{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["7(2)"],"submitter":["Buontempo F"],"pubmed_abstract":["The proteasome inhibitor bortezomib is a new targeted treatment option for refractory or relapsed acute lymphoblastic leukemia (ALL) patients. However, a limited efficacy of bortezomib alone has been reported. A terminal pro-apoptotic endoplasmic reticulum (ER) stress/unfolded protein response (UPR) is one of the several mechanisms of bortezomib-induced apoptosis. Recently, it has been documented that UPR disruption could be considered a selective anti-leukemia therapy. CX-4945, a potent casein kinase (CK) 2 inhibitor, has been found to induce apoptotic cell death in T-ALL preclinical models, via perturbation of ER/UPR pathway. In this study, we analyzed in T- and B-ALL preclinical settings, the molecular mechanisms of synergistic apoptotic effects observed after bortezomib/CX-4945 combine"],"journal":["Oncotarget"],"pagination":["1323-40"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC4811463"],"repository":["biostudies-literature"],"pubmed_title":["Synergistic cytotoxic effects of bortezomib and CK2 inhibitor CX-4945 in acute lymphoblastic leukemia: turning off the prosurvival ER chaperone BIP/Grp78 and turning on the pro-apoptotic NF-κB."],"pmcid":["PMC4811463"],"pubmed_authors":["Orsini E","Lonetti A","Neri LM","Cappellini A","Bertaina A","Pession A","Locatelli F","Martelli AM","Evangelisti C","Chiarini F","Melchionda F","Bertacchini J","Buontempo F","McCubrey JA"],"additional_accession":[]},"is_claimable":false,"name":"Synergistic cytotoxic effects of bortezomib and CK2 inhibitor CX-4945 in acute lymphoblastic leukemia: turning off the prosurvival ER chaperone BIP/Grp78 and turning on the pro-apoptotic NF-κB.","description":"The proteasome inhibitor bortezomib is a new targeted treatment option for refractory or relapsed acute lymphoblastic leukemia (ALL) patients. However, a limited efficacy of bortezomib alone has been reported. A terminal pro-apoptotic endoplasmic reticulum (ER) stress/unfolded protein response (UPR) is one of the several mechanisms of bortezomib-induced apoptosis. Recently, it has been documented that UPR disruption could be considered a selective anti-leukemia therapy. CX-4945, a potent casein kinase (CK) 2 inhibitor, has been found to induce apoptotic cell death in T-ALL preclinical models, via perturbation of ER/UPR pathway. In this study, we analyzed in T- and B-ALL preclinical settings, the molecular mechanisms of synergistic apoptotic effects observed after bortezomib/CX-4945 combine","dates":{"release":"2016-01-01T00:00:00Z","publication":"2016 Jan","modification":"2026-04-30T07:05:51.612Z","creation":"2019-03-27T03:10:32Z"},"accession":"S-EPMC4811463","cross_references":{"pubmed":["26593250"],"doi":["10.18632/oncotarget.6361"]}}