Inhibition of mutagenic translesion synthesis: A possible strategy for improving chemotherapy?

[...]mistakes introduced by TLS polymerases copying over DNA lesions introduced during the chemotherapy lead to mutations that contribute to acquired resistance. Besides the structural features of individual TLS polymerases, successful TLS also depends on interactions between these polymerases and o...

Ausführliche Beschreibung

Gespeichert in:
Bibliographische Detailangaben
Veröffentlicht in:PLoS genetics 2017-08, Vol.13 (8), p.e1006842
Hauptverfasser: Yamanaka, Kinrin, Chatterjee, Nimrat, Hemann, Michael T, Walker, Graham C
Format: Artikel
Sprache:eng
Schlagworte:
Online-Zugang:Volltext
Tags: Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
container_end_page
container_issue 8
container_start_page e1006842
container_title PLoS genetics
container_volume 13
creator Yamanaka, Kinrin
Chatterjee, Nimrat
Hemann, Michael T
Walker, Graham C
description [...]mistakes introduced by TLS polymerases copying over DNA lesions introduced during the chemotherapy lead to mutations that contribute to acquired resistance. Besides the structural features of individual TLS polymerases, successful TLS also depends on interactions between these polymerases and other cellular proteins that target and choreograph their activity. [...]targeting REV1 and REV3 might not only increase killing of cancer cells but could also potentially suppress secondary malignancies and tumor relapse. [...]the effectiveness of small molecule inhibitors of TLS polymerase could be further improved by delivery systems that could target these drugs to specific tumors in cancer patients. Because protein-protein interactions are so important for TLS, drug targets for these interaction interfaces could be promising candidates for cancer therapeutics.
doi_str_mv 10.1371/journal.pgen.1006842
format Article
fullrecord <record><control><sourceid>proquest_plos_</sourceid><recordid>TN_cdi_plos_journals_1939435786</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><doaj_id>oai_doaj_org_article_c572e3fd3acf44e48bf6682cad295255</doaj_id><sourcerecordid>1939435786</sourcerecordid><originalsourceid>FETCH-LOGICAL-c592t-c610e1bdaabbdbff448fcb755ccb418ae9f63b9f32ac88a04b4c41396a8597ce3</originalsourceid><addsrcrecordid>eNp1Uk1vEzEUtBCIlsA_QGCJc4K9_libA1VV8RGpEhe4Ytlee-No117sTaX8exyyrdoDJz_5zcwbzXsAvMVog0mLP-7TIUc9bKbexQ1GiAvaPAOXmDGybimizx_VF-BVKXuECBOyfQkuGiFwyzi_BL-3cRdMmEOKMHk4HmZd9YKFc9axDK6cGuUY510tyyd4DadUSjCDg6VCZtcfoU8ZhnHK6S7EHtqdG1OFZz0dr16DF14Pxb1Z3hX49fXLz5vv69sf37Y317dry2Qzry3HyGHTaW1MZ7ynVHhrWsasNRQL7aTnxEhPGm2F0IgaaikmkmvBZGsdWYH3Z91pSEUt0RSFJZGUsFbwitieEV3SezXlMOp8VEkH9e8j5V7pPAc7OGVZ2zjiO6JtdeKoMJ5z0VjdNZI1NdMV-LxMO5jRddbFGsXwRPRpJ4ad6tOdYowjRmQV-LAI5PTn4Mr8H8v0jLK5Zp6df5iAkTrdwD1LnW5ALTdQae8eu3sg3S-d_AVE37Og</addsrcrecordid><sourcetype>Open Website</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1939435786</pqid></control><display><type>article</type><title>Inhibition of mutagenic translesion synthesis: A possible strategy for improving chemotherapy?</title><source>MEDLINE</source><source>DOAJ Directory of Open Access Journals</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>PubMed Central</source><source>Public Library of Science (PLoS)</source><creator>Yamanaka, Kinrin ; Chatterjee, Nimrat ; Hemann, Michael T ; Walker, Graham C</creator><creatorcontrib>Yamanaka, Kinrin ; Chatterjee, Nimrat ; Hemann, Michael T ; Walker, Graham C</creatorcontrib><description>[...]mistakes introduced by TLS polymerases copying over DNA lesions introduced during the chemotherapy lead to mutations that contribute to acquired resistance. Besides the structural features of individual TLS polymerases, successful TLS also depends on interactions between these polymerases and other cellular proteins that target and choreograph their activity. [...]targeting REV1 and REV3 might not only increase killing of cancer cells but could also potentially suppress secondary malignancies and tumor relapse. [...]the effectiveness of small molecule inhibitors of TLS polymerase could be further improved by delivery systems that could target these drugs to specific tumors in cancer patients. Because protein-protein interactions are so important for TLS, drug targets for these interaction interfaces could be promising candidates for cancer therapeutics.</description><identifier>ISSN: 1553-7404</identifier><identifier>ISSN: 1553-7390</identifier><identifier>EISSN: 1553-7404</identifier><identifier>DOI: 10.1371/journal.pgen.1006842</identifier><identifier>PMID: 28817566</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Animals ; Antineoplastic Agents - pharmacology ; Antineoplastic Agents - therapeutic use ; Biology ; Biology and life sciences ; Brain cancer ; Cancer therapies ; Cell cycle ; Chemotherapy ; Deoxyribonucleic acid ; DNA ; DNA Damage ; DNA polymerase ; DNA Repair ; DNA Replication ; DNA-Directed DNA Polymerase - metabolism ; Drug resistance ; Drug Resistance, Neoplasm ; Genomes ; Humans ; Medical prognosis ; Medicine and Health Sciences ; Mutation ; Nucleic Acid Synthesis Inhibitors - pharmacology ; Nucleic Acid Synthesis Inhibitors - therapeutic use ; Proteins ; Research and Analysis Methods ; Tumors ; Viewpoints</subject><ispartof>PLoS genetics, 2017-08, Vol.13 (8), p.e1006842</ispartof><rights>2017 Public Library of Science. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited: Yamanaka K, Chatterjee N, Hemann MT, Walker GC (2017) Inhibition of mutagenic translesion synthesis: A possible strategy for improving chemotherapy? PLoS Genet 13(8): e1006842. https://doi.org/10.1371/journal.pgen.1006842</rights><rights>2017 Yamanaka et al 2017 Yamanaka et al</rights><rights>2017 Public Library of Science. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited: Yamanaka K, Chatterjee N, Hemann MT, Walker GC (2017) Inhibition of mutagenic translesion synthesis: A possible strategy for improving chemotherapy? PLoS Genet 13(8): e1006842. https://doi.org/10.1371/journal.pgen.1006842</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c592t-c610e1bdaabbdbff448fcb755ccb418ae9f63b9f32ac88a04b4c41396a8597ce3</citedby><cites>FETCH-LOGICAL-c592t-c610e1bdaabbdbff448fcb755ccb418ae9f63b9f32ac88a04b4c41396a8597ce3</cites><orcidid>0000-0001-7243-8261 ; 0000-0001-5539-4391 ; 0000-0001-6556-9423 ; 0000-0001-6776-2163</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5560539/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5560539/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,2096,2915,23845,27901,27902,53766,53768,79343,79344</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28817566$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Yamanaka, Kinrin</creatorcontrib><creatorcontrib>Chatterjee, Nimrat</creatorcontrib><creatorcontrib>Hemann, Michael T</creatorcontrib><creatorcontrib>Walker, Graham C</creatorcontrib><title>Inhibition of mutagenic translesion synthesis: A possible strategy for improving chemotherapy?</title><title>PLoS genetics</title><addtitle>PLoS Genet</addtitle><description>[...]mistakes introduced by TLS polymerases copying over DNA lesions introduced during the chemotherapy lead to mutations that contribute to acquired resistance. Besides the structural features of individual TLS polymerases, successful TLS also depends on interactions between these polymerases and other cellular proteins that target and choreograph their activity. [...]targeting REV1 and REV3 might not only increase killing of cancer cells but could also potentially suppress secondary malignancies and tumor relapse. [...]the effectiveness of small molecule inhibitors of TLS polymerase could be further improved by delivery systems that could target these drugs to specific tumors in cancer patients. Because protein-protein interactions are so important for TLS, drug targets for these interaction interfaces could be promising candidates for cancer therapeutics.</description><subject>Animals</subject><subject>Antineoplastic Agents - pharmacology</subject><subject>Antineoplastic Agents - therapeutic use</subject><subject>Biology</subject><subject>Biology and life sciences</subject><subject>Brain cancer</subject><subject>Cancer therapies</subject><subject>Cell cycle</subject><subject>Chemotherapy</subject><subject>Deoxyribonucleic acid</subject><subject>DNA</subject><subject>DNA Damage</subject><subject>DNA polymerase</subject><subject>DNA Repair</subject><subject>DNA Replication</subject><subject>DNA-Directed DNA Polymerase - metabolism</subject><subject>Drug resistance</subject><subject>Drug Resistance, Neoplasm</subject><subject>Genomes</subject><subject>Humans</subject><subject>Medical prognosis</subject><subject>Medicine and Health Sciences</subject><subject>Mutation</subject><subject>Nucleic Acid Synthesis Inhibitors - pharmacology</subject><subject>Nucleic Acid Synthesis Inhibitors - therapeutic use</subject><subject>Proteins</subject><subject>Research and Analysis Methods</subject><subject>Tumors</subject><subject>Viewpoints</subject><issn>1553-7404</issn><issn>1553-7390</issn><issn>1553-7404</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><sourceid>DOA</sourceid><recordid>eNp1Uk1vEzEUtBCIlsA_QGCJc4K9_libA1VV8RGpEhe4Ytlee-No117sTaX8exyyrdoDJz_5zcwbzXsAvMVog0mLP-7TIUc9bKbexQ1GiAvaPAOXmDGybimizx_VF-BVKXuECBOyfQkuGiFwyzi_BL-3cRdMmEOKMHk4HmZd9YKFc9axDK6cGuUY510tyyd4DadUSjCDg6VCZtcfoU8ZhnHK6S7EHtqdG1OFZz0dr16DF14Pxb1Z3hX49fXLz5vv69sf37Y317dry2Qzry3HyGHTaW1MZ7ynVHhrWsasNRQL7aTnxEhPGm2F0IgaaikmkmvBZGsdWYH3Z91pSEUt0RSFJZGUsFbwitieEV3SezXlMOp8VEkH9e8j5V7pPAc7OGVZ2zjiO6JtdeKoMJ5z0VjdNZI1NdMV-LxMO5jRddbFGsXwRPRpJ4ad6tOdYowjRmQV-LAI5PTn4Mr8H8v0jLK5Zp6df5iAkTrdwD1LnW5ALTdQae8eu3sg3S-d_AVE37Og</recordid><startdate>20170801</startdate><enddate>20170801</enddate><creator>Yamanaka, Kinrin</creator><creator>Chatterjee, Nimrat</creator><creator>Hemann, Michael T</creator><creator>Walker, Graham C</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7QP</scope><scope>7QR</scope><scope>7SS</scope><scope>7TK</scope><scope>7TM</scope><scope>7TO</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>P64</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>RC3</scope><scope>5PM</scope><scope>DOA</scope><orcidid>https://orcid.org/0000-0001-7243-8261</orcidid><orcidid>https://orcid.org/0000-0001-5539-4391</orcidid><orcidid>https://orcid.org/0000-0001-6556-9423</orcidid><orcidid>https://orcid.org/0000-0001-6776-2163</orcidid></search><sort><creationdate>20170801</creationdate><title>Inhibition of mutagenic translesion synthesis: A possible strategy for improving chemotherapy?</title><author>Yamanaka, Kinrin ; Chatterjee, Nimrat ; Hemann, Michael T ; Walker, Graham C</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c592t-c610e1bdaabbdbff448fcb755ccb418ae9f63b9f32ac88a04b4c41396a8597ce3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Animals</topic><topic>Antineoplastic Agents - pharmacology</topic><topic>Antineoplastic Agents - therapeutic use</topic><topic>Biology</topic><topic>Biology and life sciences</topic><topic>Brain cancer</topic><topic>Cancer therapies</topic><topic>Cell cycle</topic><topic>Chemotherapy</topic><topic>Deoxyribonucleic acid</topic><topic>DNA</topic><topic>DNA Damage</topic><topic>DNA polymerase</topic><topic>DNA Repair</topic><topic>DNA Replication</topic><topic>DNA-Directed DNA Polymerase - metabolism</topic><topic>Drug resistance</topic><topic>Drug Resistance, Neoplasm</topic><topic>Genomes</topic><topic>Humans</topic><topic>Medical prognosis</topic><topic>Medicine and Health Sciences</topic><topic>Mutation</topic><topic>Nucleic Acid Synthesis Inhibitors - pharmacology</topic><topic>Nucleic Acid Synthesis Inhibitors - therapeutic use</topic><topic>Proteins</topic><topic>Research and Analysis Methods</topic><topic>Tumors</topic><topic>Viewpoints</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Yamanaka, Kinrin</creatorcontrib><creatorcontrib>Chatterjee, Nimrat</creatorcontrib><creatorcontrib>Hemann, Michael T</creatorcontrib><creatorcontrib>Walker, Graham C</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Calcium &amp; Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Entomology Abstracts (Full archive)</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Health &amp; Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health &amp; Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health &amp; Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>Genetics Abstracts</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PLoS genetics</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Yamanaka, Kinrin</au><au>Chatterjee, Nimrat</au><au>Hemann, Michael T</au><au>Walker, Graham C</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Inhibition of mutagenic translesion synthesis: A possible strategy for improving chemotherapy?</atitle><jtitle>PLoS genetics</jtitle><addtitle>PLoS Genet</addtitle><date>2017-08-01</date><risdate>2017</risdate><volume>13</volume><issue>8</issue><spage>e1006842</spage><pages>e1006842-</pages><issn>1553-7404</issn><issn>1553-7390</issn><eissn>1553-7404</eissn><abstract>[...]mistakes introduced by TLS polymerases copying over DNA lesions introduced during the chemotherapy lead to mutations that contribute to acquired resistance. Besides the structural features of individual TLS polymerases, successful TLS also depends on interactions between these polymerases and other cellular proteins that target and choreograph their activity. [...]targeting REV1 and REV3 might not only increase killing of cancer cells but could also potentially suppress secondary malignancies and tumor relapse. [...]the effectiveness of small molecule inhibitors of TLS polymerase could be further improved by delivery systems that could target these drugs to specific tumors in cancer patients. Because protein-protein interactions are so important for TLS, drug targets for these interaction interfaces could be promising candidates for cancer therapeutics.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>28817566</pmid><doi>10.1371/journal.pgen.1006842</doi><orcidid>https://orcid.org/0000-0001-7243-8261</orcidid><orcidid>https://orcid.org/0000-0001-5539-4391</orcidid><orcidid>https://orcid.org/0000-0001-6556-9423</orcidid><orcidid>https://orcid.org/0000-0001-6776-2163</orcidid><oa>free_for_read</oa></addata></record>
fulltext fulltext
identifier ISSN: 1553-7404
ispartof PLoS genetics, 2017-08, Vol.13 (8), p.e1006842
issn 1553-7404
1553-7390
1553-7404
language eng
recordid cdi_plos_journals_1939435786
source MEDLINE; DOAJ Directory of Open Access Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central; Public Library of Science (PLoS)
subjects Animals
Antineoplastic Agents - pharmacology
Antineoplastic Agents - therapeutic use
Biology
Biology and life sciences
Brain cancer
Cancer therapies
Cell cycle
Chemotherapy
Deoxyribonucleic acid
DNA
DNA Damage
DNA polymerase
DNA Repair
DNA Replication
DNA-Directed DNA Polymerase - metabolism
Drug resistance
Drug Resistance, Neoplasm
Genomes
Humans
Medical prognosis
Medicine and Health Sciences
Mutation
Nucleic Acid Synthesis Inhibitors - pharmacology
Nucleic Acid Synthesis Inhibitors - therapeutic use
Proteins
Research and Analysis Methods
Tumors
Viewpoints
title Inhibition of mutagenic translesion synthesis: A possible strategy for improving chemotherapy?
url https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-02T01%3A48%3A45IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_plos_&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Inhibition%20of%20mutagenic%20translesion%20synthesis:%20A%20possible%20strategy%20for%20improving%20chemotherapy?&rft.jtitle=PLoS%20genetics&rft.au=Yamanaka,%20Kinrin&rft.date=2017-08-01&rft.volume=13&rft.issue=8&rft.spage=e1006842&rft.pages=e1006842-&rft.issn=1553-7404&rft.eissn=1553-7404&rft_id=info:doi/10.1371/journal.pgen.1006842&rft_dat=%3Cproquest_plos_%3E1939435786%3C/proquest_plos_%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1939435786&rft_id=info:pmid/28817566&rft_doaj_id=oai_doaj_org_article_c572e3fd3acf44e48bf6682cad295255&rfr_iscdi=true