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Review
. 2020 Jun 29:8:23.
doi: 10.1186/s40364-020-00202-7. eCollection 2020.

Role of DNA repair defects in predicting immunotherapy response

Jing Zhang  1 , David J H Shih  1 , Shiaw-Yih Lin  1
Affiliations
Review

Role of DNA repair defects in predicting immunotherapy response

Jing Zhang et al. Biomark Res. .

Abstract

Defect in DNA damage response (DDR) is a common feature of cancer cells, which regulates tumor growth and therapeutic response. Recently, the approval of immune checkpoint blockade (ICB) for tumors with defective mismatch repair has paved the way for investigating the role of other DDR defects in sensitizing cancer to ICB therapy. Despite great progress in understanding DDR pathways, the mechanisms that link DDR defects and ICB response remain incompletely understood. Further, the clinical activity of ICB in patients with DDR defective tumors has not been well described. Here, we discuss recent studies demonstrating that biomarkers in DDR pathways may serve as potential predictors to guide the selection of patients for ICB therapy. A better understanding of the relationship between deficiency in DDR and response to ICB would facilitate efforts in optimizing the efficacy of immunotherapy.

Keywords: Biomarkers; DNA damage response; Immune checkpoint blockade; Immunotherapy.

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Conflict of interest statement

Competing interestsThe authors declare that they have no competing interests.

Figures

Fig. 1
Fig. 1
DNA damage response regulates tumor immunity. Defects in DNA damage response can result in both immunostimulation and immunosuppression. Production of neoantigens and/or activation of the cGAS/STING pathway can initiate anti-tumor immunity
See this image and copyright information in PMC

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References

    1. Wei SC, Duffy CR, Allison JP. Fundamental mechanisms of immune checkpoint blockade therapy. Cancer Discov. 2018;8(9):1069–1086. - PubMed
    1. Akinleye A, Rasool Z. Immune checkpoint inhibitors of PD-L1 as cancer therapeutics. J Hematol Oncol. 2019;12(1):92. - PMC - PubMed
    1. Jenkins RW, Barbie DA, Flaherty KT. Mechanisms of resistance to immune checkpoint inhibitors. Br J Cancer. 2018;118(1):9–16. - PMC - PubMed
    1. Hodi FS, et al. Improved survival with ipilimumab in patients with metastatic melanoma. N Engl J Med. 2010;363(8):711–723. - PMC - PubMed
    1. Hodi FS, et al. Combined nivolumab and ipilimumab versus ipilimumab alone in patients with advanced melanoma: 2-year overall survival outcomes in a multicentre, randomised, controlled, phase 2 trial. Lancet Oncol. 2016;17(11):1558–1568. - PMC - PubMed

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