Targeting DNA Damage Response and Immune Checkpoint for Anticancer Therapy

Deficiency in DNA damage response (DDR) genes leads to impaired DNA repair functions that will induce genomic instability and facilitate cancer development. However, alterations of DDR genes can serve as biomarkers for the selection of suitable patients to receive specific therapeutics, such as immu...

Full description

Saved in:
Bibliographic Details
Published in:International journal of molecular sciences 2022-03, Vol.23 (6), p.3238
Main Authors: Huang, Jau-Ling, Chang, Yu-Tzu, Hong, Zhen-Yang, Lin, Chang-Shen
Format: Article
Language:English
Subjects:
Angiogenesis
Apoptosis
Ataxia
Biomarkers
Breast
Breast cancer
Cancer immunotherapy
Cancer therapies
Cell cycle
cGAS-STING
Chemotherapy
clinical trial
Clinical trials
Colorectal cancer
Deoxyribonucleic acid
DNA
DNA Damage
DNA damage response
DNA methylation
DNA Repair
Gene expression
Genes
Genomic instability
Growth factors
Humans
Immune checkpoint
Immune response
Immune system
Immunity
Immunotherapy
Inflammation
Interferon
Kinases
Leukemia
Mutation
Neoplasms - drug therapy
Neoplasms - genetics
Pancreatic cancer
PARP
Patients
Polymerization
Proteins
Review
RNA polymerase
Therapeutic targets
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
cited_by cdi_FETCH-LOGICAL-c478t-8bdcfda02fe8d734b08262011a007c3f480393f95d9c92adae3e97999490d70b3
cites cdi_FETCH-LOGICAL-c478t-8bdcfda02fe8d734b08262011a007c3f480393f95d9c92adae3e97999490d70b3
container_end_page
container_issue 6
container_start_page 3238
container_title International journal of molecular sciences
container_volume 23
creator Huang, Jau-Ling
Chang, Yu-Tzu
Hong, Zhen-Yang
Lin, Chang-Shen
description Deficiency in DNA damage response (DDR) genes leads to impaired DNA repair functions that will induce genomic instability and facilitate cancer development. However, alterations of DDR genes can serve as biomarkers for the selection of suitable patients to receive specific therapeutics, such as immune checkpoint blockade (ICB) therapy. In addition, certain altered DDR genes can be ideal therapeutic targets through adapting the mechanism of synthetic lethality. Recent studies indicate that targeting DDR can improve cancer immunotherapy by modulating the immune response mediated by cGAS-STING-interferon signaling. Investigations of the interplay of DDR-targeting and ICB therapies provide more effective treatment options for cancer patients. This review introduces the mechanisms of DDR and discusses their crucial roles in cancer therapy based on the concepts of synthetic lethality and ICB. The contemporary clinical trials of DDR-targeting and ICB therapies in breast, colorectal, and pancreatic cancers are included.
doi_str_mv 10.3390/ijms23063238
format article
fullrecord <record><control><sourceid>proquest_doaj_</sourceid><recordid>TN_cdi_doaj_primary_oai_doaj_org_article_01a9ae347a124b0092183afd019cef4b</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><doaj_id>oai_doaj_org_article_01a9ae347a124b0092183afd019cef4b</doaj_id><sourcerecordid>2642433504</sourcerecordid><originalsourceid>FETCH-LOGICAL-c478t-8bdcfda02fe8d734b08262011a007c3f480393f95d9c92adae3e97999490d70b3</originalsourceid><addsrcrecordid>eNpdkU2P0zAQhiMEYj_gxhlF4sKBwvgjiX1BqrosFK1AQuVsTe1JmpLYWTtB2n9PSpdVl5Mt-_HjmXmz7BWD90Jo-NDu-8QFlIIL9SQ7Z5LzBUBZPT3Zn2UXKe0BuOCFfp6diUJwVRbqPPu6wdjQ2Pomv_q2zK-wx4byH5SG4BPl6F2-7vvJU77akf01hNaPeR1ivvRja9FbivlmRxGHuxfZsxq7RC_v18vs5_WnzerL4ub75_VqebOwslLjQm2drR0Cr0m5SsgtKF5yYAwBKitqqUBoUevCaas5OiRButJaSw2ugq24zNZHrwu4N0Nse4x3JmBr_h6E2BiMc3EdGWCo5_eyQsbnj0BzpgTWDpi2VMuD6-PRNUzbnpwlP0bsHkkf3_h2Z5rw2yhdcF6yWfD2XhDD7URpNH2bLHUdegpTMryUEkBIrmb0zX_oPkzRz6M6UFwKUYCcqXdHysaQUqT6oRgG5hC4OQ18xl-fNvAA_0tY_AH4TqVr</addsrcrecordid><sourcetype>Open Website</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2642433504</pqid></control><display><type>article</type><title>Targeting DNA Damage Response and Immune Checkpoint for Anticancer Therapy</title><source>Publicly Available Content Database</source><source>PubMed Central</source><creator>Huang, Jau-Ling ; Chang, Yu-Tzu ; Hong, Zhen-Yang ; Lin, Chang-Shen</creator><creatorcontrib>Huang, Jau-Ling ; Chang, Yu-Tzu ; Hong, Zhen-Yang ; Lin, Chang-Shen</creatorcontrib><description>Deficiency in DNA damage response (DDR) genes leads to impaired DNA repair functions that will induce genomic instability and facilitate cancer development. However, alterations of DDR genes can serve as biomarkers for the selection of suitable patients to receive specific therapeutics, such as immune checkpoint blockade (ICB) therapy. In addition, certain altered DDR genes can be ideal therapeutic targets through adapting the mechanism of synthetic lethality. Recent studies indicate that targeting DDR can improve cancer immunotherapy by modulating the immune response mediated by cGAS-STING-interferon signaling. Investigations of the interplay of DDR-targeting and ICB therapies provide more effective treatment options for cancer patients. This review introduces the mechanisms of DDR and discusses their crucial roles in cancer therapy based on the concepts of synthetic lethality and ICB. The contemporary clinical trials of DDR-targeting and ICB therapies in breast, colorectal, and pancreatic cancers are included.</description><identifier>ISSN: 1422-0067</identifier><identifier>ISSN: 1661-6596</identifier><identifier>EISSN: 1422-0067</identifier><identifier>DOI: 10.3390/ijms23063238</identifier><identifier>PMID: 35328658</identifier><language>eng</language><publisher>Switzerland: MDPI AG</publisher><subject>Angiogenesis ; Apoptosis ; Ataxia ; Biomarkers ; Breast ; Breast cancer ; Cancer immunotherapy ; Cancer therapies ; Cell cycle ; cGAS-STING ; Chemotherapy ; clinical trial ; Clinical trials ; Colorectal cancer ; Deoxyribonucleic acid ; DNA ; DNA Damage ; DNA damage response ; DNA methylation ; DNA Repair ; Gene expression ; Genes ; Genomic instability ; Growth factors ; Humans ; Immune checkpoint ; Immune response ; Immune system ; Immunity ; Immunotherapy ; Inflammation ; Interferon ; Kinases ; Leukemia ; Mutation ; Neoplasms - drug therapy ; Neoplasms - genetics ; Pancreatic cancer ; PARP ; Patients ; Polymerization ; Proteins ; Review ; RNA polymerase ; Therapeutic targets</subject><ispartof>International journal of molecular sciences, 2022-03, Vol.23 (6), p.3238</ispartof><rights>2022 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2022 by the authors. 2022</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c478t-8bdcfda02fe8d734b08262011a007c3f480393f95d9c92adae3e97999490d70b3</citedby><cites>FETCH-LOGICAL-c478t-8bdcfda02fe8d734b08262011a007c3f480393f95d9c92adae3e97999490d70b3</cites><orcidid>0000-0001-7415-2187</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.proquest.com/docview/2642433504/fulltextPDF?pq-origsite=primo$$EPDF$$P50$$Gproquest$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/2642433504?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,25753,27924,27925,37012,37013,44590,53791,53793,75126</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/35328658$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Huang, Jau-Ling</creatorcontrib><creatorcontrib>Chang, Yu-Tzu</creatorcontrib><creatorcontrib>Hong, Zhen-Yang</creatorcontrib><creatorcontrib>Lin, Chang-Shen</creatorcontrib><title>Targeting DNA Damage Response and Immune Checkpoint for Anticancer Therapy</title><title>International journal of molecular sciences</title><addtitle>Int J Mol Sci</addtitle><description>Deficiency in DNA damage response (DDR) genes leads to impaired DNA repair functions that will induce genomic instability and facilitate cancer development. However, alterations of DDR genes can serve as biomarkers for the selection of suitable patients to receive specific therapeutics, such as immune checkpoint blockade (ICB) therapy. In addition, certain altered DDR genes can be ideal therapeutic targets through adapting the mechanism of synthetic lethality. Recent studies indicate that targeting DDR can improve cancer immunotherapy by modulating the immune response mediated by cGAS-STING-interferon signaling. Investigations of the interplay of DDR-targeting and ICB therapies provide more effective treatment options for cancer patients. This review introduces the mechanisms of DDR and discusses their crucial roles in cancer therapy based on the concepts of synthetic lethality and ICB. The contemporary clinical trials of DDR-targeting and ICB therapies in breast, colorectal, and pancreatic cancers are included.</description><subject>Angiogenesis</subject><subject>Apoptosis</subject><subject>Ataxia</subject><subject>Biomarkers</subject><subject>Breast</subject><subject>Breast cancer</subject><subject>Cancer immunotherapy</subject><subject>Cancer therapies</subject><subject>Cell cycle</subject><subject>cGAS-STING</subject><subject>Chemotherapy</subject><subject>clinical trial</subject><subject>Clinical trials</subject><subject>Colorectal cancer</subject><subject>Deoxyribonucleic acid</subject><subject>DNA</subject><subject>DNA Damage</subject><subject>DNA damage response</subject><subject>DNA methylation</subject><subject>DNA Repair</subject><subject>Gene expression</subject><subject>Genes</subject><subject>Genomic instability</subject><subject>Growth factors</subject><subject>Humans</subject><subject>Immune checkpoint</subject><subject>Immune response</subject><subject>Immune system</subject><subject>Immunity</subject><subject>Immunotherapy</subject><subject>Inflammation</subject><subject>Interferon</subject><subject>Kinases</subject><subject>Leukemia</subject><subject>Mutation</subject><subject>Neoplasms - drug therapy</subject><subject>Neoplasms - genetics</subject><subject>Pancreatic cancer</subject><subject>PARP</subject><subject>Patients</subject><subject>Polymerization</subject><subject>Proteins</subject><subject>Review</subject><subject>RNA polymerase</subject><subject>Therapeutic targets</subject><issn>1422-0067</issn><issn>1661-6596</issn><issn>1422-0067</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>PIMPY</sourceid><sourceid>DOA</sourceid><recordid>eNpdkU2P0zAQhiMEYj_gxhlF4sKBwvgjiX1BqrosFK1AQuVsTe1JmpLYWTtB2n9PSpdVl5Mt-_HjmXmz7BWD90Jo-NDu-8QFlIIL9SQ7Z5LzBUBZPT3Zn2UXKe0BuOCFfp6diUJwVRbqPPu6wdjQ2Pomv_q2zK-wx4byH5SG4BPl6F2-7vvJU77akf01hNaPeR1ivvRja9FbivlmRxGHuxfZsxq7RC_v18vs5_WnzerL4ub75_VqebOwslLjQm2drR0Cr0m5SsgtKF5yYAwBKitqqUBoUevCaas5OiRButJaSw2ugq24zNZHrwu4N0Nse4x3JmBr_h6E2BiMc3EdGWCo5_eyQsbnj0BzpgTWDpi2VMuD6-PRNUzbnpwlP0bsHkkf3_h2Z5rw2yhdcF6yWfD2XhDD7URpNH2bLHUdegpTMryUEkBIrmb0zX_oPkzRz6M6UFwKUYCcqXdHysaQUqT6oRgG5hC4OQ18xl-fNvAA_0tY_AH4TqVr</recordid><startdate>20220317</startdate><enddate>20220317</enddate><creator>Huang, Jau-Ling</creator><creator>Chang, Yu-Tzu</creator><creator>Hong, Zhen-Yang</creator><creator>Lin, Chang-Shen</creator><general>MDPI AG</general><general>MDPI</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>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>MBDVC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope><orcidid>https://orcid.org/0000-0001-7415-2187</orcidid></search><sort><creationdate>20220317</creationdate><title>Targeting DNA Damage Response and Immune Checkpoint for Anticancer Therapy</title><author>Huang, Jau-Ling ; Chang, Yu-Tzu ; Hong, Zhen-Yang ; Lin, Chang-Shen</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c478t-8bdcfda02fe8d734b08262011a007c3f480393f95d9c92adae3e97999490d70b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>Angiogenesis</topic><topic>Apoptosis</topic><topic>Ataxia</topic><topic>Biomarkers</topic><topic>Breast</topic><topic>Breast cancer</topic><topic>Cancer immunotherapy</topic><topic>Cancer therapies</topic><topic>Cell cycle</topic><topic>cGAS-STING</topic><topic>Chemotherapy</topic><topic>clinical trial</topic><topic>Clinical trials</topic><topic>Colorectal cancer</topic><topic>Deoxyribonucleic acid</topic><topic>DNA</topic><topic>DNA Damage</topic><topic>DNA damage response</topic><topic>DNA methylation</topic><topic>DNA Repair</topic><topic>Gene expression</topic><topic>Genes</topic><topic>Genomic instability</topic><topic>Growth factors</topic><topic>Humans</topic><topic>Immune checkpoint</topic><topic>Immune response</topic><topic>Immune system</topic><topic>Immunity</topic><topic>Immunotherapy</topic><topic>Inflammation</topic><topic>Interferon</topic><topic>Kinases</topic><topic>Leukemia</topic><topic>Mutation</topic><topic>Neoplasms - drug therapy</topic><topic>Neoplasms - genetics</topic><topic>Pancreatic cancer</topic><topic>PARP</topic><topic>Patients</topic><topic>Polymerization</topic><topic>Proteins</topic><topic>Review</topic><topic>RNA polymerase</topic><topic>Therapeutic targets</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Huang, Jau-Ling</creatorcontrib><creatorcontrib>Chang, Yu-Tzu</creatorcontrib><creatorcontrib>Hong, Zhen-Yang</creatorcontrib><creatorcontrib>Lin, Chang-Shen</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>Health &amp; Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>ProQuest Health &amp; Medical Complete (Alumni)</collection><collection>Health &amp; Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>ProQuest Research Library</collection><collection>Research Library (Corporate)</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 Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>Directory of Open Access Journals</collection><jtitle>International journal of molecular sciences</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Huang, Jau-Ling</au><au>Chang, Yu-Tzu</au><au>Hong, Zhen-Yang</au><au>Lin, Chang-Shen</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Targeting DNA Damage Response and Immune Checkpoint for Anticancer Therapy</atitle><jtitle>International journal of molecular sciences</jtitle><addtitle>Int J Mol Sci</addtitle><date>2022-03-17</date><risdate>2022</risdate><volume>23</volume><issue>6</issue><spage>3238</spage><pages>3238-</pages><issn>1422-0067</issn><issn>1661-6596</issn><eissn>1422-0067</eissn><abstract>Deficiency in DNA damage response (DDR) genes leads to impaired DNA repair functions that will induce genomic instability and facilitate cancer development. However, alterations of DDR genes can serve as biomarkers for the selection of suitable patients to receive specific therapeutics, such as immune checkpoint blockade (ICB) therapy. In addition, certain altered DDR genes can be ideal therapeutic targets through adapting the mechanism of synthetic lethality. Recent studies indicate that targeting DDR can improve cancer immunotherapy by modulating the immune response mediated by cGAS-STING-interferon signaling. Investigations of the interplay of DDR-targeting and ICB therapies provide more effective treatment options for cancer patients. This review introduces the mechanisms of DDR and discusses their crucial roles in cancer therapy based on the concepts of synthetic lethality and ICB. The contemporary clinical trials of DDR-targeting and ICB therapies in breast, colorectal, and pancreatic cancers are included.</abstract><cop>Switzerland</cop><pub>MDPI AG</pub><pmid>35328658</pmid><doi>10.3390/ijms23063238</doi><orcidid>https://orcid.org/0000-0001-7415-2187</orcidid><oa>free_for_read</oa></addata></record>
fulltext fulltext
identifier ISSN: 1422-0067
ispartof International journal of molecular sciences, 2022-03, Vol.23 (6), p.3238
issn 1422-0067
1661-6596
1422-0067
language eng
recordid cdi_doaj_primary_oai_doaj_org_article_01a9ae347a124b0092183afd019cef4b
source Publicly Available Content Database; PubMed Central
subjects Angiogenesis
Apoptosis
Ataxia
Biomarkers
Breast
Breast cancer
Cancer immunotherapy
Cancer therapies
Cell cycle
cGAS-STING
Chemotherapy
clinical trial
Clinical trials
Colorectal cancer
Deoxyribonucleic acid
DNA
DNA Damage
DNA damage response
DNA methylation
DNA Repair
Gene expression
Genes
Genomic instability
Growth factors
Humans
Immune checkpoint
Immune response
Immune system
Immunity
Immunotherapy
Inflammation
Interferon
Kinases
Leukemia
Mutation
Neoplasms - drug therapy
Neoplasms - genetics
Pancreatic cancer
PARP
Patients
Polymerization
Proteins
Review
RNA polymerase
Therapeutic targets
title Targeting DNA Damage Response and Immune Checkpoint for Anticancer Therapy
url http://sfxeu10.hosted.exlibrisgroup.com/loughborough?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-29T16%3A53%3A20IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_doaj_&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Targeting%20DNA%20Damage%20Response%20and%20Immune%20Checkpoint%20for%20Anticancer%20Therapy&rft.jtitle=International%20journal%20of%20molecular%20sciences&rft.au=Huang,%20Jau-Ling&rft.date=2022-03-17&rft.volume=23&rft.issue=6&rft.spage=3238&rft.pages=3238-&rft.issn=1422-0067&rft.eissn=1422-0067&rft_id=info:doi/10.3390/ijms23063238&rft_dat=%3Cproquest_doaj_%3E2642433504%3C/proquest_doaj_%3E%3Cgrp_id%3Ecdi_FETCH-LOGICAL-c478t-8bdcfda02fe8d734b08262011a007c3f480393f95d9c92adae3e97999490d70b3%3C/grp_id%3E%3Coa%3E%3C/oa%3E%3Curl%3E%3C/url%3E&rft_id=info:oai/&rft_pqid=2642433504&rft_id=info:pmid/35328658&rfr_iscdi=true