Emerging roles of H3K9me3, SETDB1 and SETDB2 in therapy-induced cellular reprogramming.

CONCLUSION: A number of converging phenotypes outline a stress-responsive mechanism for SETDB1 and SETDB2 activation and subsequent increased survival, providing novel insights into epigenetic biology. A clearer understanding of how SETDB1/2-mediated transcriptional reprogramming can subvert treatment responses will be invaluable in improving length and efficacy of modern therapies. PMID: 30850015 [PubMed - in process]

https://www.ncbi.nlm.nih.gov/pubmed/30850015?dopt=Abstract

Source: Clinical Breast Cancer - March 7, 2019 Category: Cancer & Oncology Authors: Torrano J, Al Emran A, Hammerlindl H, Schaider H Tags: Clin Epigenetics Source Type: research