Abstract Chromatin remodeling complexes undergo dynamic assembly of chromatin to facilitate the access to DNA packed in nucleosomes during DNA-template cellular processes. They present genetic alterations in multiple of its components in a broad range of hematological and solid malignancies. The SWI/SNF ATP-dependent chromatin remodeling complex subunits BRG1 and ARID1A were reported to act as tumor suppressors and they are mutated in a variety of human cancers including breast cancer, prostate cancer, lung cancer and pancreatic cancer. In contrast with the irreversible genomic mutations, epigenetic modifications can be reversed by therapeutic treatment. New generation of epigenetic drugs consists on specific inhibitors against chromatin associated proteins which present abnormal expression in tumors. Bromodomain and BET inhibitors block the assembly of a protein complex at a particular gene locus by impairing the interaction of the bromodomain with the acetylated lysine of a histone tail. To date, some BET inhibitors have been tested for the treatment of the rare NUT midline carcinoma disease, acute myeloid leukemia and multiple myeloma. Our aim was to find new potential biomarkers for a personalized cancer treatment with new generation epigenetic drugs. Thus, we tested whether cell lines with a component of the SWI/SNF complex disrupted (BRG1 or ARID1A) present more sensitivity to bromodomain inhibitors. Citation Format: Montserrat Pérez-Salvia, Laia Simó-Riudalbas, Manel Esteller. Effect of epigenetic drugs on chromatin remodeling complexes disrupted in cancer. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 4784. doi:10.1158/1538-7445.AM2015-4784
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