ArticleJournal for immunotherapy of cancer2026
Telmisartan increases olaparib efficacy in homologous recombination proficient tumors by augmenting type I interferon production.
Article in Journal for immunotherapy of cancer, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundPoly-ADP ribose polymerase inhibitors (PARPi) are well-known to treat tumors that are deficient in homologous recombination (HR) DNA repair. However, PARPi can treat breast cancer gene (BRCA) wild-type tumors, the mechanisms behind which are not fully elucidated. We previously reported that tumor-intrinsic programmed death ligand-1 (PD-L1) signals promote HR, and that genetic tumor PD-L1
methodsWe used control and genetically modified murine and human tumor cell lines to demonstrate signaling outcomes and treatment efficacy of olaparib and telmisartan alone or combined
resultsThe FDA-approved angiotensin II receptor blocker (ARB) antihypertensive telmisartan depleted tumor PD-L1, synergized with PARPi, and augmented PARPi-induced DNA damage. Surprisingly, telmisartan improved PARPi independently of tumor PD-L1, which expands telmisartan applicability to improve PARPi in PD-L1
conclusionsTelmisartan depletes tumor PD-L1 but has significant PD-L1-independent clinical translational potential to improve PARPi in BRCA wild-type (WT) tumors and augment tumor immunogenicity.
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