{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Xu Y"],"funding":["National Cancer Institute (NCI)","NCRR NIH HHS","NIDDK NIH HHS","NHLBI NIH HHS","NIOSH CDC HHS","National Cancer Institute","NHGRI NIH HHS","NCI NIH HHS"],"pagination":["1640-1652"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12475887"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["24(10)"],"pubmed_abstract":["Diffuse mesothelioma is a rare but highly aggressive and treatment-resistant neoplasm with low survival rates. Effective therapeutic strategies are limited, and resistance to treatment is a major obstacle. Myeloid cell leukemia (MCL)-1 and B-cell leukemia (BCL)-xL are antiapoptotic B-cell lymphoma 2 (Bcl-2) family proteins that block cell-intrinsic apoptosis through interactions on the mitochondrial outer membrane which contribute to therapeutic resistance. We investigated whether B-cell homology domain3 profiles were consistent between intra-patient fresh tumor sample, patient-derived cells, and patient-derived xenografts (PDX) by B-cell homology domain-3 profiling; we observed striking consistency which enabled cross-model comparisons. Next, we co-targeted BCL-xl and MCL-1 and noted that"],"journal":["Molecular cancer therapeutics"],"pubmed_title":["Co-Targeting BCL-xL with MCL-1 Induces Lethal Mitochondrial Dysfunction in Diffuse Mesothelioma."],"pmcid":["PMC12475887"],"funding_grant_id":["R37 CA289419","UM1 HG006348","R01 DK114356","R03 CA252685-01","R21 CA256466","U01 CA214195","R01 CA290173","S10 RR024574","R03 CA252685","U24 OH009077","P30 CA125123","R01 HL130249"],"pubmed_authors":["Vilchis M","Zhu Y","Ripley RT","Hilsenbeck SG","Surman DR","Aggison JC","Shen YH","Li N","Ramineni M","Li Y","Medina CG","Wu S","Chen X","Dobrolecki LE","Xu Y"],"additional_accession":[]},"is_claimable":false,"name":"Co-Targeting BCL-xL with MCL-1 Induces Lethal Mitochondrial Dysfunction in Diffuse Mesothelioma.","description":"Diffuse mesothelioma is a rare but highly aggressive and treatment-resistant neoplasm with low survival rates. Effective therapeutic strategies are limited, and resistance to treatment is a major obstacle. Myeloid cell leukemia (MCL)-1 and B-cell leukemia (BCL)-xL are antiapoptotic B-cell lymphoma 2 (Bcl-2) family proteins that block cell-intrinsic apoptosis through interactions on the mitochondrial outer membrane which contribute to therapeutic resistance. We investigated whether B-cell homology domain3 profiles were consistent between intra-patient fresh tumor sample, patient-derived cells, and patient-derived xenografts (PDX) by B-cell homology domain-3 profiling; we observed striking consistency which enabled cross-model comparisons. Next, we co-targeted BCL-xl and MCL-1 and noted that","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Oct","modification":"2026-06-06T17:45:20.886Z","creation":"2026-06-03T03:10:45.195Z"},"accession":"S-EPMC12475887","cross_references":{"pubmed":["40804773"],"doi":["10.1158/1535-7163.mct-24-0873","10.1158/1535-7163.MCT-24-0873"]}}