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An ex vivo organ culture screening model revealed that low temperature conditions prevent side effects of anticancer drugs
Development of chemotherapy has led to a high survival rate of cancer patients; however, the severe side effects of anticancer drugs, including organ hypoplasia, persist. To assume the side effect of anticancer drugs, we established a new ex vivo screening model and described a method for suppressin...
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Published in: | Scientific reports 2022-02, Vol.12 (1), p.3093-3093, Article 3093 |
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creator | Tian, Tian Miyazaki, Kanako Chiba, Yuta Funada, Keita Yuta, Tomomi Mizuta, Kanji Fu, Yao Kawahara, Jumpei Han, Xue Ando, Yuna Funada, Ami Yamada, Aya Iwamoto, Tsutomu Nakamura, Seiji Takahashi, Ichiro Fukumoto, Satoshi Yoshizaki, Keigo |
description | Development of chemotherapy has led to a high survival rate of cancer patients; however, the severe side effects of anticancer drugs, including organ hypoplasia, persist. To assume the side effect of anticancer drugs, we established a new ex vivo screening model and described a method for suppressing side effects. Cyclophosphamide (CPA) is a commonly used anticancer drug and causes severe side effects in developing organs with intensive proliferation, including the teeth and hair. Using the organ culture model, we found that treatment with CPA disturbed the growth of tooth germs by inducing DNA damage, apoptosis and suppressing cellular proliferation and differentiation. Furthermore, low temperature suppressed CPA-mediated inhibition of organ development. Our ex vivo and in vitro analysis revealed that low temperature impeded Rb phosphorylation and caused cell cycle arrest at the G1 phase during CPA treatment. This can prevent the CPA-mediated cell damage of DNA replication caused by the cross-linking reaction of CPA. Our findings suggest that the side effects of anticancer drugs on organ development can be avoided by maintaining the internal environment under low temperature. |
doi_str_mv | 10.1038/s41598-022-06945-7 |
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To assume the side effect of anticancer drugs, we established a new ex vivo screening model and described a method for suppressing side effects. Cyclophosphamide (CPA) is a commonly used anticancer drug and causes severe side effects in developing organs with intensive proliferation, including the teeth and hair. Using the organ culture model, we found that treatment with CPA disturbed the growth of tooth germs by inducing DNA damage, apoptosis and suppressing cellular proliferation and differentiation. Furthermore, low temperature suppressed CPA-mediated inhibition of organ development. Our ex vivo and in vitro analysis revealed that low temperature impeded Rb phosphorylation and caused cell cycle arrest at the G1 phase during CPA treatment. This can prevent the CPA-mediated cell damage of DNA replication caused by the cross-linking reaction of CPA. Our findings suggest that the side effects of anticancer drugs on organ development can be avoided by maintaining the internal environment under low temperature.</description><identifier>ISSN: 2045-2322</identifier><identifier>EISSN: 2045-2322</identifier><identifier>DOI: 10.1038/s41598-022-06945-7</identifier><identifier>PMID: 35197531</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>631/136/2060 ; 692/308/1426 ; Antineoplastic Agents - adverse effects ; Antineoplastic drugs ; Antitumor agents ; Apoptosis ; Cancer ; Cell culture ; Cell cycle ; Cell Cycle Checkpoints - drug effects ; Cell Proliferation - drug effects ; Chemotherapy ; Cyclophosphamide ; Cyclophosphamide - adverse effects ; Deoxyribonucleic acid ; DNA ; DNA biosynthesis ; DNA damage ; DNA Damage - drug effects ; DNA Replication - drug effects ; Drug development ; Drugs ; G1 phase ; G1 Phase - drug effects ; Humanities and Social Sciences ; Humans ; Hypoplasia ; Low temperature ; Models, Biological ; multidisciplinary ; Organ culture ; Organ Culture Techniques ; Phosphorylation ; Science ; Science (multidisciplinary) ; Side effects ; Temperature</subject><ispartof>Scientific reports, 2022-02, Vol.12 (1), p.3093-3093, Article 3093</ispartof><rights>The Author(s) 2022</rights><rights>2022. The Author(s).</rights><rights>The Author(s) 2022. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c679t-a332d5d9d2c066031b8314063ae65fbf5e7af9fdf71d3efef43b6972f01508163</citedby><cites>FETCH-LOGICAL-c679t-a332d5d9d2c066031b8314063ae65fbf5e7af9fdf71d3efef43b6972f01508163</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.proquest.com/docview/2632035774/fulltextPDF?pq-origsite=primo$$EPDF$$P50$$Gproquest$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/2632035774?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,25732,27903,27904,36991,36992,44569,53769,53771,74872</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/35197531$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Tian, Tian</creatorcontrib><creatorcontrib>Miyazaki, Kanako</creatorcontrib><creatorcontrib>Chiba, Yuta</creatorcontrib><creatorcontrib>Funada, Keita</creatorcontrib><creatorcontrib>Yuta, Tomomi</creatorcontrib><creatorcontrib>Mizuta, Kanji</creatorcontrib><creatorcontrib>Fu, Yao</creatorcontrib><creatorcontrib>Kawahara, Jumpei</creatorcontrib><creatorcontrib>Han, Xue</creatorcontrib><creatorcontrib>Ando, Yuna</creatorcontrib><creatorcontrib>Funada, Ami</creatorcontrib><creatorcontrib>Yamada, Aya</creatorcontrib><creatorcontrib>Iwamoto, Tsutomu</creatorcontrib><creatorcontrib>Nakamura, Seiji</creatorcontrib><creatorcontrib>Takahashi, Ichiro</creatorcontrib><creatorcontrib>Fukumoto, Satoshi</creatorcontrib><creatorcontrib>Yoshizaki, Keigo</creatorcontrib><title>An ex vivo organ culture screening model revealed that low temperature conditions prevent side effects of anticancer drugs</title><title>Scientific reports</title><addtitle>Sci Rep</addtitle><addtitle>Sci Rep</addtitle><description>Development of chemotherapy has led to a high survival rate of cancer patients; however, the severe side effects of anticancer drugs, including organ hypoplasia, persist. To assume the side effect of anticancer drugs, we established a new ex vivo screening model and described a method for suppressing side effects. Cyclophosphamide (CPA) is a commonly used anticancer drug and causes severe side effects in developing organs with intensive proliferation, including the teeth and hair. Using the organ culture model, we found that treatment with CPA disturbed the growth of tooth germs by inducing DNA damage, apoptosis and suppressing cellular proliferation and differentiation. Furthermore, low temperature suppressed CPA-mediated inhibition of organ development. Our ex vivo and in vitro analysis revealed that low temperature impeded Rb phosphorylation and caused cell cycle arrest at the G1 phase during CPA treatment. This can prevent the CPA-mediated cell damage of DNA replication caused by the cross-linking reaction of CPA. Our findings suggest that the side effects of anticancer drugs on organ development can be avoided by maintaining the internal environment under low temperature.</description><subject>631/136/2060</subject><subject>692/308/1426</subject><subject>Antineoplastic Agents - adverse effects</subject><subject>Antineoplastic drugs</subject><subject>Antitumor agents</subject><subject>Apoptosis</subject><subject>Cancer</subject><subject>Cell culture</subject><subject>Cell cycle</subject><subject>Cell Cycle Checkpoints - drug effects</subject><subject>Cell Proliferation - drug effects</subject><subject>Chemotherapy</subject><subject>Cyclophosphamide</subject><subject>Cyclophosphamide - adverse effects</subject><subject>Deoxyribonucleic acid</subject><subject>DNA</subject><subject>DNA biosynthesis</subject><subject>DNA damage</subject><subject>DNA Damage - drug effects</subject><subject>DNA Replication - drug effects</subject><subject>Drug development</subject><subject>Drugs</subject><subject>G1 phase</subject><subject>G1 Phase - 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To assume the side effect of anticancer drugs, we established a new ex vivo screening model and described a method for suppressing side effects. Cyclophosphamide (CPA) is a commonly used anticancer drug and causes severe side effects in developing organs with intensive proliferation, including the teeth and hair. Using the organ culture model, we found that treatment with CPA disturbed the growth of tooth germs by inducing DNA damage, apoptosis and suppressing cellular proliferation and differentiation. Furthermore, low temperature suppressed CPA-mediated inhibition of organ development. Our ex vivo and in vitro analysis revealed that low temperature impeded Rb phosphorylation and caused cell cycle arrest at the G1 phase during CPA treatment. This can prevent the CPA-mediated cell damage of DNA replication caused by the cross-linking reaction of CPA. 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subjects | 631/136/2060 692/308/1426 Antineoplastic Agents - adverse effects Antineoplastic drugs Antitumor agents Apoptosis Cancer Cell culture Cell cycle Cell Cycle Checkpoints - drug effects Cell Proliferation - drug effects Chemotherapy Cyclophosphamide Cyclophosphamide - adverse effects Deoxyribonucleic acid DNA DNA biosynthesis DNA damage DNA Damage - drug effects DNA Replication - drug effects Drug development Drugs G1 phase G1 Phase - drug effects Humanities and Social Sciences Humans Hypoplasia Low temperature Models, Biological multidisciplinary Organ culture Organ Culture Techniques Phosphorylation Science Science (multidisciplinary) Side effects Temperature |
title | An ex vivo organ culture screening model revealed that low temperature conditions prevent side effects of anticancer drugs |
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