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class="u-taCenter"></div><div class="profile--tab_content_container js-tab-pane tab-pane active" id="all"><div class="profile--tab_heading_container js-section-heading" data-section="Papers" id="Papers"><h3 class="profile--tab_heading_container">Papers by Snorri Thorgeirsson</h3></div><div class="js-work-strip profile--work_container" data-work-id="105178600"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/105178600/Origin_and_fate_of_oval_cells_in_dipin_induced_hepatocarcinogenesis_in_the_mouse"><img alt="Research paper thumbnail of Origin and fate of oval cells in dipin-induced hepatocarcinogenesis in the mouse" class="work-thumbnail" src="https://attachments.academia-assets.com/104703222/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/105178600/Origin_and_fate_of_oval_cells_in_dipin_induced_hepatocarcinogenesis_in_the_mouse">Origin and fate of oval cells in dipin-induced hepatocarcinogenesis in the mouse</a></div><div class="wp-workCard_item"><span>The American journal of pathology</span><span>, 1994</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">We have studied the development and differentiation of oval cells in the Dipin model of hepatocar...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">We have studied the development and differentiation of oval cells in the Dipin model of hepatocarcinogenesis in the mouse and compared this process to generation of biliary epithelial cells by bile duct ligation using light and electron microscopy. The Dipin model of hepatocarcinogenesis consists of a single injection of an alkylating drug, Dipin (1,4-bis[N,N&#39;-di(ethylene)-phosphamide]-piperazine), followed by partial hepatectomy. The Dipin treatment resulted in irreversible damage and gradual death of hepatocytes by necrosis and apoptosis. Earlier work provided evidence that regeneration of parenchyma occurred via oval cell proliferation and subsequent differentiation into hepatocytes that replaced the degenerating hepatocytes. Both autoradiographic and morphological data indicated that oval cells were derived from ductular cells of Hering canals. The first oval cells labeled with [3H]thymidine were similar in size and ultrastructure to ductular cells of Hering canals with whom...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="1ef1e1419b8e5fb7e99651aac4453ee7" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":104703222,"asset_id":105178600,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/104703222/download_file?s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="105178600"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="105178600"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 105178600; 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$(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="105178599"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/105178599/In_vivo_differentiation_of_rat_liver_oval_cells_into_hepatocytes"><img alt="Research paper thumbnail of In vivo differentiation of rat liver oval cells into hepatocytes" class="work-thumbnail" src="https://attachments.academia-assets.com/104703221/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/105178599/In_vivo_differentiation_of_rat_liver_oval_cells_into_hepatocytes">In vivo differentiation of rat liver oval cells into hepatocytes</a></div><div class="wp-workCard_item"><span>Cancer research</span><span>, Jan 15, 1989</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">The Solt-Farber protocol, in the absence of an initiating agent, was used to examine the precurso...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">The Solt-Farber protocol, in the absence of an initiating agent, was used to examine the precursor-product relationship between oval cells and hepatocytes in rat liver. The animals were administered 2-acetylaminofluorene (AAF) by gavage for 2 wk combined with partial hepatectomy 1 wk after administering AAF Two dose levels of AAF were used: 9- and 21-mg total dose for animals in Groups I and II, respectively. [3H]Thymidine was administered i.p. to one-half of the animals at Day 6 post-partial hepatectomy. Animals were sacrificed 7, 9, 11, and 13 days after surgery. Only oval cells became labeled on Day 7 in both groups. On Day 9 both labeled oval cells and labeled basophilic hepatocytes were present in Group I, whereas in Group II only oval cells remained labeled. On Days 11 and 13 both oval cells and basophilic hepatocytes were labeled in both groups. The total amount of radioactivity in Group II livers remained the same on Day 9 when only labeled oval cells were present and on Day...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="32bdca73e7d380032f9913012232910a" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":104703221,"asset_id":105178599,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/104703221/download_file?s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="105178599"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="105178599"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 105178599; 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$(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="105178598"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/105178598/Cellular_and_molecular_changes_in_the_early_stages_of_chemical_hepatocarcinogenesis_in_the_rat"><img alt="Research paper thumbnail of Cellular and molecular changes in the early stages of chemical hepatocarcinogenesis in the rat" class="work-thumbnail" src="https://attachments.academia-assets.com/104703225/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/105178598/Cellular_and_molecular_changes_in_the_early_stages_of_chemical_hepatocarcinogenesis_in_the_rat">Cellular and molecular changes in the early stages of chemical hepatocarcinogenesis in the rat</a></div><div class="wp-workCard_item"><span>Cancer research</span><span>, 1990</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">The early cellular and molecular changes in the Solt-Farber model of hepatocarcinogenesis with an...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">The early cellular and molecular changes in the Solt-Farber model of hepatocarcinogenesis with and without initiation was studied by using histochemical, immunohistochemical, and in situ hybridization techniques. Increased cellularity was observed in the periductal space in both models 32 to 56 h after partial hepatectomy. These periductal cells and Ito cells were the only cells that became labeled with tritiated thymidine in the uninitiated liver model. Forty-five to 60% of the labeled periductal cells were positive for gamma-glutamyltranspeptidase. From the periductal area the cells that were positive for antibody raised against oval cells (OV-6) infiltrated into liver parenchyma and were followed by desmin-positive Ito cells. The number of Ito cells in the uninitiated model 6 days after partial hepatectomy was 3.5 times higher in the area occupied by oval cells than elsewhere in the liver. The first alpha-fetoprotein (AFP)-positive cells appeared either as individual cells or as ...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="a1089853b2cfcf495127aef4fb2cca7c" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":104703225,"asset_id":105178598,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/104703225/download_file?s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="105178598"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="105178598"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 105178598; 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$(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="105178597"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/105178597/Low_frequency_of_p53_gene_mutation_in_tumors_induced_by_aflatoxin_B1_in_nonhuman_primates"><img alt="Research paper thumbnail of Low frequency of p53 gene mutation in tumors induced by aflatoxin B1 in nonhuman primates" class="work-thumbnail" src="https://attachments.academia-assets.com/104703233/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/105178597/Low_frequency_of_p53_gene_mutation_in_tumors_induced_by_aflatoxin_B1_in_nonhuman_primates">Low frequency of p53 gene mutation in tumors induced by aflatoxin B1 in nonhuman primates</a></div><div class="wp-workCard_item"><span>Cancer research</span><span>, Jan 15, 1992</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Aflatoxin B1 has been suggested as a causative agent for a G to T mutation at codon 249 in the p5...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Aflatoxin B1 has been suggested as a causative agent for a G to T mutation at codon 249 in the p53 gene in human hepatocellular carcinomas from southern Africa and Qidong in China. To test this hypothesis, nine tumors induced by aflatoxin B1 in nonhuman primates were analyzed for mutations in the p53 gene. These included four hepatocellular carcinomas, two cholangiocarcinomas, a spindle cell carcinoma of the bile duct, a hemangioendothelial sarcoma of the liver, and an osteogenic sarcoma of the tibia. None of the tumors showed changes at the third position of codon 249 by cleavage analysis of the HaeIII enzyme site at codon 249. A point mutation was identified in one hepatocellular carcinoma at the second position of codon 175 (G to T transversion) by sequencing analysis of the four conserved domains (II to V) in the p53 gene. These data suggest that mutations in the p53 gene are not necessary in aflatoxin B1 induced hepatocarcinogenesis in nonhuman primates. The occurrence of mutat...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="9cdcdd208b8d909f2f09041d2047c101" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":104703233,"asset_id":105178597,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/104703233/download_file?s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="105178597"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="105178597"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 105178597; 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$(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="105178596"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/105178596/DLC_1_operates_as_a_tumor_suppressor_gene_in_human_non_small_cell_lung_carcinomas"><img alt="Research paper thumbnail of DLC-1 operates as a tumor suppressor gene in human non-small cell lung carcinomas" class="work-thumbnail" src="https://attachments.academia-assets.com/104703230/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/105178596/DLC_1_operates_as_a_tumor_suppressor_gene_in_human_non_small_cell_lung_carcinomas">DLC-1 operates as a tumor suppressor gene in human non-small cell lung carcinomas</a></div><div class="wp-workCard_item"><span>Oncogene</span><span>, Jan 19, 2004</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">The deleted in liver cancer (DLC-1) gene at chromosome 8p21-22 is altered mainly by genomic delet...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">The deleted in liver cancer (DLC-1) gene at chromosome 8p21-22 is altered mainly by genomic deletion or aberrant promoter methylation in a large number of human cancers such as breast, liver, colon and prostate and is known to have an inhibitory effect on breast and liver tumor cell growth. Given the high frequency of deletion involving region 8p21-22 in human non-small cell lung carcinoma (NSCLC), we examined alterations of DLC-1 in a series of primary tumors and tumor cell lines and tested effects of DLC-1 on tumor cell growth. A significant decrease or absence of the DLC-1 mRNA expression was found in 95% of primary NSCLC (20/21) and 58% of NSCLC cell lines (11/19). Transcriptional silencing of DLC-1 was primarily associated with aberrant DNA methylation, rather than genomic deletion as 5-aza-2&#39;-deoxycytidine induced reactivation of DLC-1 expression in 82% (9/11) NSCLC cell lines showing downregulated DLC-1. It was further evidenced by an aberrant DLC-1 promoter methylation p...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="96407c98a997cbb3b85e10ccf1353c35" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":104703230,"asset_id":105178596,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/104703230/download_file?s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="105178596"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="105178596"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 105178596; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=105178596]").text(description); $(".js-view-count[data-work-id=105178596]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 105178596; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='105178596']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-a9bf3a2bc8c89fa2a77156577594264ee8a0f214d74241bc0fcd3f69f8d107ac.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); 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$(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="105178595"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/105178595/Expression_of_hepatic_transcription_factors_during_liver_development_and_oval_cell_differentiation"><img alt="Research paper thumbnail of Expression of hepatic transcription factors during liver development and oval cell differentiation" class="work-thumbnail" src="https://attachments.academia-assets.com/104703211/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/105178595/Expression_of_hepatic_transcription_factors_during_liver_development_and_oval_cell_differentiation">Expression of hepatic transcription factors during liver development and oval cell differentiation</a></div><div class="wp-workCard_item"><span>The Journal of cell biology</span><span>, 1994</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">The oval cells are thought to be the progeny of a liver stem cell compartment and strong evidence...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">The oval cells are thought to be the progeny of a liver stem cell compartment and strong evidence now exists indicating that these cells can participate in liver regeneration by differentiating into different hepatic lineages. To better understand the regulation of this process we have studied the expression of liver-enriched transcriptional factors (HNF1 alpha and HNF1 beta, HNF3 alpha, HNF3 beta, and HNF3 gamma, HNF4, C/EBP, C/EBP beta, and DBP) in an experimental model of oval cell proliferation and differentiation and compared the expression of these factors to that observed during late stages of hepatic ontogenesis. The steady-state mRNA levels of four (HNF1 alpha, HNF3 alpha, HNF4, and C/EBP beta) &quot;liver-enriched&quot; transcriptional factors gradually decrease during the late period of embryonic liver development while three factors (HNF1 beta, HNF3 beta, and DBP) increase. In the normal adult rat liver the expression of all the transcription factors are restricted to th...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="64ad9b4e725e84d8fd0d1e14bd3e4220" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":104703211,"asset_id":105178595,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/104703211/download_file?s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="105178595"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="105178595"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 105178595; 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$(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="105178594"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/105178594/The_recombinant_proregion_of_transforming_growth_factor_beta1_latency_associated_peptide_inhibits_active_transforming_growth_factor_beta1_in_transgenic_mice"><img alt="Research paper thumbnail of The recombinant proregion of transforming growth factor beta1 (latency-associated peptide) inhibits active transforming growth factor beta1 in transgenic mice" class="work-thumbnail" src="https://attachments.academia-assets.com/104703220/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/105178594/The_recombinant_proregion_of_transforming_growth_factor_beta1_latency_associated_peptide_inhibits_active_transforming_growth_factor_beta1_in_transgenic_mice">The recombinant proregion of transforming growth factor beta1 (latency-associated peptide) inhibits active transforming growth factor beta1 in transgenic mice</a></div><div class="wp-workCard_item"><span>Proceedings of the National Academy of Sciences</span><span>, 1996</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">All three isoforms of transforming growth factors beta (TGF-betal, TGF-beta2, and TGF-beta3) are ...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">All three isoforms of transforming growth factors beta (TGF-betal, TGF-beta2, and TGF-beta3) are secreted as latent complexes and activated extracellularly, leading to the release of the mature cytokines from their noncovalently associated proregions, also known as latency-associated peptides (LAPs). The LAP region of TGF-beta1 was expressed in a baculovirus expression system and purified to homogeneity. In vitro assays of growth inhibition and gene induction mediated by TGF-beta3 demonstrate that recombinant TGF-beta1 LAP is a potent inhibitor of the activities of TGF-betal, -beta2, and -beta3. Effective dosages of LAP for 50% neutralization of TGF-beta activities range from 4.7- to 80-fold molar excess depending on the TGF-beta isoform and activity examined. Using 125I-labeled LAP, we show that the intraperitoneal application route is effective for systemic administration of LAP. Comparison of concentrations of LAP in tissues shows a homogenous pattern in most organs with the exce...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="1260bad5f2e669914fd54d9444cc863e" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":104703220,"asset_id":105178594,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/104703220/download_file?s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="105178594"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="105178594"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 105178594; 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dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "1260bad5f2e669914fd54d9444cc863e" } } $('.js-work-strip[data-work-id=105178594]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":105178594,"title":"The recombinant proregion of transforming growth factor beta1 (latency-associated peptide) inhibits active transforming growth factor beta1 in transgenic mice","internal_url":"https://www.academia.edu/105178594/The_recombinant_proregion_of_transforming_growth_factor_beta1_latency_associated_peptide_inhibits_active_transforming_growth_factor_beta1_in_transgenic_mice","owner_id":43593595,"coauthors_can_edit":true,"owner":{"id":43593595,"first_name":"Snorri","middle_initials":null,"last_name":"Thorgeirsson","page_name":"SnorriThorgeirsson","domain_name":"independent","created_at":"2016-02-20T12:48:37.482-08:00","display_name":"Snorri Thorgeirsson","url":"https://independent.academia.edu/SnorriThorgeirsson"},"attachments":[{"id":104703220,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/104703220/thumbnails/1.jpg","file_name":"d5c0aabd83ba2a2365e1646fa7fae45a83d6.pdf","download_url":"https://www.academia.edu/attachments/104703220/download_file","bulk_download_file_name":"The_recombinant_proregion_of_transformin.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/104703220/d5c0aabd83ba2a2365e1646fa7fae45a83d6-libre.pdf?1690975446=\u0026response-content-disposition=attachment%3B+filename%3DThe_recombinant_proregion_of_transformin.pdf\u0026Expires=1740537650\u0026Signature=ehY5PvjpmsSMLqenhPtqCrxTIc45BAY4-dYDXoTrMHekJ6KUlz3XnvlXKyoIhav~fmRdzuGbAcXMPC992vozykkaA9CPzawlyV7MY1zPU5KSpS-ZVCR4QSqXyY0IsquGaw3hv7~ZnkhWertLnyHBh-awN4E9MqoQPB8Py~Oc1S5Fu2xd9e~w6ooqFRmq7w--ASTDwHGYKUkN9LSX8W2OYLOOPftXgniSTVuM5drwHEhb-p3gEVcauckjjmbs4RhqNNp9Czu1cYFoxyvTJbmv2r8wctmf9R4fV575oigRWKYTiGWqQO8LSCZC~SllOS7YNfDXdT4vIYy~1OKhc1cyTA__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="105178593"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/105178593/Gene_expression_profiling_demonstrates_that_TGF_%CE%B21_signals_exclusively_through_receptor_complexes_involving_Alk5_and_identifies_targets_of_TGF_%CE%B2_signaling"><img alt="Research paper thumbnail of Gene expression profiling demonstrates that TGF-β1 signals exclusively through receptor complexes involving Alk5 and identifies targets of TGF-β signaling" class="work-thumbnail" src="https://attachments.academia-assets.com/104703209/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/105178593/Gene_expression_profiling_demonstrates_that_TGF_%CE%B21_signals_exclusively_through_receptor_complexes_involving_Alk5_and_identifies_targets_of_TGF_%CE%B2_signaling">Gene expression profiling demonstrates that TGF-β1 signals exclusively through receptor complexes involving Alk5 and identifies targets of TGF-β signaling</a></div><div class="wp-workCard_item"><span>Physiological Genomics</span><span>, 2005</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Transforming growth factor-β1 (TGF-β) regulates cellular functions like proliferation, differenti...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Transforming growth factor-β1 (TGF-β) regulates cellular functions like proliferation, differentiation, and apoptosis. On the cell surface, TGF-β binds to receptor complexes consisting of TGF-β receptor type II (TβRII) and activin-like kinase receptor-5 (Alk5), and the downstream signaling is transduced by Smad and MAPK proteins. Recent data have shown that alternative receptor combinations aside from the classical pairing of TβRII/Alk5 can be relevant for TGF-β signaling. We have screened for alternative receptors for TGF-β and also for gene targets of TGF-β signaling, by performing functional assays and microarray analysis in murine embryonic fibroblast (MEF) cell lines lacking Alk5. Data from TGF-β-stimulated Alk5−/− cells show them to be completely unaffected by TGF-β. Additionally, 465 downstream targets of Alk5 signaling were identified when comparing Alk5−/− or TGF-β-stimulated Alk5+/+ MEFs with unstimulated Alk5+/+ cells. Our results demonstrate that, in MEFs, TGF-β signals ...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="631f144eb9651d336307d612cfd9c9e7" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":104703209,"asset_id":105178593,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/104703209/download_file?s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="105178593"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="105178593"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 105178593; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=105178593]").text(description); $(".js-view-count[data-work-id=105178593]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 105178593; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='105178593']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-a9bf3a2bc8c89fa2a77156577594264ee8a0f214d74241bc0fcd3f69f8d107ac.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "631f144eb9651d336307d612cfd9c9e7" } } $('.js-work-strip[data-work-id=105178593]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":105178593,"title":"Gene expression profiling demonstrates that TGF-β1 signals exclusively through receptor complexes involving Alk5 and identifies targets of TGF-β signaling","internal_url":"https://www.academia.edu/105178593/Gene_expression_profiling_demonstrates_that_TGF_%CE%B21_signals_exclusively_through_receptor_complexes_involving_Alk5_and_identifies_targets_of_TGF_%CE%B2_signaling","owner_id":43593595,"coauthors_can_edit":true,"owner":{"id":43593595,"first_name":"Snorri","middle_initials":null,"last_name":"Thorgeirsson","page_name":"SnorriThorgeirsson","domain_name":"independent","created_at":"2016-02-20T12:48:37.482-08:00","display_name":"Snorri Thorgeirsson","url":"https://independent.academia.edu/SnorriThorgeirsson"},"attachments":[{"id":104703209,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/104703209/thumbnails/1.jpg","file_name":"physiolgenomics.00303.pdf","download_url":"https://www.academia.edu/attachments/104703209/download_file","bulk_download_file_name":"Gene_expression_profiling_demonstrates_t.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/104703209/physiolgenomics.00303-libre.pdf?1690975448=\u0026response-content-disposition=attachment%3B+filename%3DGene_expression_profiling_demonstrates_t.pdf\u0026Expires=1740537650\u0026Signature=e0AuW~nnzg9SsVuvazNNcrBQELNQ3hK5IGeOt1iKpdJG1lSVpzfwMUYmUwbBikhnvzAOX~0oA786tL8af6H3khqfNa4WwhyM2nIWbvIG8t0C1i66JXtGBuvf0ZieeOJENnED399oosvtcpO~qJR67UXKlXHqooVKUv0Et36zYa3fwSh17Q9UaClNgV1gxohqcyjlA1-2VZu7k21SDMjXyQ8LtR5sfWo1MEp5456jAl821xzEmwnjUUrt0U0tIHsXrmpB7UX1euTgWft1NLChMQlDCnFOUU~XJ5GT7wUlk7XuKgRYRSJ6PdEWOOUWpBCNoendRM6CpO9YgGCRvGPTsA__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="105178592"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/105178592/Sixty_five_gene_based_risk_score_classifier_predicts_overall_survival_in_hepatocellular_carcinoma"><img alt="Research paper thumbnail of Sixty-five gene-based risk score classifier predicts overall survival in hepatocellular carcinoma" class="work-thumbnail" src="https://attachments.academia-assets.com/104703239/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/105178592/Sixty_five_gene_based_risk_score_classifier_predicts_overall_survival_in_hepatocellular_carcinoma">Sixty-five gene-based risk score classifier predicts overall survival in hepatocellular carcinoma</a></div><div class="wp-workCard_item"><span>Hepatology</span><span>, 2012</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Clinical application of the prognostic gene expression signature has been delayed due to the larg...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Clinical application of the prognostic gene expression signature has been delayed due to the large number of genes and complexity of prediction algorithms. In current study, we aim to develop an easy-to-use risk score with a limited number of genes that can robustly predict prognosis of patients with HCC. The risk score was developed by using Cox coefficient values of 65 genes in the training set (n=139) and its robustness was validated in test sets (n=292). The risk score was a highly significant predictor of overall survival (OS) in the first test cohort (P = 5.6 × 10-5 , n = 100) and the second test cohort (P = 5.0 × 10-5 , n = 192). In multivariate analysis, the risk score was significant risk factor among clinical variables examined together (hazard ratio [HR], 1.36; 95% confidential interval [CI], 1.13-1.64; P = 0.001 for OS). Conclusion-The risk score classifier we have developed can identify two clinically distinct HCC subtypes at early and late stage of the disease in a simple and highly reproducible manner across multiple data sets.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="05bc2c8d147b497769e59062cefea226" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":104703239,"asset_id":105178592,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/104703239/download_file?s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="105178592"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="105178592"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 105178592; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=105178592]").text(description); $(".js-view-count[data-work-id=105178592]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 105178592; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='105178592']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-a9bf3a2bc8c89fa2a77156577594264ee8a0f214d74241bc0fcd3f69f8d107ac.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "05bc2c8d147b497769e59062cefea226" } } $('.js-work-strip[data-work-id=105178592]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":105178592,"title":"Sixty-five gene-based risk score classifier predicts overall survival in hepatocellular carcinoma","internal_url":"https://www.academia.edu/105178592/Sixty_five_gene_based_risk_score_classifier_predicts_overall_survival_in_hepatocellular_carcinoma","owner_id":43593595,"coauthors_can_edit":true,"owner":{"id":43593595,"first_name":"Snorri","middle_initials":null,"last_name":"Thorgeirsson","page_name":"SnorriThorgeirsson","domain_name":"independent","created_at":"2016-02-20T12:48:37.482-08:00","display_name":"Snorri Thorgeirsson","url":"https://independent.academia.edu/SnorriThorgeirsson"},"attachments":[{"id":104703239,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/104703239/thumbnails/1.jpg","file_name":"pmc4060518.pdf","download_url":"https://www.academia.edu/attachments/104703239/download_file","bulk_download_file_name":"Sixty_five_gene_based_risk_score_classif.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/104703239/pmc4060518-libre.pdf?1690975436=\u0026response-content-disposition=attachment%3B+filename%3DSixty_five_gene_based_risk_score_classif.pdf\u0026Expires=1740537650\u0026Signature=e17wWf5H90UjuA0ywWRW10FYIrbvnYSvsdr6j2x8hNRMgZA93QENRGJxGWcQexLeQAAyEINt5pF-Ud9eyMjWq7nLy7r-j4TGw9vuogO3yhbwh9d36CybpFuRIlMXoxpXJk20F0O7ONfxLLsWKPJbAecdGFJOv9UrP0KdDYJuBU2Qo6cnbx0fCJyc~7FUMHbs4AeovOyxTyGJe7IbcgfgEMnJpyc~Curu83gUo2fgAzEn-x7D5Uz8j26pG8KmKIb8s8DoeCo0mQ6QM4FrNvq4UVcuJVmcHU4S~eOyCY~y0hBOgint2ihv3ukkSPX~VD6GWPP-OPiyVjWZ0wyA7X5fCA__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="105178591"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/105178591/Hepatic_precursors_derived_from_murine_embryonic_stem_cells_contribute_to_regeneration_of_injured_liver"><img alt="Research paper thumbnail of Hepatic precursors derived from murine embryonic stem cells contribute to regeneration of injured liver" class="work-thumbnail" src="https://attachments.academia-assets.com/104703224/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/105178591/Hepatic_precursors_derived_from_murine_embryonic_stem_cells_contribute_to_regeneration_of_injured_liver">Hepatic precursors derived from murine embryonic stem cells contribute to regeneration of injured liver</a></div><div class="wp-workCard_item"><span>Hepatology</span><span>, 2006</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="a70a71a302432eb4cbda4b24da47be4b" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":104703224,"asset_id":105178591,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/104703224/download_file?s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="105178591"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="105178591"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 105178591; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=105178591]").text(description); $(".js-view-count[data-work-id=105178591]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 105178591; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='105178591']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-a9bf3a2bc8c89fa2a77156577594264ee8a0f214d74241bc0fcd3f69f8d107ac.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "a70a71a302432eb4cbda4b24da47be4b" } } $('.js-work-strip[data-work-id=105178591]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":105178591,"title":"Hepatic precursors derived from murine embryonic stem cells contribute to regeneration of injured liver","internal_url":"https://www.academia.edu/105178591/Hepatic_precursors_derived_from_murine_embryonic_stem_cells_contribute_to_regeneration_of_injured_liver","owner_id":43593595,"coauthors_can_edit":true,"owner":{"id":43593595,"first_name":"Snorri","middle_initials":null,"last_name":"Thorgeirsson","page_name":"SnorriThorgeirsson","domain_name":"independent","created_at":"2016-02-20T12:48:37.482-08:00","display_name":"Snorri Thorgeirsson","url":"https://independent.academia.edu/SnorriThorgeirsson"},"attachments":[{"id":104703224,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/104703224/thumbnails/1.jpg","file_name":"20070122-fulltext.pdf","download_url":"https://www.academia.edu/attachments/104703224/download_file","bulk_download_file_name":"Hepatic_precursors_derived_from_murine_e.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/104703224/20070122-fulltext-libre.pdf?1690975438=\u0026response-content-disposition=attachment%3B+filename%3DHepatic_precursors_derived_from_murine_e.pdf\u0026Expires=1740537650\u0026Signature=B0RJCwNRR2V31i3byE4sr69gHusxEjGw2TF2IkImUGtA5YSkoboAfp7fdRu53O4ZCX3cG5vSdgrbEQSig0DOAmJVk0k-D4SVyZmXk5eXjaAXaVl1futCRNxLJ72zAdgEveJURIqPlIRUTsU5-xmZRMvsz~qt7BN7-zyfbR6suLtUCbhkYog5jUKTn7XEK2fyvEH-cXf2LCoju1YWPkQwtnXijsT7I6G5KQ~7mRVf9oF1QvMErfjYZ1A-xSj24-gHSeeVPO4r2gaJzyun0wvXwbgyxGoFt~oAFX8xqVrPxbE4oVm1DQFE7ouRxM1ZODFvdtgF9KwKBVe131x99RhgJw__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="105178590"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/105178590/DLC_1_a_Rho_GTPase_activating_protein_with_tumor_suppressor_function_is_essential_for_embryonic_development"><img alt="Research paper thumbnail of DLC-1, a Rho GTPase-activating protein with tumor suppressor function, is essential for embryonic development" class="work-thumbnail" src="https://attachments.academia-assets.com/104703231/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/105178590/DLC_1_a_Rho_GTPase_activating_protein_with_tumor_suppressor_function_is_essential_for_embryonic_development">DLC-1, a Rho GTPase-activating protein with tumor suppressor function, is essential for embryonic development</a></div><div class="wp-workCard_item"><span>FEBS Letters</span><span>, 2005</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">DLC-1 (deleted in liver cancer 1) is a Rho GTPaseactivating protein that is able to inhibit cell ...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">DLC-1 (deleted in liver cancer 1) is a Rho GTPaseactivating protein that is able to inhibit cell growth and suppress tumorigenesis. We have used homologous recombination to inactivate the mouse DLC-1 gene (Arhgap7). Mice heterozygous for the targeted allele were phenotypically normal, but homozygous mutant embryos did not survive beyond 10.5 days post coitum. Histological analysis revealed that DLC-1 À/À embryos had defects in the neural tube, brain, heart, and placenta. Cultured fibroblasts from DLC-1-deficient embryos displayed alterations in the organization of actin filaments and focal adhesions.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="3dba4ad413937729d8d955234a4e99e6" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":104703231,"asset_id":105178590,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/104703231/download_file?s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="105178590"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="105178590"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 105178590; 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$(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="105178589"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/105178589/Role_of_Growth_Hormone_GH_in_Liver_Regeneration"><img alt="Research paper thumbnail of Role of Growth Hormone (GH) in Liver Regeneration" class="work-thumbnail" src="https://attachments.academia-assets.com/104703208/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/105178589/Role_of_Growth_Hormone_GH_in_Liver_Regeneration">Role of Growth Hormone (GH) in Liver Regeneration</a></div><div class="wp-workCard_item"><span>Endocrinology</span><span>, 2004</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Liver regeneration is a fundamental mechanism by which the liver responds to injury. This process...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Liver regeneration is a fundamental mechanism by which the liver responds to injury. This process is regulated by endogenous growth factors and cytokines, and it involves proliferation of all mature cells that exist within the intact organ. To understand the role of the GH/IGF-I axis in liver regeneration, we performed partial hepatectomies in three groups of mice: GH antagonist (GHa) transgenic mice, in which the action of GH is blocked; liver IGF-I-deficient mice that lack IGF-I specifically in the liver and also lack the acid-labile subunit (ALS; LID+ALSKO mice), in which IGF-I levels are very low and GH secretion is increased; and control mice. Interestingly, the survival rate of GHa transgenic mice was dramatically reduced after partial hepatectomy (57%) compared with the survival rate of controls (100%) or LID+ALSKO mice (88%). In control mice, the liver was completely regenerated after 4 d, whereas liver regeneration required 7 d in LID+ALSKO mice. In contrast, in GHa mice, l...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="27ab88e0cfe42271066f809b4b9687d7" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":104703208,"asset_id":105178589,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/104703208/download_file?s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="105178589"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="105178589"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 105178589; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=105178589]").text(description); $(".js-view-count[data-work-id=105178589]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 105178589; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='105178589']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-a9bf3a2bc8c89fa2a77156577594264ee8a0f214d74241bc0fcd3f69f8d107ac.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); 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$(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="105178588"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/105178588/Genomic_copy_number_alterations_with_transcriptional_deregulation_at_6p_identify_an_aggressive_HCC_phenotype"><img alt="Research paper thumbnail of Genomic copy number alterations with transcriptional deregulation at 6p identify an aggressive HCC phenotype" class="work-thumbnail" src="https://attachments.academia-assets.com/104703207/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/105178588/Genomic_copy_number_alterations_with_transcriptional_deregulation_at_6p_identify_an_aggressive_HCC_phenotype">Genomic copy number alterations with transcriptional deregulation at 6p identify an aggressive HCC phenotype</a></div><div class="wp-workCard_item"><span>Carcinogenesis</span><span>, 2013</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Genomic analyses have revealed the enormous heterogeneity in essentially all cancer types. Howeve...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Genomic analyses have revealed the enormous heterogeneity in essentially all cancer types. However, the identification of precise subtypes, which are biologically informative and clinically useful, remains a challenge. The application of integrative analysis of multilayered genomic profiles to define the chromosomal regions of genomic copy number alterations with concomitant transcriptional deregulation is posited to provide a promising strategy to identify driver targets. In this study, we performed an integrative analysis of the DNA copy numbers and gene expression profiles of hepatocellular carcinoma (HCC). By comparing DNA copy numbers between HCC subtypes based on gene expression pattern, we revealed the DNA copy number alteration with concordant gene expression changes at 6p21-p24 particularly in the HCC subtype of aggressive phenotype without expressing stemness genes. Among the genes at 6p21-p24, we identified IER3 as a potential driver. The clinical utility of IER3 copy numbers was demonstrated by validating its clinical correlation with independent cohorts. In addition, short hairpin RNA-mediated knockdown experiment revealed the functional relevance of IER3 in liver cancer progression. In conclusion, our results suggest that genomic copy number alterations with transcriptional deregulation at 6p21-p24 identify an aggressive HCC phenotype and a novel functional biomarker.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="0011fc4fcad1a2db3cc4e784ddc94836" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":104703207,"asset_id":105178588,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/104703207/download_file?s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="105178588"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="105178588"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 105178588; 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$(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="105178587"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/105178587/Short_term_carcinogenicity_testing_of_2_amino_1_methyl_6_phenylimidazo_4_5_b_pyridine_PhIP_and_2_amino_3_methylimidazo_4_5_f_quinoline_IQ_in_E%CE%BC_pim_1_transgenic_mice"><img alt="Research paper thumbnail of Short-term carcinogenicity testing of 2-amino-1-methyl-6-phenylimidazo[4, 5- b ]pyridine (PhIP) and 2-amino-3-methylimidazo[4, 5-f]quinoline (IQ) in Eμ- pim -1 transgenic mice" class="work-thumbnail" src="https://attachments.academia-assets.com/104703219/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/105178587/Short_term_carcinogenicity_testing_of_2_amino_1_methyl_6_phenylimidazo_4_5_b_pyridine_PhIP_and_2_amino_3_methylimidazo_4_5_f_quinoline_IQ_in_E%CE%BC_pim_1_transgenic_mice">Short-term carcinogenicity testing of 2-amino-1-methyl-6-phenylimidazo[4, 5- b ]pyridine (PhIP) and 2-amino-3-methylimidazo[4, 5-f]quinoline (IQ) in Eμ- pim -1 transgenic mice</a></div><div class="wp-workCard_item"><span>Carcinogenesis</span><span>, 1996</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">The usefulness of transgenic E(j.-pi/n-l mice over-expressing the pim-1 oncogene in lymphoid tiss...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">The usefulness of transgenic E(j.-pi/n-l mice over-expressing the pim-1 oncogene in lymphoid tissues, as sensitive test organisms was studied in a short-term carcinogenicity study. The mice were fed standard diet Altromin 1314 supplemented either with 0.03% 2-amino-l-methyl-6phenylimidazo[4,5-ft]pyridine (PhIP) for 7 months or with 0.03% 2-amino-3-methylimidazo[4,5-/|quinoline (IQ) for 6 months. PhIP and IQ are heterocyclic amines formed during cooking of meat and fish and are mutagenic to bacteria and cultured mammalian cells. PhIP is a potent mouse lymphomagen, while IQ is a liver carcinogen and also causes lung tumors and tumors of the forestomach in mice. We found that transgenic E\i-pim-l mice are highly susceptible to PhIP induced lymphomagenesis but do not respond to the IQ treatment PhIP feeding of E\i-pim-l mice not only increased the total number of T-ceU lymphomas but also decreased the latency time compared to either transgenic or wild-type controls. The effect was most pronounced in the treated female E\i-pim-l mice, which showed a higher incidence of PhIP induced T-cell lymphomas than transgenic males and a strongly reduced latency period after PhIP treatment compared to nontransgenic mice. Our results suggest that the transgenic Eji-/H/n-l mouse may be a useful model for short-term carcinogenicity screening of potential genotoxic carcinogens having the lymphoid system as target tissue. The carcinogen IQ which does not have the lymphoid system as a target was not recognized in this model.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="2dadb16472ac6355a47d02e033e7ad11" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":104703219,"asset_id":105178587,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/104703219/download_file?s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="105178587"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="105178587"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 105178587; 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At present, it is challenging to identify patients with high risk of recurrence, which would warrant additional therapies. In this study, we sought to analyze a recently developed metastasis-related gene signature for its utility in predicting HCC survival, using 2 independent cohorts consisting of a total of 386 patients who received radical resection. Cohort 1 contained 247 predominantly HBV-positive cases analyzed with an Affymetrix platform, whereas cohort 2 contained 139 cases with mixed etiology analyzed with the NCI Oligo Set microarray platform. We employed a survival risk prediction algorithm with training, test, and independent cross-validation strategies and found that the gene signature is predictive of overall and disease-free survival. Importantly, risk was significantly predicted independently of clinical characteristics and microarray platform. In add...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="bdd3fc53614333cef24ca76a888f2c7d" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":104703205,"asset_id":105178586,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/104703205/download_file?s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="105178586"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="105178586"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 105178586; 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In this issue of Cancer Cell, Pilati and colleagues present an integrative multi-''omics''-based analysis of HCA and identify recurrent genetic alterations associated with adenoma-carcinoma transition and new drugable targets.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="f2a480d930a665340473793957d8b589" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":104703218,"asset_id":105178585,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/104703218/download_file?s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="105178585"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="105178585"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 105178585; 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$(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="105178584"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/105178584/Origin_and_Structural_Evolution_of_the_Early_Proliferating_Oval_Cells_in_Rat_Liver"><img alt="Research paper thumbnail of Origin and Structural Evolution of the Early Proliferating Oval Cells in Rat Liver" class="work-thumbnail" src="https://attachments.academia-assets.com/104703232/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/105178584/Origin_and_Structural_Evolution_of_the_Early_Proliferating_Oval_Cells_in_Rat_Liver">Origin and Structural Evolution of the Early Proliferating Oval Cells in Rat Liver</a></div><div class="wp-workCard_item"><span>The American Journal of Pathology</span><span>, 2001</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="e46984b6947b0a810676ac8fda25f318" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":104703232,"asset_id":105178584,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/104703232/download_file?s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="105178584"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="105178584"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 105178584; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=105178584]").text(description); $(".js-view-count[data-work-id=105178584]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 105178584; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='105178584']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-a9bf3a2bc8c89fa2a77156577594264ee8a0f214d74241bc0fcd3f69f8d107ac.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); 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$(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="105178538"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/105178538/Alterations_of_tumor_suppressor_genes_and_allelic_losses_in_human_hepatocellular_carcinomas_in_China"><img alt="Research paper thumbnail of Alterations of tumor suppressor genes and allelic losses in human hepatocellular carcinomas in China" class="work-thumbnail" src="https://attachments.academia-assets.com/104703177/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/105178538/Alterations_of_tumor_suppressor_genes_and_allelic_losses_in_human_hepatocellular_carcinomas_in_China">Alterations of tumor suppressor genes and allelic losses in human hepatocellular carcinomas in China</a></div><div class="wp-workCard_item"><span>Cancer research</span><span>, 1994</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Aflatoxin B1 has been suggested as a causative agent for a G to T mutation at codon 249 in the p5...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Aflatoxin B1 has been suggested as a causative agent for a G to T mutation at codon 249 in the p53 gene in human hepatocellular carcinomas (HCC) from southern Africa and Qidong in China. The objective of the present work was to test the hypothesis that exposure to aflatoxin B1 either alone or coincident with other environmental carcinogens might be associated with allelic losses occurring during development of human hepatocarcinogenesis in China. The HCCs were obtained from two different areas in China: Qidong, where exposure to hepatitis B virus (HBV) and aflatoxin B1 is high; and Beijing, where exposure to HBV is high but that of aflatoxin B1 is low. We analyzed the tumors for mutations in the p53 gene and loss of heterozygosity for the p53, Rb, and APC genes and at marker loci on chromosomes 4, 13, and 16. Frequencies of mutation, loss, and aberration (mutation and loss) of the p53 gene in 25 HCCs from Qidong were 60, 58, and 80%, respectively. The frequencies in 9 HCCs from Beij...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="486ff567ad2fbc064892b31ae6663a64" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":104703177,"asset_id":105178538,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/104703177/download_file?s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="105178538"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="105178538"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 105178538; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=105178538]").text(description); $(".js-view-count[data-work-id=105178538]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 105178538; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='105178538']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-a9bf3a2bc8c89fa2a77156577594264ee8a0f214d74241bc0fcd3f69f8d107ac.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "486ff567ad2fbc064892b31ae6663a64" } } $('.js-work-strip[data-work-id=105178538]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":105178538,"title":"Alterations of tumor suppressor genes and allelic losses in human hepatocellular carcinomas in China","internal_url":"https://www.academia.edu/105178538/Alterations_of_tumor_suppressor_genes_and_allelic_losses_in_human_hepatocellular_carcinomas_in_China","owner_id":43593595,"coauthors_can_edit":true,"owner":{"id":43593595,"first_name":"Snorri","middle_initials":null,"last_name":"Thorgeirsson","page_name":"SnorriThorgeirsson","domain_name":"independent","created_at":"2016-02-20T12:48:37.482-08:00","display_name":"Snorri Thorgeirsson","url":"https://independent.academia.edu/SnorriThorgeirsson"},"attachments":[{"id":104703177,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/104703177/thumbnails/1.jpg","file_name":"281.full.pdf","download_url":"https://www.academia.edu/attachments/104703177/download_file","bulk_download_file_name":"Alterations_of_tumor_suppressor_genes_an.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/104703177/281.full-libre.pdf?1690975459=\u0026response-content-disposition=attachment%3B+filename%3DAlterations_of_tumor_suppressor_genes_an.pdf\u0026Expires=1740537650\u0026Signature=bHKeqAOVlDrzM7mJhauUsJT4xMT9K6ToPNEldnEZZSvhelwaddVM-Lu2bL0~5vyWS9SdQM5WmLF0KTgNi6WiHy43sJonllsnFD2bR3FsIJvNK~vmIg93~QfGFlrvwM3YaMzdem9f0SroCks4zR-KLH2~L1hlJudP9pIkc9cVbMW4LEWCnvUEvvHKT7bagyCarcKTn3ZyF8HOaiJLpWg0F~DydfouBaOYBuP4a2ck3YibcdZSx6HIXb80Np7VlCOqTnzGtr3~qls3TTcSZCSTMaPZSQGekBZHvcZnkYsX2KbIUHBUp-n0rP8nIVurwbv0O6r-NVXKO31J8yubDD6ajQ__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="101056351"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/101056351/Hepatic_regeneration_in_vitamin_A_deficient_rats_changes_in_the_expression_of_transforming_growth_factor_alpha_epidermal_growth_factor_receptor_and_retinoic_acid_receptors_alpha_and_beta"><img alt="Research paper thumbnail of Hepatic regeneration in vitamin A-deficient rats: changes in the expression of transforming growth factor alpha/epidermal growth factor receptor and retinoic acid receptors alpha and beta" class="work-thumbnail" src="https://attachments.academia-assets.com/101701347/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/101056351/Hepatic_regeneration_in_vitamin_A_deficient_rats_changes_in_the_expression_of_transforming_growth_factor_alpha_epidermal_growth_factor_receptor_and_retinoic_acid_receptors_alpha_and_beta">Hepatic regeneration in vitamin A-deficient rats: changes in the expression of transforming growth factor alpha/epidermal growth factor receptor and retinoic acid receptors alpha and beta</a></div><div class="wp-workCard_item"><span>Cell growth & differentiation : the molecular biology journal of the American Association for Cancer Research</span><span>, 1994</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">We have studied the effect of vitamin A deficiency on the expression of transforming growth facto...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">We have studied the effect of vitamin A deficiency on the expression of transforming growth factor alpha (TGF-alpha), hepatocyte growth factor, acidic fibroblast growth factor, and TGF-beta 1 after partial hepatectomy of vitamin A-supplemented and vitamin A-deficient rats. In addition, the expressions of epidermal growth factor receptor and retinoic acid receptors alpha (RAR alpha) and beta (RAR beta) were studied. Partial hepatectomy was performed on the animals from the vitamin A-supplemented and -deficient groups at the age of 10 weeks when the weights of the animals on the deficient diet had reached a plateau. Two animals from each group were sacrificed before the operation and also 12, 24, 48, and 72 h and 5 days after the operation. Partial hepatectomy of the vitamin A-deficient rats leads to a focal necrosis of liver followed by a rapid restoration of liver mass. Expression of the TGF-alpha and epidermal growth factor receptor was highly elevated in the livers of deficient an...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="06d3ef79a3bc995ddfbf328726e507a2" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":101701347,"asset_id":101056351,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/101701347/download_file?s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="101056351"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="101056351"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 101056351; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=101056351]").text(description); $(".js-view-count[data-work-id=101056351]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 101056351; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='101056351']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-a9bf3a2bc8c89fa2a77156577594264ee8a0f214d74241bc0fcd3f69f8d107ac.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); 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$(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="101056350"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/101056350/Analysis_of_c_myc_expression_in_a_human_hepatoma_cell_line"><img alt="Research paper thumbnail of Analysis of c-myc expression in a human hepatoma cell line" class="work-thumbnail" src="https://attachments.academia-assets.com/101701252/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/101056350/Analysis_of_c_myc_expression_in_a_human_hepatoma_cell_line">Analysis of c-myc expression in a human hepatoma cell line</a></div><div class="wp-workCard_item"><span>Cancer research</span><span>, 1987</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">A tumorigenic human hepatoma cell line, Hep G2, has been shown to have high steady-state levels o...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">A tumorigenic human hepatoma cell line, Hep G2, has been shown to have high steady-state levels of c-myc transcripts compared to normal human liver. We have now characterized c-myc expression in Hep G2 cells with regard to message stability, gene rearrangements, gene amplification, chromosomal translocations, promoter utilization, and the effects of protein synthesis inhibitors. We have determined that the half-life of the Hep G2 c-myc transcript is approximately 20 min and conclude that the high steady-state level of c-myc mRNA is not the result of a specific stabilization of the c-myc message but probably results from increased c-myc gene transcription. c-myc expression in Hep G2 cells appears to be constitutive, since it remains constant in different cell growth states (log phase versus nondividing cells). The high constitutive expression of the c-myc gene in Hep G2 cells could not be explained by gene amplification, gene rearrangements, or chromosomal translocations. However, ba...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="57769a99ce988fc1368e62fa3546faa6" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":101701252,"asset_id":101056350,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/101701252/download_file?s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="101056350"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="101056350"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 101056350; 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$(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> </div><div class="profile--tab_content_container js-tab-pane tab-pane" data-section-id="4649791" id="papers"><div class="js-work-strip profile--work_container" data-work-id="105178600"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/105178600/Origin_and_fate_of_oval_cells_in_dipin_induced_hepatocarcinogenesis_in_the_mouse"><img alt="Research paper thumbnail of Origin and fate of oval cells in dipin-induced hepatocarcinogenesis in the mouse" class="work-thumbnail" src="https://attachments.academia-assets.com/104703222/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/105178600/Origin_and_fate_of_oval_cells_in_dipin_induced_hepatocarcinogenesis_in_the_mouse">Origin and fate of oval cells in dipin-induced hepatocarcinogenesis in the mouse</a></div><div class="wp-workCard_item"><span>The American journal of pathology</span><span>, 1994</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">We have studied the development and differentiation of oval cells in the Dipin model of hepatocar...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">We have studied the development and differentiation of oval cells in the Dipin model of hepatocarcinogenesis in the mouse and compared this process to generation of biliary epithelial cells by bile duct ligation using light and electron microscopy. The Dipin model of hepatocarcinogenesis consists of a single injection of an alkylating drug, Dipin (1,4-bis[N,N&#39;-di(ethylene)-phosphamide]-piperazine), followed by partial hepatectomy. The Dipin treatment resulted in irreversible damage and gradual death of hepatocytes by necrosis and apoptosis. Earlier work provided evidence that regeneration of parenchyma occurred via oval cell proliferation and subsequent differentiation into hepatocytes that replaced the degenerating hepatocytes. Both autoradiographic and morphological data indicated that oval cells were derived from ductular cells of Hering canals. The first oval cells labeled with [3H]thymidine were similar in size and ultrastructure to ductular cells of Hering canals with whom...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="1ef1e1419b8e5fb7e99651aac4453ee7" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":104703222,"asset_id":105178600,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/104703222/download_file?s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="105178600"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="105178600"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 105178600; 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$(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="105178599"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/105178599/In_vivo_differentiation_of_rat_liver_oval_cells_into_hepatocytes"><img alt="Research paper thumbnail of In vivo differentiation of rat liver oval cells into hepatocytes" class="work-thumbnail" src="https://attachments.academia-assets.com/104703221/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/105178599/In_vivo_differentiation_of_rat_liver_oval_cells_into_hepatocytes">In vivo differentiation of rat liver oval cells into hepatocytes</a></div><div class="wp-workCard_item"><span>Cancer research</span><span>, Jan 15, 1989</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">The Solt-Farber protocol, in the absence of an initiating agent, was used to examine the precurso...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">The Solt-Farber protocol, in the absence of an initiating agent, was used to examine the precursor-product relationship between oval cells and hepatocytes in rat liver. The animals were administered 2-acetylaminofluorene (AAF) by gavage for 2 wk combined with partial hepatectomy 1 wk after administering AAF Two dose levels of AAF were used: 9- and 21-mg total dose for animals in Groups I and II, respectively. [3H]Thymidine was administered i.p. to one-half of the animals at Day 6 post-partial hepatectomy. Animals were sacrificed 7, 9, 11, and 13 days after surgery. Only oval cells became labeled on Day 7 in both groups. On Day 9 both labeled oval cells and labeled basophilic hepatocytes were present in Group I, whereas in Group II only oval cells remained labeled. On Days 11 and 13 both oval cells and basophilic hepatocytes were labeled in both groups. The total amount of radioactivity in Group II livers remained the same on Day 9 when only labeled oval cells were present and on Day...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="32bdca73e7d380032f9913012232910a" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":104703221,"asset_id":105178599,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/104703221/download_file?s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="105178599"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="105178599"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 105178599; 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$(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="105178598"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/105178598/Cellular_and_molecular_changes_in_the_early_stages_of_chemical_hepatocarcinogenesis_in_the_rat"><img alt="Research paper thumbnail of Cellular and molecular changes in the early stages of chemical hepatocarcinogenesis in the rat" class="work-thumbnail" src="https://attachments.academia-assets.com/104703225/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/105178598/Cellular_and_molecular_changes_in_the_early_stages_of_chemical_hepatocarcinogenesis_in_the_rat">Cellular and molecular changes in the early stages of chemical hepatocarcinogenesis in the rat</a></div><div class="wp-workCard_item"><span>Cancer research</span><span>, 1990</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">The early cellular and molecular changes in the Solt-Farber model of hepatocarcinogenesis with an...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">The early cellular and molecular changes in the Solt-Farber model of hepatocarcinogenesis with and without initiation was studied by using histochemical, immunohistochemical, and in situ hybridization techniques. Increased cellularity was observed in the periductal space in both models 32 to 56 h after partial hepatectomy. These periductal cells and Ito cells were the only cells that became labeled with tritiated thymidine in the uninitiated liver model. Forty-five to 60% of the labeled periductal cells were positive for gamma-glutamyltranspeptidase. From the periductal area the cells that were positive for antibody raised against oval cells (OV-6) infiltrated into liver parenchyma and were followed by desmin-positive Ito cells. The number of Ito cells in the uninitiated model 6 days after partial hepatectomy was 3.5 times higher in the area occupied by oval cells than elsewhere in the liver. The first alpha-fetoprotein (AFP)-positive cells appeared either as individual cells or as ...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="a1089853b2cfcf495127aef4fb2cca7c" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":104703225,"asset_id":105178598,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/104703225/download_file?s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="105178598"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="105178598"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 105178598; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=105178598]").text(description); $(".js-view-count[data-work-id=105178598]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 105178598; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='105178598']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-a9bf3a2bc8c89fa2a77156577594264ee8a0f214d74241bc0fcd3f69f8d107ac.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); 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$(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="105178597"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/105178597/Low_frequency_of_p53_gene_mutation_in_tumors_induced_by_aflatoxin_B1_in_nonhuman_primates"><img alt="Research paper thumbnail of Low frequency of p53 gene mutation in tumors induced by aflatoxin B1 in nonhuman primates" class="work-thumbnail" src="https://attachments.academia-assets.com/104703233/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/105178597/Low_frequency_of_p53_gene_mutation_in_tumors_induced_by_aflatoxin_B1_in_nonhuman_primates">Low frequency of p53 gene mutation in tumors induced by aflatoxin B1 in nonhuman primates</a></div><div class="wp-workCard_item"><span>Cancer research</span><span>, Jan 15, 1992</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Aflatoxin B1 has been suggested as a causative agent for a G to T mutation at codon 249 in the p5...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Aflatoxin B1 has been suggested as a causative agent for a G to T mutation at codon 249 in the p53 gene in human hepatocellular carcinomas from southern Africa and Qidong in China. To test this hypothesis, nine tumors induced by aflatoxin B1 in nonhuman primates were analyzed for mutations in the p53 gene. These included four hepatocellular carcinomas, two cholangiocarcinomas, a spindle cell carcinoma of the bile duct, a hemangioendothelial sarcoma of the liver, and an osteogenic sarcoma of the tibia. None of the tumors showed changes at the third position of codon 249 by cleavage analysis of the HaeIII enzyme site at codon 249. A point mutation was identified in one hepatocellular carcinoma at the second position of codon 175 (G to T transversion) by sequencing analysis of the four conserved domains (II to V) in the p53 gene. These data suggest that mutations in the p53 gene are not necessary in aflatoxin B1 induced hepatocarcinogenesis in nonhuman primates. The occurrence of mutat...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="9cdcdd208b8d909f2f09041d2047c101" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":104703233,"asset_id":105178597,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/104703233/download_file?s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="105178597"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="105178597"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 105178597; 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dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "9cdcdd208b8d909f2f09041d2047c101" } } $('.js-work-strip[data-work-id=105178597]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":105178597,"title":"Low frequency of p53 gene mutation in tumors induced by aflatoxin B1 in nonhuman primates","internal_url":"https://www.academia.edu/105178597/Low_frequency_of_p53_gene_mutation_in_tumors_induced_by_aflatoxin_B1_in_nonhuman_primates","owner_id":43593595,"coauthors_can_edit":true,"owner":{"id":43593595,"first_name":"Snorri","middle_initials":null,"last_name":"Thorgeirsson","page_name":"SnorriThorgeirsson","domain_name":"independent","created_at":"2016-02-20T12:48:37.482-08:00","display_name":"Snorri Thorgeirsson","url":"https://independent.academia.edu/SnorriThorgeirsson"},"attachments":[{"id":104703233,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/104703233/thumbnails/1.jpg","file_name":"1044.full.pdf","download_url":"https://www.academia.edu/attachments/104703233/download_file","bulk_download_file_name":"Low_frequency_of_p53_gene_mutation_in_tu.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/104703233/1044.full-libre.pdf?1690975435=\u0026response-content-disposition=attachment%3B+filename%3DLow_frequency_of_p53_gene_mutation_in_tu.pdf\u0026Expires=1740537650\u0026Signature=J2dyUSg~4C9YwSgAmq5VyiT6beEIAWtDMaCdurAkEvMzclydq2dfs5L2QRovRaIRNPnwg61R76v6OOBZQDlat6tUx0SmIJwJfKm8I6jxcVPi11Z1ENUALHC9cbAuhPI24jvbKh8UKWauawprqg88MFEdROfVg6GKPQPaGmrCpf8xlDBl6AMLilFiVI7K21kT51n5TBHKoMtGsgZ6wmcAslBCI0JI~TOPDVMEsSQmJWEgRkQMuRGQKOlu8KTOLJIpF8-u5mTR0rnCfQwehziwIgiQVhweg~KMO6FItwk0rttPOdTZKbpTeyOQWDmljJ7s1tKAHb9ttDhwpo5X4Hl34w__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="105178596"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/105178596/DLC_1_operates_as_a_tumor_suppressor_gene_in_human_non_small_cell_lung_carcinomas"><img alt="Research paper thumbnail of DLC-1 operates as a tumor suppressor gene in human non-small cell lung carcinomas" class="work-thumbnail" src="https://attachments.academia-assets.com/104703230/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/105178596/DLC_1_operates_as_a_tumor_suppressor_gene_in_human_non_small_cell_lung_carcinomas">DLC-1 operates as a tumor suppressor gene in human non-small cell lung carcinomas</a></div><div class="wp-workCard_item"><span>Oncogene</span><span>, Jan 19, 2004</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">The deleted in liver cancer (DLC-1) gene at chromosome 8p21-22 is altered mainly by genomic delet...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">The deleted in liver cancer (DLC-1) gene at chromosome 8p21-22 is altered mainly by genomic deletion or aberrant promoter methylation in a large number of human cancers such as breast, liver, colon and prostate and is known to have an inhibitory effect on breast and liver tumor cell growth. Given the high frequency of deletion involving region 8p21-22 in human non-small cell lung carcinoma (NSCLC), we examined alterations of DLC-1 in a series of primary tumors and tumor cell lines and tested effects of DLC-1 on tumor cell growth. A significant decrease or absence of the DLC-1 mRNA expression was found in 95% of primary NSCLC (20/21) and 58% of NSCLC cell lines (11/19). Transcriptional silencing of DLC-1 was primarily associated with aberrant DNA methylation, rather than genomic deletion as 5-aza-2&#39;-deoxycytidine induced reactivation of DLC-1 expression in 82% (9/11) NSCLC cell lines showing downregulated DLC-1. It was further evidenced by an aberrant DLC-1 promoter methylation p...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="96407c98a997cbb3b85e10ccf1353c35" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":104703230,"asset_id":105178596,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/104703230/download_file?s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="105178596"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="105178596"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 105178596; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=105178596]").text(description); $(".js-view-count[data-work-id=105178596]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 105178596; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='105178596']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-a9bf3a2bc8c89fa2a77156577594264ee8a0f214d74241bc0fcd3f69f8d107ac.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); 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$(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="105178595"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/105178595/Expression_of_hepatic_transcription_factors_during_liver_development_and_oval_cell_differentiation"><img alt="Research paper thumbnail of Expression of hepatic transcription factors during liver development and oval cell differentiation" class="work-thumbnail" src="https://attachments.academia-assets.com/104703211/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/105178595/Expression_of_hepatic_transcription_factors_during_liver_development_and_oval_cell_differentiation">Expression of hepatic transcription factors during liver development and oval cell differentiation</a></div><div class="wp-workCard_item"><span>The Journal of cell biology</span><span>, 1994</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">The oval cells are thought to be the progeny of a liver stem cell compartment and strong evidence...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">The oval cells are thought to be the progeny of a liver stem cell compartment and strong evidence now exists indicating that these cells can participate in liver regeneration by differentiating into different hepatic lineages. To better understand the regulation of this process we have studied the expression of liver-enriched transcriptional factors (HNF1 alpha and HNF1 beta, HNF3 alpha, HNF3 beta, and HNF3 gamma, HNF4, C/EBP, C/EBP beta, and DBP) in an experimental model of oval cell proliferation and differentiation and compared the expression of these factors to that observed during late stages of hepatic ontogenesis. The steady-state mRNA levels of four (HNF1 alpha, HNF3 alpha, HNF4, and C/EBP beta) &quot;liver-enriched&quot; transcriptional factors gradually decrease during the late period of embryonic liver development while three factors (HNF1 beta, HNF3 beta, and DBP) increase. In the normal adult rat liver the expression of all the transcription factors are restricted to th...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="64ad9b4e725e84d8fd0d1e14bd3e4220" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":104703211,"asset_id":105178595,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/104703211/download_file?s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="105178595"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="105178595"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 105178595; 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$(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="105178594"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/105178594/The_recombinant_proregion_of_transforming_growth_factor_beta1_latency_associated_peptide_inhibits_active_transforming_growth_factor_beta1_in_transgenic_mice"><img alt="Research paper thumbnail of The recombinant proregion of transforming growth factor beta1 (latency-associated peptide) inhibits active transforming growth factor beta1 in transgenic mice" class="work-thumbnail" src="https://attachments.academia-assets.com/104703220/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/105178594/The_recombinant_proregion_of_transforming_growth_factor_beta1_latency_associated_peptide_inhibits_active_transforming_growth_factor_beta1_in_transgenic_mice">The recombinant proregion of transforming growth factor beta1 (latency-associated peptide) inhibits active transforming growth factor beta1 in transgenic mice</a></div><div class="wp-workCard_item"><span>Proceedings of the National Academy of Sciences</span><span>, 1996</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">All three isoforms of transforming growth factors beta (TGF-betal, TGF-beta2, and TGF-beta3) are ...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">All three isoforms of transforming growth factors beta (TGF-betal, TGF-beta2, and TGF-beta3) are secreted as latent complexes and activated extracellularly, leading to the release of the mature cytokines from their noncovalently associated proregions, also known as latency-associated peptides (LAPs). The LAP region of TGF-beta1 was expressed in a baculovirus expression system and purified to homogeneity. In vitro assays of growth inhibition and gene induction mediated by TGF-beta3 demonstrate that recombinant TGF-beta1 LAP is a potent inhibitor of the activities of TGF-betal, -beta2, and -beta3. Effective dosages of LAP for 50% neutralization of TGF-beta activities range from 4.7- to 80-fold molar excess depending on the TGF-beta isoform and activity examined. Using 125I-labeled LAP, we show that the intraperitoneal application route is effective for systemic administration of LAP. Comparison of concentrations of LAP in tissues shows a homogenous pattern in most organs with the exce...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="1260bad5f2e669914fd54d9444cc863e" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":104703220,"asset_id":105178594,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/104703220/download_file?s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="105178594"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="105178594"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 105178594; 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dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "1260bad5f2e669914fd54d9444cc863e" } } $('.js-work-strip[data-work-id=105178594]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":105178594,"title":"The recombinant proregion of transforming growth factor beta1 (latency-associated peptide) inhibits active transforming growth factor beta1 in transgenic mice","internal_url":"https://www.academia.edu/105178594/The_recombinant_proregion_of_transforming_growth_factor_beta1_latency_associated_peptide_inhibits_active_transforming_growth_factor_beta1_in_transgenic_mice","owner_id":43593595,"coauthors_can_edit":true,"owner":{"id":43593595,"first_name":"Snorri","middle_initials":null,"last_name":"Thorgeirsson","page_name":"SnorriThorgeirsson","domain_name":"independent","created_at":"2016-02-20T12:48:37.482-08:00","display_name":"Snorri Thorgeirsson","url":"https://independent.academia.edu/SnorriThorgeirsson"},"attachments":[{"id":104703220,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/104703220/thumbnails/1.jpg","file_name":"d5c0aabd83ba2a2365e1646fa7fae45a83d6.pdf","download_url":"https://www.academia.edu/attachments/104703220/download_file","bulk_download_file_name":"The_recombinant_proregion_of_transformin.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/104703220/d5c0aabd83ba2a2365e1646fa7fae45a83d6-libre.pdf?1690975446=\u0026response-content-disposition=attachment%3B+filename%3DThe_recombinant_proregion_of_transformin.pdf\u0026Expires=1740537650\u0026Signature=ehY5PvjpmsSMLqenhPtqCrxTIc45BAY4-dYDXoTrMHekJ6KUlz3XnvlXKyoIhav~fmRdzuGbAcXMPC992vozykkaA9CPzawlyV7MY1zPU5KSpS-ZVCR4QSqXyY0IsquGaw3hv7~ZnkhWertLnyHBh-awN4E9MqoQPB8Py~Oc1S5Fu2xd9e~w6ooqFRmq7w--ASTDwHGYKUkN9LSX8W2OYLOOPftXgniSTVuM5drwHEhb-p3gEVcauckjjmbs4RhqNNp9Czu1cYFoxyvTJbmv2r8wctmf9R4fV575oigRWKYTiGWqQO8LSCZC~SllOS7YNfDXdT4vIYy~1OKhc1cyTA__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="105178593"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/105178593/Gene_expression_profiling_demonstrates_that_TGF_%CE%B21_signals_exclusively_through_receptor_complexes_involving_Alk5_and_identifies_targets_of_TGF_%CE%B2_signaling"><img alt="Research paper thumbnail of Gene expression profiling demonstrates that TGF-β1 signals exclusively through receptor complexes involving Alk5 and identifies targets of TGF-β signaling" class="work-thumbnail" src="https://attachments.academia-assets.com/104703209/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/105178593/Gene_expression_profiling_demonstrates_that_TGF_%CE%B21_signals_exclusively_through_receptor_complexes_involving_Alk5_and_identifies_targets_of_TGF_%CE%B2_signaling">Gene expression profiling demonstrates that TGF-β1 signals exclusively through receptor complexes involving Alk5 and identifies targets of TGF-β signaling</a></div><div class="wp-workCard_item"><span>Physiological Genomics</span><span>, 2005</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Transforming growth factor-β1 (TGF-β) regulates cellular functions like proliferation, differenti...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Transforming growth factor-β1 (TGF-β) regulates cellular functions like proliferation, differentiation, and apoptosis. On the cell surface, TGF-β binds to receptor complexes consisting of TGF-β receptor type II (TβRII) and activin-like kinase receptor-5 (Alk5), and the downstream signaling is transduced by Smad and MAPK proteins. Recent data have shown that alternative receptor combinations aside from the classical pairing of TβRII/Alk5 can be relevant for TGF-β signaling. We have screened for alternative receptors for TGF-β and also for gene targets of TGF-β signaling, by performing functional assays and microarray analysis in murine embryonic fibroblast (MEF) cell lines lacking Alk5. Data from TGF-β-stimulated Alk5−/− cells show them to be completely unaffected by TGF-β. Additionally, 465 downstream targets of Alk5 signaling were identified when comparing Alk5−/− or TGF-β-stimulated Alk5+/+ MEFs with unstimulated Alk5+/+ cells. Our results demonstrate that, in MEFs, TGF-β signals ...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="631f144eb9651d336307d612cfd9c9e7" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":104703209,"asset_id":105178593,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/104703209/download_file?s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="105178593"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="105178593"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 105178593; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=105178593]").text(description); $(".js-view-count[data-work-id=105178593]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 105178593; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='105178593']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-a9bf3a2bc8c89fa2a77156577594264ee8a0f214d74241bc0fcd3f69f8d107ac.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "631f144eb9651d336307d612cfd9c9e7" } } $('.js-work-strip[data-work-id=105178593]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":105178593,"title":"Gene expression profiling demonstrates that TGF-β1 signals exclusively through receptor complexes involving Alk5 and identifies targets of TGF-β signaling","internal_url":"https://www.academia.edu/105178593/Gene_expression_profiling_demonstrates_that_TGF_%CE%B21_signals_exclusively_through_receptor_complexes_involving_Alk5_and_identifies_targets_of_TGF_%CE%B2_signaling","owner_id":43593595,"coauthors_can_edit":true,"owner":{"id":43593595,"first_name":"Snorri","middle_initials":null,"last_name":"Thorgeirsson","page_name":"SnorriThorgeirsson","domain_name":"independent","created_at":"2016-02-20T12:48:37.482-08:00","display_name":"Snorri Thorgeirsson","url":"https://independent.academia.edu/SnorriThorgeirsson"},"attachments":[{"id":104703209,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/104703209/thumbnails/1.jpg","file_name":"physiolgenomics.00303.pdf","download_url":"https://www.academia.edu/attachments/104703209/download_file","bulk_download_file_name":"Gene_expression_profiling_demonstrates_t.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/104703209/physiolgenomics.00303-libre.pdf?1690975448=\u0026response-content-disposition=attachment%3B+filename%3DGene_expression_profiling_demonstrates_t.pdf\u0026Expires=1740537650\u0026Signature=e0AuW~nnzg9SsVuvazNNcrBQELNQ3hK5IGeOt1iKpdJG1lSVpzfwMUYmUwbBikhnvzAOX~0oA786tL8af6H3khqfNa4WwhyM2nIWbvIG8t0C1i66JXtGBuvf0ZieeOJENnED399oosvtcpO~qJR67UXKlXHqooVKUv0Et36zYa3fwSh17Q9UaClNgV1gxohqcyjlA1-2VZu7k21SDMjXyQ8LtR5sfWo1MEp5456jAl821xzEmwnjUUrt0U0tIHsXrmpB7UX1euTgWft1NLChMQlDCnFOUU~XJ5GT7wUlk7XuKgRYRSJ6PdEWOOUWpBCNoendRM6CpO9YgGCRvGPTsA__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="105178592"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/105178592/Sixty_five_gene_based_risk_score_classifier_predicts_overall_survival_in_hepatocellular_carcinoma"><img alt="Research paper thumbnail of Sixty-five gene-based risk score classifier predicts overall survival in hepatocellular carcinoma" class="work-thumbnail" src="https://attachments.academia-assets.com/104703239/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/105178592/Sixty_five_gene_based_risk_score_classifier_predicts_overall_survival_in_hepatocellular_carcinoma">Sixty-five gene-based risk score classifier predicts overall survival in hepatocellular carcinoma</a></div><div class="wp-workCard_item"><span>Hepatology</span><span>, 2012</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Clinical application of the prognostic gene expression signature has been delayed due to the larg...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Clinical application of the prognostic gene expression signature has been delayed due to the large number of genes and complexity of prediction algorithms. In current study, we aim to develop an easy-to-use risk score with a limited number of genes that can robustly predict prognosis of patients with HCC. The risk score was developed by using Cox coefficient values of 65 genes in the training set (n=139) and its robustness was validated in test sets (n=292). The risk score was a highly significant predictor of overall survival (OS) in the first test cohort (P = 5.6 × 10-5 , n = 100) and the second test cohort (P = 5.0 × 10-5 , n = 192). In multivariate analysis, the risk score was significant risk factor among clinical variables examined together (hazard ratio [HR], 1.36; 95% confidential interval [CI], 1.13-1.64; P = 0.001 for OS). Conclusion-The risk score classifier we have developed can identify two clinically distinct HCC subtypes at early and late stage of the disease in a simple and highly reproducible manner across multiple data sets.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="05bc2c8d147b497769e59062cefea226" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":104703239,"asset_id":105178592,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/104703239/download_file?s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="105178592"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="105178592"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 105178592; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=105178592]").text(description); $(".js-view-count[data-work-id=105178592]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 105178592; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='105178592']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-a9bf3a2bc8c89fa2a77156577594264ee8a0f214d74241bc0fcd3f69f8d107ac.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "05bc2c8d147b497769e59062cefea226" } } $('.js-work-strip[data-work-id=105178592]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":105178592,"title":"Sixty-five gene-based risk score classifier predicts overall survival in hepatocellular carcinoma","internal_url":"https://www.academia.edu/105178592/Sixty_five_gene_based_risk_score_classifier_predicts_overall_survival_in_hepatocellular_carcinoma","owner_id":43593595,"coauthors_can_edit":true,"owner":{"id":43593595,"first_name":"Snorri","middle_initials":null,"last_name":"Thorgeirsson","page_name":"SnorriThorgeirsson","domain_name":"independent","created_at":"2016-02-20T12:48:37.482-08:00","display_name":"Snorri Thorgeirsson","url":"https://independent.academia.edu/SnorriThorgeirsson"},"attachments":[{"id":104703239,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/104703239/thumbnails/1.jpg","file_name":"pmc4060518.pdf","download_url":"https://www.academia.edu/attachments/104703239/download_file","bulk_download_file_name":"Sixty_five_gene_based_risk_score_classif.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/104703239/pmc4060518-libre.pdf?1690975436=\u0026response-content-disposition=attachment%3B+filename%3DSixty_five_gene_based_risk_score_classif.pdf\u0026Expires=1740537650\u0026Signature=e17wWf5H90UjuA0ywWRW10FYIrbvnYSvsdr6j2x8hNRMgZA93QENRGJxGWcQexLeQAAyEINt5pF-Ud9eyMjWq7nLy7r-j4TGw9vuogO3yhbwh9d36CybpFuRIlMXoxpXJk20F0O7ONfxLLsWKPJbAecdGFJOv9UrP0KdDYJuBU2Qo6cnbx0fCJyc~7FUMHbs4AeovOyxTyGJe7IbcgfgEMnJpyc~Curu83gUo2fgAzEn-x7D5Uz8j26pG8KmKIb8s8DoeCo0mQ6QM4FrNvq4UVcuJVmcHU4S~eOyCY~y0hBOgint2ihv3ukkSPX~VD6GWPP-OPiyVjWZ0wyA7X5fCA__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="105178591"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/105178591/Hepatic_precursors_derived_from_murine_embryonic_stem_cells_contribute_to_regeneration_of_injured_liver"><img alt="Research paper thumbnail of Hepatic precursors derived from murine embryonic stem cells contribute to regeneration of injured liver" class="work-thumbnail" src="https://attachments.academia-assets.com/104703224/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/105178591/Hepatic_precursors_derived_from_murine_embryonic_stem_cells_contribute_to_regeneration_of_injured_liver">Hepatic precursors derived from murine embryonic stem cells contribute to regeneration of injured liver</a></div><div class="wp-workCard_item"><span>Hepatology</span><span>, 2006</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="a70a71a302432eb4cbda4b24da47be4b" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":104703224,"asset_id":105178591,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/104703224/download_file?s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="105178591"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="105178591"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 105178591; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=105178591]").text(description); $(".js-view-count[data-work-id=105178591]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 105178591; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='105178591']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-a9bf3a2bc8c89fa2a77156577594264ee8a0f214d74241bc0fcd3f69f8d107ac.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "a70a71a302432eb4cbda4b24da47be4b" } } $('.js-work-strip[data-work-id=105178591]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":105178591,"title":"Hepatic precursors derived from murine embryonic stem cells contribute to regeneration of injured liver","internal_url":"https://www.academia.edu/105178591/Hepatic_precursors_derived_from_murine_embryonic_stem_cells_contribute_to_regeneration_of_injured_liver","owner_id":43593595,"coauthors_can_edit":true,"owner":{"id":43593595,"first_name":"Snorri","middle_initials":null,"last_name":"Thorgeirsson","page_name":"SnorriThorgeirsson","domain_name":"independent","created_at":"2016-02-20T12:48:37.482-08:00","display_name":"Snorri Thorgeirsson","url":"https://independent.academia.edu/SnorriThorgeirsson"},"attachments":[{"id":104703224,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/104703224/thumbnails/1.jpg","file_name":"20070122-fulltext.pdf","download_url":"https://www.academia.edu/attachments/104703224/download_file","bulk_download_file_name":"Hepatic_precursors_derived_from_murine_e.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/104703224/20070122-fulltext-libre.pdf?1690975438=\u0026response-content-disposition=attachment%3B+filename%3DHepatic_precursors_derived_from_murine_e.pdf\u0026Expires=1740537650\u0026Signature=B0RJCwNRR2V31i3byE4sr69gHusxEjGw2TF2IkImUGtA5YSkoboAfp7fdRu53O4ZCX3cG5vSdgrbEQSig0DOAmJVk0k-D4SVyZmXk5eXjaAXaVl1futCRNxLJ72zAdgEveJURIqPlIRUTsU5-xmZRMvsz~qt7BN7-zyfbR6suLtUCbhkYog5jUKTn7XEK2fyvEH-cXf2LCoju1YWPkQwtnXijsT7I6G5KQ~7mRVf9oF1QvMErfjYZ1A-xSj24-gHSeeVPO4r2gaJzyun0wvXwbgyxGoFt~oAFX8xqVrPxbE4oVm1DQFE7ouRxM1ZODFvdtgF9KwKBVe131x99RhgJw__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="105178590"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/105178590/DLC_1_a_Rho_GTPase_activating_protein_with_tumor_suppressor_function_is_essential_for_embryonic_development"><img alt="Research paper thumbnail of DLC-1, a Rho GTPase-activating protein with tumor suppressor function, is essential for embryonic development" class="work-thumbnail" src="https://attachments.academia-assets.com/104703231/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/105178590/DLC_1_a_Rho_GTPase_activating_protein_with_tumor_suppressor_function_is_essential_for_embryonic_development">DLC-1, a Rho GTPase-activating protein with tumor suppressor function, is essential for embryonic development</a></div><div class="wp-workCard_item"><span>FEBS Letters</span><span>, 2005</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">DLC-1 (deleted in liver cancer 1) is a Rho GTPaseactivating protein that is able to inhibit cell ...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">DLC-1 (deleted in liver cancer 1) is a Rho GTPaseactivating protein that is able to inhibit cell growth and suppress tumorigenesis. We have used homologous recombination to inactivate the mouse DLC-1 gene (Arhgap7). Mice heterozygous for the targeted allele were phenotypically normal, but homozygous mutant embryos did not survive beyond 10.5 days post coitum. Histological analysis revealed that DLC-1 À/À embryos had defects in the neural tube, brain, heart, and placenta. Cultured fibroblasts from DLC-1-deficient embryos displayed alterations in the organization of actin filaments and focal adhesions.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="3dba4ad413937729d8d955234a4e99e6" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":104703231,"asset_id":105178590,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/104703231/download_file?s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="105178590"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="105178590"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 105178590; 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$(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="105178589"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/105178589/Role_of_Growth_Hormone_GH_in_Liver_Regeneration"><img alt="Research paper thumbnail of Role of Growth Hormone (GH) in Liver Regeneration" class="work-thumbnail" src="https://attachments.academia-assets.com/104703208/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/105178589/Role_of_Growth_Hormone_GH_in_Liver_Regeneration">Role of Growth Hormone (GH) in Liver Regeneration</a></div><div class="wp-workCard_item"><span>Endocrinology</span><span>, 2004</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Liver regeneration is a fundamental mechanism by which the liver responds to injury. This process...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Liver regeneration is a fundamental mechanism by which the liver responds to injury. This process is regulated by endogenous growth factors and cytokines, and it involves proliferation of all mature cells that exist within the intact organ. To understand the role of the GH/IGF-I axis in liver regeneration, we performed partial hepatectomies in three groups of mice: GH antagonist (GHa) transgenic mice, in which the action of GH is blocked; liver IGF-I-deficient mice that lack IGF-I specifically in the liver and also lack the acid-labile subunit (ALS; LID+ALSKO mice), in which IGF-I levels are very low and GH secretion is increased; and control mice. Interestingly, the survival rate of GHa transgenic mice was dramatically reduced after partial hepatectomy (57%) compared with the survival rate of controls (100%) or LID+ALSKO mice (88%). In control mice, the liver was completely regenerated after 4 d, whereas liver regeneration required 7 d in LID+ALSKO mice. In contrast, in GHa mice, l...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="27ab88e0cfe42271066f809b4b9687d7" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":104703208,"asset_id":105178589,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/104703208/download_file?s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="105178589"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="105178589"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 105178589; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=105178589]").text(description); $(".js-view-count[data-work-id=105178589]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 105178589; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='105178589']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-a9bf3a2bc8c89fa2a77156577594264ee8a0f214d74241bc0fcd3f69f8d107ac.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); 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$(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="105178588"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/105178588/Genomic_copy_number_alterations_with_transcriptional_deregulation_at_6p_identify_an_aggressive_HCC_phenotype"><img alt="Research paper thumbnail of Genomic copy number alterations with transcriptional deregulation at 6p identify an aggressive HCC phenotype" class="work-thumbnail" src="https://attachments.academia-assets.com/104703207/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/105178588/Genomic_copy_number_alterations_with_transcriptional_deregulation_at_6p_identify_an_aggressive_HCC_phenotype">Genomic copy number alterations with transcriptional deregulation at 6p identify an aggressive HCC phenotype</a></div><div class="wp-workCard_item"><span>Carcinogenesis</span><span>, 2013</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Genomic analyses have revealed the enormous heterogeneity in essentially all cancer types. Howeve...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Genomic analyses have revealed the enormous heterogeneity in essentially all cancer types. However, the identification of precise subtypes, which are biologically informative and clinically useful, remains a challenge. The application of integrative analysis of multilayered genomic profiles to define the chromosomal regions of genomic copy number alterations with concomitant transcriptional deregulation is posited to provide a promising strategy to identify driver targets. In this study, we performed an integrative analysis of the DNA copy numbers and gene expression profiles of hepatocellular carcinoma (HCC). By comparing DNA copy numbers between HCC subtypes based on gene expression pattern, we revealed the DNA copy number alteration with concordant gene expression changes at 6p21-p24 particularly in the HCC subtype of aggressive phenotype without expressing stemness genes. Among the genes at 6p21-p24, we identified IER3 as a potential driver. The clinical utility of IER3 copy numbers was demonstrated by validating its clinical correlation with independent cohorts. In addition, short hairpin RNA-mediated knockdown experiment revealed the functional relevance of IER3 in liver cancer progression. In conclusion, our results suggest that genomic copy number alterations with transcriptional deregulation at 6p21-p24 identify an aggressive HCC phenotype and a novel functional biomarker.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="0011fc4fcad1a2db3cc4e784ddc94836" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":104703207,"asset_id":105178588,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/104703207/download_file?s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="105178588"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="105178588"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 105178588; 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$(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="105178587"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/105178587/Short_term_carcinogenicity_testing_of_2_amino_1_methyl_6_phenylimidazo_4_5_b_pyridine_PhIP_and_2_amino_3_methylimidazo_4_5_f_quinoline_IQ_in_E%CE%BC_pim_1_transgenic_mice"><img alt="Research paper thumbnail of Short-term carcinogenicity testing of 2-amino-1-methyl-6-phenylimidazo[4, 5- b ]pyridine (PhIP) and 2-amino-3-methylimidazo[4, 5-f]quinoline (IQ) in Eμ- pim -1 transgenic mice" class="work-thumbnail" src="https://attachments.academia-assets.com/104703219/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/105178587/Short_term_carcinogenicity_testing_of_2_amino_1_methyl_6_phenylimidazo_4_5_b_pyridine_PhIP_and_2_amino_3_methylimidazo_4_5_f_quinoline_IQ_in_E%CE%BC_pim_1_transgenic_mice">Short-term carcinogenicity testing of 2-amino-1-methyl-6-phenylimidazo[4, 5- b ]pyridine (PhIP) and 2-amino-3-methylimidazo[4, 5-f]quinoline (IQ) in Eμ- pim -1 transgenic mice</a></div><div class="wp-workCard_item"><span>Carcinogenesis</span><span>, 1996</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">The usefulness of transgenic E(j.-pi/n-l mice over-expressing the pim-1 oncogene in lymphoid tiss...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">The usefulness of transgenic E(j.-pi/n-l mice over-expressing the pim-1 oncogene in lymphoid tissues, as sensitive test organisms was studied in a short-term carcinogenicity study. The mice were fed standard diet Altromin 1314 supplemented either with 0.03% 2-amino-l-methyl-6phenylimidazo[4,5-ft]pyridine (PhIP) for 7 months or with 0.03% 2-amino-3-methylimidazo[4,5-/|quinoline (IQ) for 6 months. PhIP and IQ are heterocyclic amines formed during cooking of meat and fish and are mutagenic to bacteria and cultured mammalian cells. PhIP is a potent mouse lymphomagen, while IQ is a liver carcinogen and also causes lung tumors and tumors of the forestomach in mice. We found that transgenic E\i-pim-l mice are highly susceptible to PhIP induced lymphomagenesis but do not respond to the IQ treatment PhIP feeding of E\i-pim-l mice not only increased the total number of T-ceU lymphomas but also decreased the latency time compared to either transgenic or wild-type controls. The effect was most pronounced in the treated female E\i-pim-l mice, which showed a higher incidence of PhIP induced T-cell lymphomas than transgenic males and a strongly reduced latency period after PhIP treatment compared to nontransgenic mice. Our results suggest that the transgenic Eji-/H/n-l mouse may be a useful model for short-term carcinogenicity screening of potential genotoxic carcinogens having the lymphoid system as target tissue. The carcinogen IQ which does not have the lymphoid system as a target was not recognized in this model.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="2dadb16472ac6355a47d02e033e7ad11" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":104703219,"asset_id":105178587,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/104703219/download_file?s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="105178587"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="105178587"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 105178587; 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At present, it is challenging to identify patients with high risk of recurrence, which would warrant additional therapies. In this study, we sought to analyze a recently developed metastasis-related gene signature for its utility in predicting HCC survival, using 2 independent cohorts consisting of a total of 386 patients who received radical resection. Cohort 1 contained 247 predominantly HBV-positive cases analyzed with an Affymetrix platform, whereas cohort 2 contained 139 cases with mixed etiology analyzed with the NCI Oligo Set microarray platform. We employed a survival risk prediction algorithm with training, test, and independent cross-validation strategies and found that the gene signature is predictive of overall and disease-free survival. Importantly, risk was significantly predicted independently of clinical characteristics and microarray platform. In add...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="bdd3fc53614333cef24ca76a888f2c7d" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":104703205,"asset_id":105178586,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/104703205/download_file?s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="105178586"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="105178586"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 105178586; 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In this issue of Cancer Cell, Pilati and colleagues present an integrative multi-''omics''-based analysis of HCA and identify recurrent genetic alterations associated with adenoma-carcinoma transition and new drugable targets.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="f2a480d930a665340473793957d8b589" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":104703218,"asset_id":105178585,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/104703218/download_file?s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="105178585"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="105178585"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 105178585; 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$(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="105178584"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/105178584/Origin_and_Structural_Evolution_of_the_Early_Proliferating_Oval_Cells_in_Rat_Liver"><img alt="Research paper thumbnail of Origin and Structural Evolution of the Early Proliferating Oval Cells in Rat Liver" class="work-thumbnail" src="https://attachments.academia-assets.com/104703232/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/105178584/Origin_and_Structural_Evolution_of_the_Early_Proliferating_Oval_Cells_in_Rat_Liver">Origin and Structural Evolution of the Early Proliferating Oval Cells in Rat Liver</a></div><div class="wp-workCard_item"><span>The American Journal of Pathology</span><span>, 2001</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="e46984b6947b0a810676ac8fda25f318" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":104703232,"asset_id":105178584,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/104703232/download_file?s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="105178584"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="105178584"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 105178584; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=105178584]").text(description); $(".js-view-count[data-work-id=105178584]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 105178584; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='105178584']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-a9bf3a2bc8c89fa2a77156577594264ee8a0f214d74241bc0fcd3f69f8d107ac.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); 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$(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="105178538"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/105178538/Alterations_of_tumor_suppressor_genes_and_allelic_losses_in_human_hepatocellular_carcinomas_in_China"><img alt="Research paper thumbnail of Alterations of tumor suppressor genes and allelic losses in human hepatocellular carcinomas in China" class="work-thumbnail" src="https://attachments.academia-assets.com/104703177/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/105178538/Alterations_of_tumor_suppressor_genes_and_allelic_losses_in_human_hepatocellular_carcinomas_in_China">Alterations of tumor suppressor genes and allelic losses in human hepatocellular carcinomas in China</a></div><div class="wp-workCard_item"><span>Cancer research</span><span>, 1994</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Aflatoxin B1 has been suggested as a causative agent for a G to T mutation at codon 249 in the p5...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Aflatoxin B1 has been suggested as a causative agent for a G to T mutation at codon 249 in the p53 gene in human hepatocellular carcinomas (HCC) from southern Africa and Qidong in China. The objective of the present work was to test the hypothesis that exposure to aflatoxin B1 either alone or coincident with other environmental carcinogens might be associated with allelic losses occurring during development of human hepatocarcinogenesis in China. The HCCs were obtained from two different areas in China: Qidong, where exposure to hepatitis B virus (HBV) and aflatoxin B1 is high; and Beijing, where exposure to HBV is high but that of aflatoxin B1 is low. We analyzed the tumors for mutations in the p53 gene and loss of heterozygosity for the p53, Rb, and APC genes and at marker loci on chromosomes 4, 13, and 16. Frequencies of mutation, loss, and aberration (mutation and loss) of the p53 gene in 25 HCCs from Qidong were 60, 58, and 80%, respectively. The frequencies in 9 HCCs from Beij...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="486ff567ad2fbc064892b31ae6663a64" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":104703177,"asset_id":105178538,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/104703177/download_file?s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="105178538"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="105178538"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 105178538; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=105178538]").text(description); $(".js-view-count[data-work-id=105178538]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 105178538; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='105178538']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-a9bf3a2bc8c89fa2a77156577594264ee8a0f214d74241bc0fcd3f69f8d107ac.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "486ff567ad2fbc064892b31ae6663a64" } } $('.js-work-strip[data-work-id=105178538]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":105178538,"title":"Alterations of tumor suppressor genes and allelic losses in human hepatocellular carcinomas in China","internal_url":"https://www.academia.edu/105178538/Alterations_of_tumor_suppressor_genes_and_allelic_losses_in_human_hepatocellular_carcinomas_in_China","owner_id":43593595,"coauthors_can_edit":true,"owner":{"id":43593595,"first_name":"Snorri","middle_initials":null,"last_name":"Thorgeirsson","page_name":"SnorriThorgeirsson","domain_name":"independent","created_at":"2016-02-20T12:48:37.482-08:00","display_name":"Snorri Thorgeirsson","url":"https://independent.academia.edu/SnorriThorgeirsson"},"attachments":[{"id":104703177,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/104703177/thumbnails/1.jpg","file_name":"281.full.pdf","download_url":"https://www.academia.edu/attachments/104703177/download_file","bulk_download_file_name":"Alterations_of_tumor_suppressor_genes_an.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/104703177/281.full-libre.pdf?1690975459=\u0026response-content-disposition=attachment%3B+filename%3DAlterations_of_tumor_suppressor_genes_an.pdf\u0026Expires=1740537650\u0026Signature=bHKeqAOVlDrzM7mJhauUsJT4xMT9K6ToPNEldnEZZSvhelwaddVM-Lu2bL0~5vyWS9SdQM5WmLF0KTgNi6WiHy43sJonllsnFD2bR3FsIJvNK~vmIg93~QfGFlrvwM3YaMzdem9f0SroCks4zR-KLH2~L1hlJudP9pIkc9cVbMW4LEWCnvUEvvHKT7bagyCarcKTn3ZyF8HOaiJLpWg0F~DydfouBaOYBuP4a2ck3YibcdZSx6HIXb80Np7VlCOqTnzGtr3~qls3TTcSZCSTMaPZSQGekBZHvcZnkYsX2KbIUHBUp-n0rP8nIVurwbv0O6r-NVXKO31J8yubDD6ajQ__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="101056351"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/101056351/Hepatic_regeneration_in_vitamin_A_deficient_rats_changes_in_the_expression_of_transforming_growth_factor_alpha_epidermal_growth_factor_receptor_and_retinoic_acid_receptors_alpha_and_beta"><img alt="Research paper thumbnail of Hepatic regeneration in vitamin A-deficient rats: changes in the expression of transforming growth factor alpha/epidermal growth factor receptor and retinoic acid receptors alpha and beta" class="work-thumbnail" src="https://attachments.academia-assets.com/101701347/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/101056351/Hepatic_regeneration_in_vitamin_A_deficient_rats_changes_in_the_expression_of_transforming_growth_factor_alpha_epidermal_growth_factor_receptor_and_retinoic_acid_receptors_alpha_and_beta">Hepatic regeneration in vitamin A-deficient rats: changes in the expression of transforming growth factor alpha/epidermal growth factor receptor and retinoic acid receptors alpha and beta</a></div><div class="wp-workCard_item"><span>Cell growth & differentiation : the molecular biology journal of the American Association for Cancer Research</span><span>, 1994</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">We have studied the effect of vitamin A deficiency on the expression of transforming growth facto...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">We have studied the effect of vitamin A deficiency on the expression of transforming growth factor alpha (TGF-alpha), hepatocyte growth factor, acidic fibroblast growth factor, and TGF-beta 1 after partial hepatectomy of vitamin A-supplemented and vitamin A-deficient rats. In addition, the expressions of epidermal growth factor receptor and retinoic acid receptors alpha (RAR alpha) and beta (RAR beta) were studied. Partial hepatectomy was performed on the animals from the vitamin A-supplemented and -deficient groups at the age of 10 weeks when the weights of the animals on the deficient diet had reached a plateau. Two animals from each group were sacrificed before the operation and also 12, 24, 48, and 72 h and 5 days after the operation. Partial hepatectomy of the vitamin A-deficient rats leads to a focal necrosis of liver followed by a rapid restoration of liver mass. Expression of the TGF-alpha and epidermal growth factor receptor was highly elevated in the livers of deficient an...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="06d3ef79a3bc995ddfbf328726e507a2" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":101701347,"asset_id":101056351,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/101701347/download_file?s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="101056351"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="101056351"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 101056351; 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$(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="101056350"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/101056350/Analysis_of_c_myc_expression_in_a_human_hepatoma_cell_line"><img alt="Research paper thumbnail of Analysis of c-myc expression in a human hepatoma cell line" class="work-thumbnail" src="https://attachments.academia-assets.com/101701252/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/101056350/Analysis_of_c_myc_expression_in_a_human_hepatoma_cell_line">Analysis of c-myc expression in a human hepatoma cell line</a></div><div class="wp-workCard_item"><span>Cancer research</span><span>, 1987</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">A tumorigenic human hepatoma cell line, Hep G2, has been shown to have high steady-state levels o...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">A tumorigenic human hepatoma cell line, Hep G2, has been shown to have high steady-state levels of c-myc transcripts compared to normal human liver. We have now characterized c-myc expression in Hep G2 cells with regard to message stability, gene rearrangements, gene amplification, chromosomal translocations, promoter utilization, and the effects of protein synthesis inhibitors. We have determined that the half-life of the Hep G2 c-myc transcript is approximately 20 min and conclude that the high steady-state level of c-myc mRNA is not the result of a specific stabilization of the c-myc message but probably results from increased c-myc gene transcription. c-myc expression in Hep G2 cells appears to be constitutive, since it remains constant in different cell growth states (log phase versus nondividing cells). The high constitutive expression of the c-myc gene in Hep G2 cells could not be explained by gene amplification, gene rearrangements, or chromosomal translocations. However, ba...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="57769a99ce988fc1368e62fa3546faa6" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":101701252,"asset_id":101056350,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/101701252/download_file?s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="101056350"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="101056350"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 101056350; 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