GATA2 promotes castration-resistant prostate cancer development by suppressing IFN-β axis-mediated antitumor immunity.

Castration-resistant prostate cancer (CRPC) nearly inevitably develops after long-term treatment with androgen deprivation therapy (ADT), leading to significant mortality. Investigating the mechanisms driving CRPC development is imperative. Here, we determined that the pioneer transcription factor GATA2, which is frequently amplified in CRPC patients, inhibits interferon (IFN)-β-mediated antitumor immunity, thereby promoting CRPC progression.

ATRX loss suppresses the type I interferon response in sarcoma cells through chromatin remodeling.

Sarcomas constitute a heterogeneous group of mesenchymal cancers and are particularly common in children and adolescents, leading to significant lethality. Therefore, it is necessary to understand the underlying mechanisms by which genetic alterations promote sarcoma progression. Here, we demonstrate that loss-of-function of , a member of the SWI/SNF DNA-remodeling family, represses the interferon (IFN)-β response by inducing chromatin remodeling in sarcoma cells.