The authors use statistical and machine learning approaches to connect features of the spatial organization of the TIME to outcomes for patients with high-grade serous carcinoma, finding several spatial features with significant univariate correlations and/or high relative importance in high-dimensional predictive models.

The authors show that calorie restriction significantly enhances NK cell–mediated antitumor immunity through the transcription factor Eomesodermin. The data highlight a link between calorie restriction and NK cell–mediated tumor immunosurveillance and have potential for clinical translation.

Immune function declines with age. The authors show that loss of tumor antigen–specific CD8⁺ T cells drives tumor growth and resistance to anti–PD-1 immunotherapy in aged mice, providing insight for designing immunotherapies for elderly patients.

The authors show that CCR6 regulates Treg activity via increased glucose metabolism. Ablating Ccr6 in Tregs prevents their activation in the context of tumors. This immuno-metabolic mechanism regulating Treg activation in tumors provides a new immunotherapeutic target.

The authors show that organ site is a critical determinant of immune composition in the metastatic tumor microenvironment. Consideration of organ site may be critical to enable effective immunotherapy for patients with metastatic breast cancer.

CAR-NK cell therapeutic potency against solid tumors is suppressed by the hostile tumor microenvironment. The authors show genetic engineering to express catalase and alginate hydrogel encapsulation improve CAR-NK cell tumor infiltration, persistence, and efficacy in multiple TNBC models.

The authors demonstrate that tumor-associated antigen burden correlates with the efficacy of immune checkpoint inhibition in patients with tumor mutation burden–low and PDL1-negative tumors, who would otherwise have a low response rate and limited access to this treatment.

New approaches are needed to augment efficacy of anti–PD-1 therapy in HCC. The authors uncover a mechanism by which CX3CR1⁺ TAMs promote T-cell exhaustion and limit anti–PD-1 efficacy in HCC models, revealing potential new immunotherapy targets for HCC.

The authors identify a subset of CD36⁺ macrophages with proinflammatory phenotype that interact with ZCCHC12⁺ tumor cells in PTC and promote tumor progression. Accumulation of CD36⁺ proinflammatory macrophages is associated with recurrence, suggesting ways to predict patient outcomes.

To overcome challenges with oADV therapy, the authors engineered an oADV to have self-biomineralization capacity. Self-biomineralized oADV shifted the suppressive tumor immune microenvironment from a “cold” to “hot” state, enhancing antitumor immunity in several mouse models.