Cell-autonomous inflammation of BRCA1-deficient ovarian cancers drives both tumor-intrinsic immunoreactivity and immune resistance via STING

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Marine Bruand; Matteo Morotti; Mathieu Desbuisson; Hualing Zhang; Catherine Ronet; Michal Bassani-Sternberg; Iain A. McNeish; Elizabeth M. Swisher; Mauro Delorenzi; Melita Irving

doi:10.1016/j.celrep.2021.109412

Cell-autonomous inflammation of BRCA1-deficient ovarian cancers drives both tumor-intrinsic immunoreactivity and immune resistance via STING

Marine Bruand & Melita Irving et al.

In this study, we investigate mechanisms leading to inflammation and immunoreactivity in ovarian tumors with homologous recombination deficiency (HRD). BRCA1 loss is found to lead to transcriptional reprogramming in tumor cells and cell-intrinsic inflammation involving type I interferon (IFN) and stimulator of IFN genes (STING). BRCA1-mutated (BRCA1

Cell-autonomous inflammation of BRCA1-deficient ovarian cancers drives both tumor-intrinsic immunoreactivity and immune resistance via STING

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