Abstract
Tumor-specific homologous recombination (HR) DNA defects and the phosphatidylinositol 3-kinase (PI3K)-AKT pathway are commonly implicated in tumorigenesis, and preclinical studies have shown synergistic effects of poly (ADP-ribose) polymerase (PARP) with PI3K-AKT inhibitors. Both pathways modulate the tumor immune microenvironment by regulation of tumor-infiltrating lymphocytes and reduction of Treg cells. We hypothesized that triplet combination of immunotherapy with PARP and PI3K-AKT pathway inhibition is tolerable and may demonstrate activity in pts with relevant pathway defects.
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