{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Lang F"],"funding":["National Cancer Institute","NCI NIH HHS","National Institutes of Health"],"pagination":["1083-1096"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11145461"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["26(6)"],"pubmed_abstract":["<h4>Background</h4>The cell cycle is tightly regulated by checkpoints, which play a vital role in controlling its progression and timing. Cancer cells exploit the G2/M checkpoint, which serves as a resistance mechanism against genotoxic anticancer treatments, allowing for DNA repair prior to cell division. Manipulating cell cycle timing has emerged as a potential strategy to augment the effectiveness of DNA damage-based therapies.<h4>Methods</h4>In this study, we conducted a forward genome-wide CRISPR/Cas9 screening with repeated exposure to the alkylating agent temozolomide (TMZ) to investigate the mechanisms underlying tumor cell survival under genotoxic stress.<h4>Results</h4>Our findings revealed that canonical DNA repair pathways, including the Ataxia-telangiectasia mutated (ATM)/Fanc"],"journal":["Neuro-oncology"],"pubmed_title":["Abrogation of the G2/M checkpoint as a chemosensitization approach for alkylating agents."],"pmcid":["PMC11145461"],"funding_grant_id":["75N91019D00024"],"pubmed_authors":["Elmogazy O","Zhang M","Cappell SD","Song H","Yang C","Lang F","Sun Z","Zhang W","Aladjem MI","Cornwell JA","Kaur K","Aregger M","Wu X"],"additional_accession":[]},"is_claimable":false,"name":"Abrogation of the G2/M checkpoint as a chemosensitization approach for alkylating agents.","description":"<h4>Background</h4>The cell cycle is tightly regulated by checkpoints, which play a vital role in controlling its progression and timing. Cancer cells exploit the G2/M checkpoint, which serves as a resistance mechanism against genotoxic anticancer treatments, allowing for DNA repair prior to cell division. Manipulating cell cycle timing has emerged as a potential strategy to augment the effectiveness of DNA damage-based therapies.<h4>Methods</h4>In this study, we conducted a forward genome-wide CRISPR/Cas9 screening with repeated exposure to the alkylating agent temozolomide (TMZ) to investigate the mechanisms underlying tumor cell survival under genotoxic stress.<h4>Results</h4>Our findings revealed that canonical DNA repair pathways, including the Ataxia-telangiectasia mutated (ATM)/Fanc","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Jun","modification":"2025-04-22T16:58:18.041Z","creation":"2025-04-06T01:55:04.766Z"},"accession":"S-EPMC11145461","cross_references":{"pubmed":["38134889"],"doi":["10.1093/neuonc/noad252"]}}