{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Bugide S"],"funding":["NCI NIH HHS"],"pagination":["e2218118120"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9942844"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["120(4)"],"pubmed_abstract":["Although epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (EGFRi) are approved for treating EGFR-mutant lung adenocarcinoma (LUAD), emergence of acquired resistance limits their clinical benefits. Several mechanisms for acquired resistance to EGFRi in LUAD have been identified; however, the molecular basis for this resistance remains unknown in ~30% of LUAD. Chromatin and DNA modifiers and their regulators play important roles in determining response to anticancer therapies. Therefore, to identify nongenetic mechanisms of EGFRi resistance in LUAD, we performed an epigenome-wide shRNA screen targeting 363 human epigenetic regulator genes. This screen identified loss of the transcriptional repressor chromobox homolog 5 (CBX5) as a driver of EGFRi resistance in EGFR-mutant L"],"journal":["Proceedings of the National Academy of Sciences of the United States of America"],"pubmed_title":["CBX5 loss drives EGFR inhibitor resistance and results in therapeutically actionable vulnerabilities in lung cancer."],"pmcid":["PMC9942844"],"funding_grant_id":["R01 CA257046","R01 CA233481","R03 CA248913","R01 CA218008"],"pubmed_authors":["Gupta R","Wajapeyee N","Edwards YJK","Green MR","Bugide S"],"additional_accession":[]},"is_claimable":false,"name":"CBX5 loss drives EGFR inhibitor resistance and results in therapeutically actionable vulnerabilities in lung cancer.","description":"Although epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (EGFRi) are approved for treating EGFR-mutant lung adenocarcinoma (LUAD), emergence of acquired resistance limits their clinical benefits. Several mechanisms for acquired resistance to EGFRi in LUAD have been identified; however, the molecular basis for this resistance remains unknown in ~30% of LUAD. Chromatin and DNA modifiers and their regulators play important roles in determining response to anticancer therapies. Therefore, to identify nongenetic mechanisms of EGFRi resistance in LUAD, we performed an epigenome-wide shRNA screen targeting 363 human epigenetic regulator genes. This screen identified loss of the transcriptional repressor chromobox homolog 5 (CBX5) as a driver of EGFRi resistance in EGFR-mutant L","dates":{"release":"2023-01-01T00:00:00Z","publication":"2023 Jan","modification":"2025-04-04T22:54:35.064Z","creation":"2025-04-04T22:54:35.064Z"},"accession":"S-EPMC9942844","cross_references":{"pubmed":["36652476"],"doi":["10.1073/pnas.2218118120"]}}