Stanford Medicine study discovers what's behind heart cell damage from chemotherapy

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<div class="cmp-image"> <img src="/content/dam/sm-news/images/2024/11/wu-crispr-1-.jpg" class="cmp-image__image" alt="Stanford Medicine study discovers what's behind heart cell damage from chemotherapy" style=" background-image: url(/etc.clientlibs/stanford/clientlibs/clientlib-core/resources/images/no-profile-photo.jpg); background-size: cover; background-position: center; background-repeat: no-repeat; "/> <div class="cmp-teaser__caption"><p>A sarcomere, or part of a cardiomyocyte that helps heart cells beat, retains its structure after treatment with indisulam and doxorubicin. (The blue dot is the nucleus of the cell.)<br /> <i>Joseph Wu lab</i></p> </div> </div> </div> <div class="cmp-teaser__content"> <p class="cmp-teaser__pretitle"> <a class="tags" href="https://med.stanford.edu/news/topics/cardiology.html"> Cardiology </a> <span class="date">November 27, 2024</span> </p> <h1 class="cmp-teaser__title"> Stanford Medicine study discovers what's behind heart cell damage from chemotherapy </h1> <div class="cmp-teaser__description"><p>Researchers used a new screening technique to identify genes involved in heart cell damage during a common chemotherapy treatment. They also found a drug that may be able to prevent it.</p></div> </div> </div> </div> <div class="socialshare container responsivegrid" is="stanford-socialshare"><div class="cmp-socialshare"> <h5 class="cmp-socialshare__title">Share Article:</h5> <a id="button-0eb8bde9c5" class="cmp-button" aria-label="Facebook" data-cmp-clickable data-cmp-data-layer="{"button-0eb8bde9c5":{"@type":"stanford/components/button","dc:title":"Facebook","xdm:linkURL":"https://www.facebook.com/sharer/sharer.php"}}" href="https://www.facebook.com/sharer/sharer.php"> <span class="cmp-button__icon cmp-button__icon--icon-facebook-f" aria-hidden="true"></span> <span class="cmp-button__text">Facebook</span> </a> <a id="button-ba85f536cc" class="cmp-button" aria-label="LinkedIn" data-cmp-clickable data-cmp-data-layer="{"button-ba85f536cc":{"@type":"stanford/components/button","dc:title":"LinkedIn","xdm:linkURL":"https://www.linkedin.com/sharing/share-offsite/"}}" href="https://www.linkedin.com/sharing/share-offsite/"> <span class="cmp-button__icon cmp-button__icon--icon-linkedin-in" aria-hidden="true"></span> <span class="cmp-button__text">LinkedIn</span> </a> <a id="button-839c9306ca" class="cmp-button" aria-label="Twitter" data-cmp-clickable data-cmp-data-layer="{"button-839c9306ca":{"@type":"stanford/components/button","dc:title":"Twitter","xdm:linkURL":"https://twitter.com/intent/tweet"}}" href="https://twitter.com/intent/tweet"> <span class="cmp-button__icon cmp-button__icon--icon-x-twitter" aria-hidden="true"></span> <span class="cmp-button__text">Twitter</span> </a> <a id="button-28a72c1b45" class="cmp-button" aria-label="Email" data-cmp-clickable data-cmp-data-layer="{"button-28a72c1b45":{"@type":"stanford/components/button","dc:title":"Email","xdm:linkURL":"mailto:"}}" href="mailto:"> <span class="cmp-button__icon cmp-button__icon--icon-envelope-fill" aria-hidden="true"></span> <span class="cmp-button__text">Email</span> </a> </div></div> <div class="articleAbstract text" is="stanford-text"> </div> <article class="article element container responsivegrid" is="stanford-article"> <div class="container responsivegrid columns:2 layout:1to3" is="stanford-container"> <div id="container-9193c59388" class="cmp-container"> <div class="container responsivegrid" is="stanford-container"> <div id="container-b4669e2c21" class="cmp-container"> </div> </div> <div class="contentfragment modifier:featured" is="stanford-contentfragment"> <section id="contentfragment-1b82025064" class="cmp-contentfragment cmp-contentfragment--heart-cell-chemotherapy" data-cmp-contentfragment-model="stanford/models/article" data-cmp-data-layer="{"contentfragment-1b82025064":{"@type":"stanford/components/contentfragment","repo:modifyDate":"2024-10-21T18:58:11Z","dc:title":"Stanford Medicine study discovers what's behind heart cell damage from chemotherapy","elements":[{"xdm:text":" <p>Using a gene-screening method they created, Stanford Medicine researchers may have discovered why an effective chemotherapy damages heart cells - and they have identified a drug that could keep the heart cells beating.</p><p>The chemotherapy, doxorubicin, kills cancer cells, but it also causes heart cells to beat out of rhythm, organize incorrectly or die. If used in high doses or for extended periods, the drug can lead to heart failure, limiting its use despite its effectiveness in treating cancer.</p><p>\"We've always wanted to find a way to stave off this toxicity,\" said <a href=\"https://profiles.stanford.edu/joseph-wu\">Joseph Wu</a>, MD, PhD, a professor of cardiovascular medicine and the director of the <a href=\"https://med.stanford.edu/cvi.html\">Stanford Cardiovascular Institute</a>.</p><p>Wu and <a href=\"https://profiles.stanford.edu/stanleyqi\">Stanley Qi</a>, PhD, an associate professor in bioengineering and a scholar at <a href=\"https://chemh.stanford.edu/\">Sarafan ChEM-H</a>, created a genetic screening tool that harnesses CRISPR, a gene-editing technology, to uncover genes that may be involved in doxorubicin-induced heart damage. The screen pinpointed a gene that seemed to be one of the key vehicles through which doxorubicin inflicted damage.</p><p>\"This CRISPR screen is a valid tool for drug discovery,\" said Wu, the Simon H. Stertzer, MD, Professor. \"That, to me, is the key take-home message of the study.\"</p><p>Wu and Qi share the senior authorship of the <a href=\"https://www.sciencedirect.com/science/article/pii/S1934590924003692?dgcid=author\">paper</a>, published in <i>Cell Stem Cell</i> Nov. 7, describing the research. Chun Liu, PhD, an assistant professor at the Medical College of Wisconsin and a former Stanford Medicine postdoctoral researcher, and <a href=\"https://profiles.stanford.edu/mengcheng-shen\">Mengcheng Shen</a>, PhD, a researcher and instructor at the institute, are the lead authors on the paper.</p><h3>Genetic needle in a haystack</h3><p>The researchers knew that doxorubicin caused harm to heart cells, but they didn't know which genes were involved in the damage. They narrowed their search to 2,300 genes that existing drugs already target.</p>\n<p class=\"contentFragment-image-left\"> <img src=\"/content/dam/sm-news/images/2022/12/Joseph-Wu2.jpg\" alt=\"test\"> Joseph Wu\r\n</p>\n <p>\"Most of the time, when you do a drug screen, you know what the target gene is, and then you screen for drugs that block that gene,\" Qi said. But in this case, Wu and Qi didn't know the target gene, so they used a new genetic screening technique to observe the effects of doxorubicin on heart cells that were derived from induced pluripotent stem cells, which can give rise to any cell in the body.</p><p>The researchers used CRISPR to turn on or turn off one of the 2,300 genes in the heart cells such that each cell had only one gene changed. They then doused those cells with doxorubicin and noted which ones survived. The question then was, Why did they survive? To find out, the researchers sequenced the DNA of each cell, looking for genetic markers.</p><p>They found that the healthiest cells after doxorubicin treatment lacked a gene called CA12, which catalyzes reactions involving carbon dioxide to maintain a variety of the body's functions, such as respiration and the formation of saliva. The researchers did more genetic tests, deleting CA12 from heart cells and confirming their suspicion: Cells without CA12 resisted doxorubicin-induced toxicity. The details of what the gene does during doxorubicin treatment are not yet clear, Wu said, but he hopes to figure that out.</p><h3>Searching for a solution</h3><p>Once Wu and his team pegged CA12 as a genetic factor in doxorubicin toxicity, they wanted to find a way to stop the CA12 protein from damaging heart cells. They picked 40 drugs that inhibit carbonic anhydrase proteins such as CA12. They gave the drugs, along with doxorubicin, to groups of heart cells that were not genetically edited. They compared the groups' survival rate to find which cells stayed healthiest throughout the treatment.</p>\n<p class=\"contentFragment-image-right\"> <img src=\"/content/dam/sm/sm-news/images/2015/01/qi-lei-stanley-150.jpg\" alt=\"test\"> Stanley Qi\r\n</p>\n <p>A drug called indisulam, currently being studied as a potential cancer treatment, helped cardiomyocytes survive doxorubicin toxicity. Indisulam protected the heart cells' ability to relax and contract and aided in maintaining cellular processes.</p><p>The next step was to test indisulam in a living organism. They treated mice with doxorubicin, then fed one of two groups indisulam. The mice that had indisulam along with the doxorubicin fared better, with stronger heart function and fewer signs of heart atrophy. Their heart cells also maintained their structure better.</p><p>The researchers are interested in how indisulam stops CA12 activity and plan to do more tests on the drug candidate to curb doxorubicin's toxicity. They also hope to study how multiple genes interact in heart cell damage rather than focusing on one gene's effect at a time.</p><p>The researchers likewise have big goals for their newly developed CRISPR screen, hoping to apply the technology beyond heart cell toxicity. \"It's a proof of principle,\" Wu said. \"In the future you could use it for other types of toxicity or diseases. We think it's a very powerful tool.\"</p><p>Researchers from the Medical College of Wisconsin, Greenstone Biosciences, the University of North Texas, and the City of Hope Comprehensive Cancer Center also contributed to the study.</p><p>The study was supported by the National Institutes of Health (grants R01 HL141371, R01 HL141851, R01 HL145676, R01 HL150693, R01 HL171102, R01 CA266470, R21 CA270609, P01 HL141851, K99/R00 K99HL166693 and K99HL166773), the American Heart Association, Chan Zuckerberg Biohub, the National Science Foundation and the California Institute of Regenerative Medicine. Stanford's Cardiovascular Institute also supported the work.</p>","xdm:title":"Content"}]}}" data-cmp-contentfragment-path="/content/dam/content-fragments/articles/all-news/2024/11/heart-cell-chemotherapy"> <div class="cmp-contentfragment__elements"> <div> <div class="aem-Grid aem-Grid--12 aem-Grid--default--12 "> </div> </div> <div> <p>Using a gene-screening method they created, Stanford Medicine researchers may have discovered why an effective chemotherapy damages heart cells - and they have identified a drug that could keep the heart cells beating.</p> <div> <div class="aem-Grid aem-Grid--12 aem-Grid--default--12 "> </div> </div> <p>The chemotherapy, doxorubicin, kills cancer cells, but it also causes heart cells to beat out of rhythm, organize incorrectly or die. If used in high doses or for extended periods, the drug can lead to heart failure, limiting its use despite its effectiveness in treating cancer.</p> <div> <div class="aem-Grid aem-Grid--12 aem-Grid--default--12 "> </div> </div> <p>"We've always wanted to find a way to stave off this toxicity," said <a href="https://profiles.stanford.edu/joseph-wu">Joseph Wu</a>, MD, PhD, a professor of cardiovascular medicine and the director of the <a href="https://med.stanford.edu/cvi.html">Stanford Cardiovascular Institute</a>.</p> <div> <div class="aem-Grid aem-Grid--12 aem-Grid--default--12 "> </div> </div> <p>Wu and <a href="https://profiles.stanford.edu/stanleyqi">Stanley Qi</a>, PhD, an associate professor in bioengineering and a scholar at <a href="https://chemh.stanford.edu/">Sarafan ChEM-H</a>, created a genetic screening tool that harnesses CRISPR, a gene-editing technology, to uncover genes that may be involved in doxorubicin-induced heart damage. The screen pinpointed a gene that seemed to be one of the key vehicles through which doxorubicin inflicted damage.</p> <div> <div class="aem-Grid aem-Grid--12 aem-Grid--default--12 "> </div> </div> <p>"This CRISPR screen is a valid tool for drug discovery," said Wu, the Simon H. Stertzer, MD, Professor. "That, to me, is the key take-home message of the study."</p> <div> <div class="aem-Grid aem-Grid--12 aem-Grid--default--12 "> </div> </div> <p>Wu and Qi share the senior authorship of the <a href="https://www.sciencedirect.com/science/article/pii/S1934590924003692?dgcid=author">paper</a>, published in <i>Cell Stem Cell</i> Nov. 7, describing the research. Chun Liu, PhD, an assistant professor at the Medical College of Wisconsin and a former Stanford Medicine postdoctoral researcher, and <a href="https://profiles.stanford.edu/mengcheng-shen">Mengcheng Shen</a>, PhD, a researcher and instructor at the institute, are the lead authors on the paper.</p> <div> <div class="aem-Grid aem-Grid--12 aem-Grid--default--12 "> </div> </div> <h3>Genetic needle in a haystack</h3> <div> <div class="aem-Grid aem-Grid--12 aem-Grid--default--12 "> </div> </div> <p>The researchers knew that doxorubicin caused harm to heart cells, but they didn't know which genes were involved in the damage. They narrowed their search to 2,300 genes that existing drugs already target.</p> <p class="contentFragment-image-left"> <img src="/content/dam/sm-news/images/2022/12/Joseph-Wu2.jpg" alt="test" /> Joseph Wu </p> <div> <div class="aem-Grid aem-Grid--12 aem-Grid--default--12 "> </div> </div> <p>"Most of the time, when you do a drug screen, you know what the target gene is, and then you screen for drugs that block that gene," Qi said. But in this case, Wu and Qi didn't know the target gene, so they used a new genetic screening technique to observe the effects of doxorubicin on heart cells that were derived from induced pluripotent stem cells, which can give rise to any cell in the body.</p> <div> <div class="aem-Grid aem-Grid--12 aem-Grid--default--12 "> </div> </div> <p>The researchers used CRISPR to turn on or turn off one of the 2,300 genes in the heart cells such that each cell had only one gene changed. They then doused those cells with doxorubicin and noted which ones survived. The question then was, Why did they survive? To find out, the researchers sequenced the DNA of each cell, looking for genetic markers.</p> <div> <div class="aem-Grid aem-Grid--12 aem-Grid--default--12 "> </div> </div> <p>They found that the healthiest cells after doxorubicin treatment lacked a gene called CA12, which catalyzes reactions involving carbon dioxide to maintain a variety of the body's functions, such as respiration and the formation of saliva. The researchers did more genetic tests, deleting CA12 from heart cells and confirming their suspicion: Cells without CA12 resisted doxorubicin-induced toxicity. The details of what the gene does during doxorubicin treatment are not yet clear, Wu said, but he hopes to figure that out.</p> <div> <div class="aem-Grid aem-Grid--12 aem-Grid--default--12 "> </div> </div> <h3>Searching for a solution</h3> <div> <div class="aem-Grid aem-Grid--12 aem-Grid--default--12 "> </div> </div> <p>Once Wu and his team pegged CA12 as a genetic factor in doxorubicin toxicity, they wanted to find a way to stop the CA12 protein from damaging heart cells. They picked 40 drugs that inhibit carbonic anhydrase proteins such as CA12. They gave the drugs, along with doxorubicin, to groups of heart cells that were not genetically edited. They compared the groups' survival rate to find which cells stayed healthiest throughout the treatment.</p> <p class="contentFragment-image-right"> <img src="/content/dam/sm/sm-news/images/2015/01/qi-lei-stanley-150.jpg" alt="test" /> Stanley Qi </p> <div> <div class="aem-Grid aem-Grid--12 aem-Grid--default--12 "> </div> </div> <p>A drug called indisulam, currently being studied as a potential cancer treatment, helped cardiomyocytes survive doxorubicin toxicity. Indisulam protected the heart cells' ability to relax and contract and aided in maintaining cellular processes.</p> <div> <div class="aem-Grid aem-Grid--12 aem-Grid--default--12 "> </div> </div> <p>The next step was to test indisulam in a living organism. They treated mice with doxorubicin, then fed one of two groups indisulam. The mice that had indisulam along with the doxorubicin fared better, with stronger heart function and fewer signs of heart atrophy. Their heart cells also maintained their structure better.</p> <div> <div class="aem-Grid aem-Grid--12 aem-Grid--default--12 "> </div> </div> <p>The researchers are interested in how indisulam stops CA12 activity and plan to do more tests on the drug candidate to curb doxorubicin's toxicity. They also hope to study how multiple genes interact in heart cell damage rather than focusing on one gene's effect at a time.</p> <div> <div class="aem-Grid aem-Grid--12 aem-Grid--default--12 "> </div> </div> <p>The researchers likewise have big goals for their newly developed CRISPR screen, hoping to apply the technology beyond heart cell toxicity. "It's a proof of principle," Wu said. "In the future you could use it for other types of toxicity or diseases. We think it's a very powerful tool."</p> <div> <div class="aem-Grid aem-Grid--12 aem-Grid--default--12 "> </div> </div> <p>Researchers from the Medical College of Wisconsin, Greenstone Biosciences, the University of North Texas, and the City of Hope Comprehensive Cancer Center also contributed to the study.</p> <div> <div class="aem-Grid aem-Grid--12 aem-Grid--default--12 "> </div> </div> <p>The study was supported by the National Institutes of Health (grants R01 HL141371, R01 HL141851, R01 HL145676, R01 HL150693, R01 HL171102, R01 CA266470, R21 CA270609, P01 HL141851, K99/R00 K99HL166693 and K99HL166773), the American Heart Association, Chan Zuckerberg Biohub, the National Science Foundation and the California Institute of Regenerative Medicine. Stanford's Cardiovascular Institute also supported the work.</p> <div> <div class="aem-Grid aem-Grid--12 aem-Grid--default--12 "> </div> </div> </div> </div> </section> </div> </div> </div> </article> <div class="experiencefragment" is="stanford-experiencefragment"> <div id="experiencefragment-d0e317641d" class="cmp-experiencefragment cmp-experiencefragment--about-stanford-medicine"> <div id="container-f836ec7112" class="cmp-container"> <div class="text" is="stanford-text"> <div data-cmp-data-layer="{"text-6631c0e627":{"@type":"stanford/components/text","repo:modifyDate":"2024-12-20T18:54:21Z","xdm:text":"<p><b>About Stanford Medicine</b></p>\r\n<p><a href=\"https://med.stanford.edu/\">Stanford Medicine</a> is an integrated academic health system comprising the <a href=\"https://med.stanford.edu/school.html\">Stanford School of Medicine</a> and adult and pediatric health care delivery systems. 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Stanford Medicine study discovers what's behind heart cell damage from chemotherapy