Immune Niche Formation in Engineered Mouse Models Reveals Mechanisms of Tumor Dormancy.

ABSTRACT: Residual tumor cells can persist in a dormant state during clinical remissions that may last decades. The mechanisms that lead to such growth control vs. eventual reactivation and macroscopic tumor outgrowth remain unclear. Here, we report data from a mouse model that reveals a key role of host immunity and the cellular and molecular mechanisms that control tumor dormancy. Abrogation of myeloid-specific TGF-βRII expression (TβRII^myeKO) resulted in an IFN-γ rich immune microenvironment. IFN-γ in turn elevated KLF4-mediated SLURP1 production in malignant cells, which is critical to the tumor cell quiescent state through interruption of fibronectin-integrin signaling pathways. The dormant tumor lesions were located in spatially localized immune niches rich in NK cells, cDCs, monocy

SUBMITTER: Ahad A 

PROVIDER: S-EPMC12190759 | biostudies-literature | 2025 Apr

REPOSITORIES: biostudies-literature