Reduction of fibrosis and immune suppressive cells in ErbB2-dependent tumorigenesis by an LXR agonist.

ABSTRACT: One of the central challenges for cancer therapy is the identification of factors in the tumor microenvironment that increase tumor progression and prevent immune surveillance. One such element associated with breast cancer is stromal fibrosis, a histopathologic criterion for invasive cancer and poor survival. Fibrosis is caused by inflammatory factors and remodeling of the extracellular matrix that elicit an immune tolerant microenvironment. To address the role of fibrosis in tumorigenesis, we developed NeuT/ATTAC transgenic mice expressing a constitutively active NeuT/erbB2 transgene, and an inducible, fat-directed caspase-8 fusion protein, which upon activation results in selective and partial ablation of mammary fat and its replacement with fibrotic tissue. Induction of fibrosis in Neu

SUBMITTER: Sheng G 

PROVIDER: S-EPMC8007044 | biostudies-literature | 2021

REPOSITORIES: biostudies-literature