OASIS Repository@POSTECHLIBRARY: 유전체 스크리닝을 이용한 교모세포종 세포주의 유전형 특이적 암 취약성과 temozolomide 내성 메커니즘 규명

<!DOCTYPE html> <html lang="ko"> <head> <title>OASIS Repository@POSTECHLIBRARY: 유전체 스크리닝을 이용한 교모세포종 세포주의 유전형 특이적 암 취약성과 temozolomide 내성 메커니즘 규명</title> <meta http-equiv="Content-Type" content="text/html; charset=UTF-8" /> <meta name="Generator" content="DSpace 5.5" /> <meta name="viewport" content="width=device-width, initial-scale=1.0"> <meta http-equiv="X-UA-Compatible" content="IE=edge"> <meta name="description" content="Postech OASIS Repository" /> <meta name="keywords" content="오아시스,레포지토리,리포지터리,저장소,포스텍,박태준학술정보관,포항공과대학교,포항공대,POSTECH,Pohang University of Science and Technology,도서관,IR,연구업적,학술실적,연구성과,dspace" /> <link rel="shortcut icon" href="/favicon.ico" type="image/x-icon"/> <link rel="search" type="application/opensearchdescription+xml" href="/open-search/description.xml" title="DSpace" /> <link rel="schema.DCTERMS" href="http://purl.org/dc/terms/" /> <link rel="schema.DC" href="http://purl.org/dc/elements/1.1/" /> <link rel="schema.OAK" href="http://www.oak.go.kr/terms/" /> <meta name="OAK.author" content="한승엽" scheme="OAK.AUTHOR" /> <meta name="DCTERMS.dateAccepted" content="2024-08-23T16:36:27Z" scheme="DCTERMS.W3CDTF" /> <meta name="DCTERMS.available" content="2024-08-23T16:36:27Z" scheme="DCTERMS.W3CDTF" /> <meta name="DCTERMS.issued" content="2024" scheme="DCTERMS.W3CDTF" /> <meta name="DC.identifier" content="OAK-2015-10710" /> <meta name="DC.identifier" content="http://postech.dcollection.net/common/orgView/200000808553" xml:lang="ko_KR" scheme="DCTERMS.URI" /> <meta name="DC.identifier" content="https://oasis.postech.ac.kr/handle/2014.oak/124100" scheme="DCTERMS.URI" /> <meta name="DC.description" content="Master" /> <meta name="DCTERMS.abstract" content="Glioblastoma (GBM) is a malignant brain tumor that accounts for 15.4% of all primary CNS tumors and brain tumors [1]. 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For this, I developed the GBMEGFRvIII;CDKN2A KO cell line by utilizing the GBMEGFRvIII cell line from previous research [7] and conducted bulk RNA-seq and genome-wide CRISPR-Cas9 screening [12]. My research demonstrates that the transcriptional pattern of GBMEGFRvIII and GBMEGFRvIII;CDKN2A KO is distinct and lipid-associated metabolic pathways play important roles in the fitness and TMZ sensitivity of GBMEGFRvIII;CDKN2A KO. The understanding of essential genes and cancer vulnerabilities in GBMEGFRvIII and GBMEGFRvIII;CDKN2A KO is expected to be useful in investigating GBM therapeutic targets related to CDKN2A deletion and EGFRvIII and developing personalized GBM medicines." /> <meta name="DC.language" content="eng" /> <meta name="DC.publisher" content="포항공과대학교" /> <meta name="DC.title" content="유전체 스크리닝을 이용한 교모세포종 세포주의 유전형 특이적 암 취약성과 temozolomide 내성 메커니즘 규명" /> <meta name="DC.type" content="Thesis" /> <meta name="DC.contributor" content="생명과학과" /> <meta name="DC.date" content="2024- 8" scheme="DCTERMS.W3CDTF" /> <meta name="citation_keywords" content="Thesis" /> <meta name="citation_dissertation_institution" content="포항공과대학교" /> <meta name="citation_title" content="유전체 스크리닝을 이용한 교모세포종 세포주의 유전형 특이적 암 취약성과 temozolomide 내성 메커니즘 규명" /> <meta name="citation_dissertation_name" content="유전체 스크리닝을 이용한 교모세포종 세포주의 유전형 특이적 암 취약성과 temozolomide 내성 메커니즘 규명" /> <meta name="citation_author" content="한승엽" /> <meta name="citation_date" content="2024" /> <meta name="citation_abstract_html_url" content="https://oasis.postech.ac.kr/handle/2014.oak/124100" /> <link rel="stylesheet" href="/css/bootstrap.min.css" defer /> <link rel="stylesheet" href="/css/layout.css" async /> <link rel="stylesheet" href="/css/mquery.css" defer /> <link rel="stylesheet" href="/css/slidebars.css" defer />  <link rel="stylesheet" href="/css/owl.carousel.css" defer />  <link rel="stylesheet" href="/css/owl.theme.css" defer /> <link rel="stylesheet" href="/css/bootstrap-partof.css" defer /> <script src="/js/jquery-1.9.1.min.js"></script> <script src="/js/jquery-ui.js"></script> <script src="/js/bootstrap.min.js"></script> <script src="/js/owl.carousel.min.js"></script> <script src="/js/common.js" defer></script> <script src="/utils.js" defer></script> <script src="/static/js/holder.js" defer></script> <script src="/static/js/choice-support.js" defer></script> <script src="/js/ms-clarity.js"></script> <script async src="https://www.googletagmanager.com/gtag/js?id=G-B9EHYYGM78"></script> <script> window.dataLayer = window.dataLayer || []; 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The prognosis of GBM patients is very poor and temozolomide (TMZ) chemotherapy improves the dismal prognosis of GBM [2, 3]. However, the accumulation of mutations in GBM forms inter-tumor heterogeneity and allows the acquisition of TMZ resistance in GBM making GBM therapeutic strategies more complex [4-6]. EGFRvIII is one of the most common mutations in GBM and is a sufficient condition for gliomagenesis [7-9]. Deletion of the CDKN2A gene cooperates with EGFRvIII and shortens the latency period of EGFRvIII- mediated gliomagenesis [7, 10]. CDKN2A deletion is associated with poor overall survival of GBM patients [11]. Here I showed context-specific essential genes and genotype-specific cancer vulnerabilities in the mouse EGFRvIII GBM cell line (GBMEGFRvIII) and CDKN2A KO EGFRvIII GBM cell line (GBMEGFRvIII;CDKN2A KO). For this, I developed the GBMEGFRvIII;CDKN2A KO cell line by utilizing the GBMEGFRvIII cell line from previous research [7] and conducted bulk RNA-seq and genome-wide CRISPR-Cas9 screening [12]. My research demonstrates that the transcriptional pattern of GBMEGFRvIII and GBMEGFRvIII;CDKN2A KO is distinct and lipid-associated metabolic pathways play important roles in the fitness and TMZ sensitivity of GBMEGFRvIII;CDKN2A KO. The understanding of essential genes and cancer vulnerabilities in GBMEGFRvIII and GBMEGFRvIII;CDKN2A KO is expected to be useful in investigating GBM therapeutic targets related to CDKN2A deletion and EGFRvIII and developing personalized GBM medicines.</dd></dl> <dl><dt>URI</dt><dd><a href="http://postech.dcollection.net/common/orgView/200000808553" class="link_type">http://postech.dcollection.net/common/orgView/200000808553</a><br /><a href="https://oasis.postech.ac.kr/handle/2014.oak/124100" class="link_type">https://oasis.postech.ac.kr/handle/2014.oak/124100</a></dd></dl> <dl><dt>Article Type</dt><dd>Thesis</dd></dl> <dl class="file_item_dl"><dt>Files in This Item:</dt> <dd class="file_download">There are no files associated with this item.</dd> </dl> </div> <div class="record_bt_box"> <a href="/handle/2014.oak/124100?mode=full">Show full item record</a> </div> <div class="al_right"> </div> <div class="sns_wrap"> <div class="sns_box"> <p class="qr_box"><img src="https://api.qrserver.com/v1/create-qr-code/?size=66x66&data=https://oasis.postech.ac.kr/handle/2014.oak/124100" alt="qr_code"></p> <div class="sns_inner"> <ul> <li> <p><a href="http://www.mendeley.com/import/?url=https://oasis.postech.ac.kr/handle/2014.oak/124100" target="_blank"><img src="/image/common/mendeley_icon.gif" alt="mendeley" /></a></p> <p class="twitter_box"> <a href="https://twitter.com/share" class="tweet_bt twitter-share-button" data-lang="en" data-size="large" data-dnt="true">트윗하기</a> <script> !function(d, s, id) { var js, fjs = d.getElementsByTagName(s)[0]; if (!d.getElementById(id)) { js = d.createElement(s); js.id = id; js.src = "//platform.twitter.com/widgets.js"; fjs.parentNode.insertBefore(js, fjs); } }(document, "script", "twitter-wjs"); </script> </p> </li> <li class="facebook_li"> <span id="fb-root"></span> <script> (function(d, s, id) { var js, fjs = d.getElementsByTagName(s)[0]; if (d.getElementById(id)) return; js = d.createElement(s); js.id = id; js.src = "//connect.facebook.net/ko_KR/all.js#xfbml=1"; fjs.parentNode.insertBefore(js, fjs); }(document, 'script', 'facebook-jssdk')); </script> <span class="fb-like" data-send="true" data-layout="standard" data-width="450" data-show-faces="false" data-font="verdana"></span> </li> </ul> </div> </div> <p class="sns_text"> <span> Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.</span> </p> </div> </div> </div>  <div class="sub_right_box"> <div class="w_cc"> <h4 class="widget_title">Communities & Collection</h4> <ul> <li><a href="/handle/2014.oak/398" class="cc_item">General Graduate School of Life Science (일반대학원 생명과학과)</a> <ul> <li><a href="/handle/2014.oak/399">1. 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OASIS Repository@POSTECHLIBRARY: 유전체 스크리닝을 이용한 교모세포종 세포주의 유전형 특이적 암 취약성과 temozolomide 내성 메커니즘 규명