ArticleJournal for immunotherapy of cancer2026
PARP inhibition combined with a T-cell receptor β chain-directed antibody fusion molecule drives polyclonal antitumor immunity and tumor regression.
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. It is linked to trial NCT02484404 (Phase I/II Study of the Anti-Programmed Death Ligand-1 Antibody Durvalumab), which is not on this map. Not yet cited in PubMed.
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The trial behind it
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Phase I/II Study of the Anti-Programmed Death Ligand-1 Antibody Durvalumab (MEDI4736) in Combination With Olaparib and/or Cediranib for Advanced Solid Tumors and Advanced or Recurrent Ovarian, Triple Negative Breast, Lung, Prostate and Colorectal Cancers
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16 authors.
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Abstract
backgroundMetastatic castration-resistant prostate cancer (mCRPC) remains an aggressive disease with limited response to systemic therapies despite androgen deprivation. Immune-excluded prostate tumors are typically resistant to immunotherapy. STAR0602 is a selective bifunctional T-cell agonist composed of an antibody targeting Vβ6 and Vβ10 T-cell receptor chains fused to human interleukin-2 that selectively expands Vβ6
methodsThe antitumor activity of the PARP inhibitor olaparib combined with mSTAR1302, the murine surrogate of STAR0602, was evaluated in TRAMP-C2 and RM-1 prostate tumor models. Tumor growth, survival, and immune responses were assessed by flow cytometry and functional depletion studies. The role of tumor-intrinsic TRAIL-R2 signaling was evaluated using a TRAIL-R2 knockout TRAMP-C2 model, and clinical relevance was explored by assessing TRAIL-R2 expression in tumor samples from patients treated with olaparib in a Phase 2 clinical trial (NCT02484404).
resultsCombination therapy with olaparib and mSTAR1302 induced significant tumor regression and improved survival compared with either agent alone. Treatment increased tumor-infiltrating lymphocytes, expanded activated Vβ13
conclusionsThese findings suggest that combining tumor-sensitizing therapies with selective T-cell activation may represent a broader strategy to overcome immune exclusion in solid tumors. Together, these results provide mechanistic rationale for clinical evaluation of olaparib in combination with STAR0602 in patients with mCRPC who have progressed on androgen deprivation therapy.
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