The authors show that microparticle-mediated delivery of Cxcl9 recruits effector T cells to the tumor site and delays relapse. The data suggest an adjuvant approach to boost the immune response in combination with targeted therapy or immunotherapy.

Transcriptional profiling reveals that tumor-infiltrating lymphocytes (TILs) with low TCR affinity to a tumor-associated antigen exhibit progenitor-like phenotypes and increased quiescence, whereas higher affinity TCR TILs exhibit more cell division and faster progression to T-cell exhaustion programs.

The authors identify podofilox as an enhancer of the cGAMP–STING signaling pathway. By altering STING trafficking, podofilox promotes STING activation and antitumor responses in vitro and in vivo, suggesting an approach to enhance STING agonist cancer immunotherapy.

Tumor-derived netrin-1 enhances the immunosuppressive function of myeloid-derived suppressor–cell (MDSC) via interaction with A2BR, facilitating the development of tumors. These findings highlight netrin-1 as a regulator of antitumor immune responses and potential therapeutic target in colorectal cancer.

Mathematical modeling of myeloid-derived suppressor–cell (MDSC) dynamics reveals MDSC–NK cell interactions as a crucial predictor of outcomes in breast-to-lung metastasis and a possible therapeutic target.

Glioblastoma is frequently refractory to radiation, chemotherapy, and immunotherapy. The authors show in genetic mouse models that the mutational profile of glioblastoma influences the tumor immune microenvironment and offers a pharmacological means to sensitize glioblastoma to checkpoint immunotherapy.

By analyzing all 31 SWI/SNF complex genes, the authors show SWI/SNF complex alterations are associated with improved clinical outcomes following immune checkpoint inhibitor (ICI) therapy across cancer types, suggesting that such alterations could serve as a prognostic biomarker for ICI therapy.

Histone deacetylase 3 (HDAC3) is shown to regulate expression of genes encoding chemokines CXCL9/10/11, as well as impact antitumor immune–cell recruitment in the tumor microenvironment. The data highlight how targeting HDAC3 could boost antitumor immune responses.

The authors show in ovarian cancer that IL15 induces a negative feedback loop driven by upregulation of the PD-1/PD-L1 checkpoint axis partly through NK cell–produced IFNγ. Addition of immune checkpoint blockade synergizes with IL15, improving cytokine-driven immunotherapy.

Hedgehog signaling metabolically programs and supports differentiation and activity of regulatory T cells (Treg). Inhibiting Hedgehog shifts Tregs into inflammatory Th17 cells and creates an immune-reactive tumor microenvironment, paving the way for novel combinatorial approaches to treat triple-negative breast cancer.