Abstract
Immune checkpoint inhibitors (ICI) have emerged as a powerful oncologic treatment modality for patients with different solid tumors. Unfortunately, the efficacy of ICI monotherapy in ovarian cancer is limited, and combination therapy provides a new opportunity for immunotherapy in ovarian cancer. DNA damage repair (DDR) pathways play central roles in the maintenance of genomic integrity and promote the progression of cancer. A deficiency in DDR genes can cause different degrees of DNA damage that enhance local antigen release, resulting in systemic antitumor immune responses. Thus, the combination of DDR inhibitors with ICI represents an attractive therapeutic strategy with the potential to improve the clinical outcomes of patients with ovarian cancer. In this review, we provide an overview of the interconnectivity between DDR pathway deficiency and immune response, summarize available clinical trials on the combination therapy in ovarian cancer, and discuss the potential predictive biomarkers that can be utilized to guide the use of combination therapy.
Highlights
Immune checkpoint inhibitors (ICI), such as CTLA-1, PD-1, and PD-L1, have emerged as a powerful oncologic treatment modality and have become a standard treatment for patients with different tumor types [1, 2]
poly(ADP ribose) polymerase (PARP) inhibitors were initially designed for BRCA mutations in patients with ovarian cancer
Owing to the modest response of monotherapy in ovarian cancer, the combination therapy of PARP inhibitors with ICI agents provides an opportunity to increase the effectiveness of therapy
Summary
Immune checkpoint inhibitors (ICI), such as CTLA-1, PD-1, and PD-L1, have emerged as a powerful oncologic treatment modality and have become a standard treatment for patients with different tumor types [1, 2]. A phase III study on patients with platinum-sensitive recurrent ovarian cancer taking PARP inhibitors as maintenance therapy found that these patients had longer progression-free survival compared with the placebo group, independent of the BRCA1/2 mutation status or other HR repair gene status [7].
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