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ArticleOnline nowOpen access Affiliations & Notes 1Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA 02215, USA 2Department of Medicine, Brigham and Women’s Hospital, Boston, MA 02115, USA 3Department of Medicine, Harvard Medical School, Boston, MA 02115, USA 4Institute for Precision Medicine, University of Pittsburgh, Pittsburgh, PA 15260, USA 5Department of Cancer Immunology and Virology, Dana-Farber Cancer Institute, Boston, MA 02215, USA 6Department of Immunology,...
Abstract Enzalutamide is a potent second-generation antiandrogen commonly used to treat hormone-sensitive and castration-resistant prostate cancer (CRPC) patients. While initially effective, the disease almost always develops resistance. Given that many enzalutamide-resistant tumors lack specific somatic mutations, there is strong evidence that epigenetic factors can cause enzalutamide resistance.
Abstract KMT2C and KMT2D, encoding histone H3 lysine 4 methyltransferases, are among the most commonly mutated genes in triple-negative breast cancer (TNBC). However, how these mutations may shape epigenomic and transcriptomic landscapes to promote tumorigenesis is largely unknown. Here we describe that deletion of Kmt2c or Kmt2d in non-metastatic murine models of TNBC drives metastasis, especially to the brain.
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