Blocking cancer-fibroblast mutualism inhibits proliferation of endocrine resistant breast cancer.

ABSTRACT: In early-stage estrogen receptor-positive (ER+) breast cancer, resistance to endocrine therapy (ET) and CDK4/6 inhibitors (CDK4/6i) often involves a shift away from estrogen-driven proliferation. The nature and source of compensatory growth signals driving cancer proliferation remain unknown but represent direct therapeutic targets of resistant cells. By analyzing single-cell RNA-sequencing data from serial biopsies of patient tumors, we elucidated compensatory growth signaling pathways activated in ET +CDK4/6i resistant cancer cells, along with the intercellular growth signal communications within the tumor microenvironment. In most patient tumors, resistant cancer cells increased ERBB growth pathway activity during treatment, only partially through ERBB receptor upregulation. Concurrentl

SUBMITTER: Jason Griffiths 

PROVIDER: S-SCDT-10_1038-S44320-025-00104-6 | biostudies-other |

REPOSITORIES: biostudies-other