{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["4"],"submitter":["Bolden JE"],"pubmed_abstract":["The identification of recurrent somatic mutations in genes encoding epigenetic enzymes has provided a strong rationale for the development of compounds that target the epigenome for the treatment of cancer. This notion is supported by biochemical studies demonstrating aberrant recruitment of epigenetic enzymes such as histone deacetylases (HDACs) and histone methyltransferases to promoter regions through association with oncogenic fusion proteins such as PML-RARα and AML1-ETO. HDAC inhibitors (HDACi) are potent inducers of tumor cell apoptosis; however, it remains unclear why tumor cells are more sensitive to HDACi-induced cell death than normal cells. Herein, we assessed the biological and molecular responses of isogenic normal and transformed cells to the FDA-approved HDACi vorinostat an"],"journal":["Cell death & disease"],"pagination":["e519"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC3734831"],"repository":["biostudies-literature"],"pubmed_title":["HDAC inhibitors induce tumor-cell-selective pro-apoptotic transcriptional responses."],"pmcid":["PMC3734831"],"pubmed_authors":["Jankowski K","Bolden JE","MacKenzie KL","Smyth GK","Shi W","Cluse L","Martin BP","Kan CY","Johnstone RW"],"additional_accession":[]},"is_claimable":false,"name":"HDAC inhibitors induce tumor-cell-selective pro-apoptotic transcriptional responses.","description":"The identification of recurrent somatic mutations in genes encoding epigenetic enzymes has provided a strong rationale for the development of compounds that target the epigenome for the treatment of cancer. This notion is supported by biochemical studies demonstrating aberrant recruitment of epigenetic enzymes such as histone deacetylases (HDACs) and histone methyltransferases to promoter regions through association with oncogenic fusion proteins such as PML-RARα and AML1-ETO. HDAC inhibitors (HDACi) are potent inducers of tumor cell apoptosis; however, it remains unclear why tumor cells are more sensitive to HDACi-induced cell death than normal cells. Herein, we assessed the biological and molecular responses of isogenic normal and transformed cells to the FDA-approved HDACi vorinostat an","dates":{"release":"2013-01-01T00:00:00Z","publication":"2013 Feb","modification":"2026-05-30T07:35:03.038Z","creation":"2025-07-28T03:04:15.874Z"},"accession":"S-EPMC3734831","cross_references":{"pubmed":["23449455"],"doi":["10.1038/cddis.2013.9"]}}