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      Alterations of DNA damage response pathway: Biomarker and therapeutic strategy for cancer immunotherapy

      review-article
      Author(s): a , b , a , b , a , a , a , a , b , a , b , a , a , ∗ , a , ∗
      Publication date (Electronic):
      Journal: Acta Pharmaceutica Sinica. B
      Publisher: Elsevier
      Keywords: DNA damage response, DNA repair, Immunotherapy, Genomic instability, Tumor microenvironment, PD-1, PD-L1, cGAS–STING, ATM, ataxia-telangiectasia mutated, ATR, ataxia telangiectasia and Rad3 related, BAP1, BRCA1-associated protein 1, BER, base excision repair, BRAF, v-RAF murine sarcoma viral oncogene homologue B, BRCA, breast cancer susceptibility gene, cGAS, cyclic GMP–AMP synthase, CHEK, cell-cycle checkpoint kinase, CHK1, checkpoint kinase 1, DAMP, damage-associated molecular patterns, DDR, DNA damage response, DR, direct repair, DSBs, double-strand breaks, GSK3β, glycogen synthase kinase 3β, HMGB1, high mobility group box-1, HRR, homologous recombination repair, ICI, immune checkpoint inhibitor, IFNγ, interferon gamma, IHC, immunohistochemistry, IRF1, interferon regulatory factor 1, JAK, Janus kinase, MAD1, mitotic arrest deficient-like 1, MGMT, O6-methylguanine methyltransferase, MLH1, MutL homolog 1, MMR, mismatch repair, MNT, MAX network transcriptional repressor, MSH2/6, MutS protein homologue-2/6, MSI, microsatellite instability, MUTYH, MutY homolog, MyD88, myeloid differentiation factor 88, NEK1, NIMA-related kinase 1, NER, nucleotide excision repair, NGS, next generation sequencing, NHEJ, nonhomologous end-joining, NIMA, never-in-mitosis A, NSCLC, non-small cell lung cancer, ORR, objective response rate, OS, overall survival, PALB2, partner and localizer of BRCA2, PARP, poly-ADP ribose polymerase, PCR, polymerase chain reaction, PD-1, programmed death 1, PD-L1, programmed death ligand 1, PFS, progression-free survival, RAD51C, RAD51 homolog C, RB1, retinoblastoma 1, RPA, replication protein A, RSR, replication stress response, SCNAs, somatic copy number alterations, ssDNA, single-stranded DNA, STAT, signal transducer and activator of transcription, STING, stimulator of interferon genes, TBK1, TANK-binding kinase 1, TILs, tumor-infiltrating lymphocytes, TLR4, Toll-like receptor 4, TMB, tumor mutational burden, TME, tumor microenvironment, TP53, tumor protein P53, TRIF, Toll-interleukin 1 receptor domain-containing adaptor inducing INF-β, FDA, United State Food and Drug Administration, XRCC4, X-ray repair cross complementing protein 4

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          Abstract

          Genomic instability remains an enabling feature of cancer and promotes malignant transformation. Alterations of DNA damage response (DDR) pathways allow genomic instability, generate neoantigens, upregulate the expression of programmed death ligand 1 (PD-L1) and interact with signaling such as cyclic GMP–AMP synthase-stimulator of interferon genes (cGAS–STING) signaling. Here, we review the basic knowledge of DDR pathways, mechanisms of genomic instability induced by DDR alterations, impacts of DDR alterations on immune system, and the potential applications of DDR alterations as biomarkers and therapeutic targets in cancer immunotherapy.

          Graphical abstract

          This review summarizes basic knowledge of DNA damage response (DDR) pathways, mechanisms of genomic instability induced by DDR alterations, impacts of DDR alterations on immune system, and its potential applications as therapeutic targets in cancer immunotherapy.

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          Global Cancer Statistics 2018: GLOBOCAN Estimates of Incidence and Mortality Worldwide for 36 Cancers in 185 Countries

          Ahmedin Jemal, Lindsey A Torre, Rebecca Siegel … (2018)
          This article provides a status report on the global burden of cancer worldwide using the GLOBOCAN 2018 estimates of cancer incidence and mortality produced by the International Agency for Research on Cancer, with a focus on geographic variability across 20 world regions. There will be an estimated 18.1 million new cancer cases (17.0 million excluding nonmelanoma skin cancer) and 9.6 million cancer deaths (9.5 million excluding nonmelanoma skin cancer) in 2018. In both sexes combined, lung cancer is the most commonly diagnosed cancer (11.6% of the total cases) and the leading cause of cancer death (18.4% of the total cancer deaths), closely followed by female breast cancer (11.6%), prostate cancer (7.1%), and colorectal cancer (6.1%) for incidence and colorectal cancer (9.2%), stomach cancer (8.2%), and liver cancer (8.2%) for mortality. Lung cancer is the most frequent cancer and the leading cause of cancer death among males, followed by prostate and colorectal cancer (for incidence) and liver and stomach cancer (for mortality). Among females, breast cancer is the most commonly diagnosed cancer and the leading cause of cancer death, followed by colorectal and lung cancer (for incidence), and vice versa (for mortality); cervical cancer ranks fourth for both incidence and mortality. The most frequently diagnosed cancer and the leading cause of cancer death, however, substantially vary across countries and within each country depending on the degree of economic development and associated social and life style factors. It is noteworthy that high-quality cancer registry data, the basis for planning and implementing evidence-based cancer control programs, are not available in most low- and middle-income countries. The Global Initiative for Cancer Registry Development is an international partnership that supports better estimation, as well as the collection and use of local data, to prioritize and evaluate national cancer control efforts. CA: A Cancer Journal for Clinicians 2018;0:1-31. © 2018 American Cancer Society.
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            Hallmarks of Cancer: The Next Generation

            Douglas Hanahan, Robert A. Weinberg (2011)
            The hallmarks of cancer comprise six biological capabilities acquired during the multistep development of human tumors. The hallmarks constitute an organizing principle for rationalizing the complexities of neoplastic disease. They include sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, and activating invasion and metastasis. Underlying these hallmarks are genome instability, which generates the genetic diversity that expedites their acquisition, and inflammation, which fosters multiple hallmark functions. Conceptual progress in the last decade has added two emerging hallmarks of potential generality to this list-reprogramming of energy metabolism and evading immune destruction. In addition to cancer cells, tumors exhibit another dimension of complexity: they contain a repertoire of recruited, ostensibly normal cells that contribute to the acquisition of hallmark traits by creating the "tumor microenvironment." Recognition of the widespread applicability of these concepts will increasingly affect the development of new means to treat human cancer. Copyright © 2011 Elsevier Inc. All rights reserved.
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              Cancer statistics, 2020

              Rebecca Siegel, Kimberly D Miller, Ahmedin Jemal (2020)
              Each year, the American Cancer Society estimates the numbers of new cancer cases and deaths that will occur in the United States and compiles the most recent data on population-based cancer occurrence. Incidence data (through 2016) were collected by the Surveillance, Epidemiology, and End Results Program; the National Program of Cancer Registries; and the North American Association of Central Cancer Registries. Mortality data (through 2017) were collected by the National Center for Health Statistics. In 2020, 1,806,590 new cancer cases and 606,520 cancer deaths are projected to occur in the United States. The cancer death rate rose until 1991, then fell continuously through 2017, resulting in an overall decline of 29% that translates into an estimated 2.9 million fewer cancer deaths than would have occurred if peak rates had persisted. This progress is driven by long-term declines in death rates for the 4 leading cancers (lung, colorectal, breast, prostate); however, over the past decade (2008-2017), reductions slowed for female breast and colorectal cancers, and halted for prostate cancer. In contrast, declines accelerated for lung cancer, from 3% annually during 2008 through 2013 to 5% during 2013 through 2017 in men and from 2% to almost 4% in women, spurring the largest ever single-year drop in overall cancer mortality of 2.2% from 2016 to 2017. Yet lung cancer still caused more deaths in 2017 than breast, prostate, colorectal, and brain cancers combined. Recent mortality declines were also dramatic for melanoma of the skin in the wake of US Food and Drug Administration approval of new therapies for metastatic disease, escalating to 7% annually during 2013 through 2017 from 1% during 2006 through 2010 in men and women aged 50 to 64 years and from 2% to 3% in those aged 20 to 49 years; annual declines of 5% to 6% in individuals aged 65 years and older are particularly striking because rates in this age group were increasing prior to 2013. It is also notable that long-term rapid increases in liver cancer mortality have attenuated in women and stabilized in men. In summary, slowing momentum for some cancers amenable to early detection is juxtaposed with notable gains for other common cancers.
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                Author and article information

                Contributors
                Yayi He
                Caicun Zhou
                Journal
                Journal ID (nlm-ta): Acta Pharm Sin B
                Journal ID (iso-abbrev): Acta Pharm Sin B
                Title: Acta Pharmaceutica Sinica. B
                Publisher: Elsevier
                ISSN (Print): 2211-3835
                ISSN (Electronic): 2211-3843
                Publication date PMC-release: 06 January 2021
                Publication date (Print): October 2021
                Publication date (Electronic): 06 January 2021
                Volume: 11
                Issue: 10
                Pages: 2983-2994
                Affiliations
                [a ]Department of Medical Oncology, Shanghai Pulmonary Hospital, Tongji University Medical School Cancer Institute, Tongji University School of Medicine, Shanghai 200433, China
                [b ]Medical School, Tongji University, Shanghai 200433, China
                Author notes
                Article
                Publisher Item ID: S2211-3835(21)00008-3
                DOI: 10.1016/j.apsb.2021.01.003
                PMC ID: 8546664
                PubMed ID: 34729299
                SO-VID: 02e85392-5b8a-49fd-9033-b8715e073727
                Copyright © © 2021 Chinese Pharmaceutical Association and Institute of Materia Medica, Chinese Academy of Medical Sciences. Production and hosting by Elsevier B.V.
                License:

                This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

                History
                Date received : 23 September 2020
                Date revision received : 25 October 2020
                Date accepted : 3 November 2020
                Categories
                Subject: Review

                Keywords: dna damage response,dna repair,immunotherapy,genomic instability,tumor microenvironment,pd-1,pd-l1,cgas–sting,atm, ataxia-telangiectasia mutated,atr, ataxia telangiectasia and rad3 related,bap1, brca1-associated protein 1,ber, base excision repair,braf, v-raf murine sarcoma viral oncogene homologue b,brca, breast cancer susceptibility gene,cgas, cyclic gmp–amp synthase,chek, cell-cycle checkpoint kinase,chk1, checkpoint kinase 1,damp, damage-associated molecular patterns,ddr, dna damage response,dr, direct repair,dsbs, double-strand breaks,gsk3β, glycogen synthase kinase 3β,hmgb1, high mobility group box-1,hrr, homologous recombination repair,ici, immune checkpoint inhibitor,ifnγ, interferon gamma,ihc, immunohistochemistry,irf1, interferon regulatory factor 1,jak, janus kinase,mad1, mitotic arrest deficient-like 1,mgmt, o6-methylguanine methyltransferase,mlh1, mutl homolog 1,mmr, mismatch repair,mnt, max network transcriptional repressor,msh2/6, muts protein homologue-2/6,msi, microsatellite instability,mutyh, muty homolog,myd88, myeloid differentiation factor 88,nek1, nima-related kinase 1,ner, nucleotide excision repair,ngs, next generation sequencing,nhej, nonhomologous end-joining,nima, never-in-mitosis a,nsclc, non-small cell lung cancer,orr, objective response rate,os, overall survival,palb2, partner and localizer of brca2,parp, poly-adp ribose polymerase,pcr, polymerase chain reaction,pd-1, programmed death 1,pd-l1, programmed death ligand 1,pfs, progression-free survival,rad51c, rad51 homolog c,rb1, retinoblastoma 1,rpa, replication protein a,rsr, replication stress response,scnas, somatic copy number alterations,ssdna, single-stranded dna,stat, signal transducer and activator of transcription,sting, stimulator of interferon genes,tbk1, tank-binding kinase 1,tils, tumor-infiltrating lymphocytes,tlr4, toll-like receptor 4,tmb, tumor mutational burden,tme, tumor microenvironment,tp53, tumor protein p53,trif, toll-interleukin 1 receptor domain-containing adaptor inducing inf-β,fda, united state food and drug administration,xrcc4, x-ray repair cross complementing protein 4
                Data availability:
                Keywords: dna damage response, dna repair, immunotherapy, genomic instability, tumor microenvironment, pd-1, pd-l1, cgas–sting, atm, ataxia-telangiectasia mutated, atr, ataxia telangiectasia and rad3 related, bap1, brca1-associated protein 1, ber, base excision repair, braf, v-raf murine sarcoma viral oncogene homologue b, brca, breast cancer susceptibility gene, cgas, cyclic gmp–amp synthase, chek, cell-cycle checkpoint kinase, chk1, checkpoint kinase 1, damp, damage-associated molecular patterns, ddr, dna damage response, dr, direct repair, dsbs, double-strand breaks, gsk3β, glycogen synthase kinase 3β, hmgb1, high mobility group box-1, hrr, homologous recombination repair, ici, immune checkpoint inhibitor, ifnγ, interferon gamma, ihc, immunohistochemistry, irf1, interferon regulatory factor 1, jak, janus kinase, mad1, mitotic arrest deficient-like 1, mgmt, o6-methylguanine methyltransferase, mlh1, mutl homolog 1, mmr, mismatch repair, mnt, max network transcriptional repressor, msh2/6, muts protein homologue-2/6, msi, microsatellite instability, mutyh, muty homolog, myd88, myeloid differentiation factor 88, nek1, nima-related kinase 1, ner, nucleotide excision repair, ngs, next generation sequencing, nhej, nonhomologous end-joining, nima, never-in-mitosis a, nsclc, non-small cell lung cancer, orr, objective response rate, os, overall survival, palb2, partner and localizer of brca2, parp, poly-adp ribose polymerase, pcr, polymerase chain reaction, pd-1, programmed death 1, pd-l1, programmed death ligand 1, pfs, progression-free survival, rad51c, rad51 homolog c, rb1, retinoblastoma 1, rpa, replication protein a, rsr, replication stress response, scnas, somatic copy number alterations, ssdna, single-stranded dna, stat, signal transducer and activator of transcription, sting, stimulator of interferon genes, tbk1, tank-binding kinase 1, tils, tumor-infiltrating lymphocytes, tlr4, toll-like receptor 4, tmb, tumor mutational burden, tme, tumor microenvironment, tp53, tumor protein p53, trif, toll-interleukin 1 receptor domain-containing adaptor inducing inf-β, fda, united state food and drug administration, xrcc4, x-ray repair cross complementing protein 4

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