Using integrated multiomic and spatially resolved single-cell profiling of high-grade serous ovarian cancer, Perez-Villatoro and colleagues show that tumor cell-intrinsic MHC class II (MHCII) expression and the organization of tumor-stroma interface niches are major determinants of endogenous antitumor immune activity and clinical outcome. These data argue against models based solely on bulk immune infiltration and instead support a context-dependent framework in which tumor cell state (particularly MHCII expression), spatial immune topology, and prior therapeutic exposure collectively shape the magnitude and quality of immune pressure during disease evolution. See related article by Perez-Villatoro et al., p. 1100.
Conejo-Garcia et al. (Mon,) studied this question.