Journal
CANCER DISCOVERY
Volume 7, Issue 7, Pages 675-693Publisher
AMER ASSOC CANCER RESEARCH
DOI: 10.1158/2159-8290.CD-17-0226
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Funding
- American Society of Radiation Oncology (ASTRO)
- Bladder Cancer Advocacy Network (BCAN)
- Harvard Catalyst, The Harvard Clinical and Translational Science Center (National Center for Research Resources
- National Center for Advancing Translational Sciences, National Institutes of Health [KL2 TR001100]
- Ovarian Cancer Research Fund Alliance
- Melanoma Research Alliance
- Susan F. Smith Center for Women's Cancers
- Department of Defense Ovarian Cancer Research Program (DOD OCRP) [W81XWH-15-1-0564]
- Stand Up To Cancer-Ovarian Cancer Research Fund-Ovarian Cancer National Alliance-National Ovarian Cancer Coalition Dream Team Translational Research Grant [SU2C-AACR-DT16-15]
- U.S. National Institutes of Health [R01DK43889, R37HL052725, P01HL048546, P50CA168504]
- Breast Cancer Research Foundation
- Ludwig Center at Harvard
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DNA-damaging agents are widely used in clinical oncology and exploit deficiencies in tumor DNA repair. Given the expanding role of immune checkpoint blockade as a therapeutic strategy, the interaction of tumor DNA damage with the immune system has recently come into focus, and it is now clear that the tumor DNA repair landscape has an important role in driving response to immune checkpoint blockade. Here, we summarize the mechanisms by which DNA damage and genomic instability have been found to shape the antitumor immune response and describe clinical efforts to use DNA repair biomarkers to guide use of immune-directed therapies. Significance: Only a subset of patients respond to immune checkpoint blockade, and reliable predictive biomarkers of response are needed to guide therapy decisions. DNA repair deficiency is common among tumors, and emerging experimental and clinical evidence suggests that features of genomic instability are associated with response to immune-directed therapies. (C) 2017 AACR.
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