Our recent study demonstrates that SETDB1 promotes endometrial cancer progression through both cancer cell-intrinsic and immune-mediated mechanisms. Loss of SETDB1 suppresses tumor growth, alters transcriptional programs, and enhances anti-tumor immune responses, revealing new therapeutic vulnerabilities in aggressive endometrial cancers.

We established an integrated platform of 53 patient-derived xenografts (PDXs) and matched patient-derived cancer cell models from 103 endometrial cancer specimens. Using high-throughput screening of 179 FDA-approved oncology drugs, we identified multiple therapeutic vulnerabilities that were not predicted by current standard-of-care approaches, providing a valuable resource for precision oncology and translational drug discovery.