{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["9(18)"],"submitter":["Congras A"],"pubmed_abstract":["Systemic anaplastic large-cell lymphoma (ALCL) is a childhood T cell neoplasm defined by the presence or absence of translocations that lead to the ectopic expression of anaplastic lymphoma kinase (ALK), with nucleophosmin-ALK (NPM-ALK) fusions being the most common. Polychemotherapy involving doxorubicin is the standard first-line treatment but for the 25 to 35% of patients who relapse and develop resistance the prognosis remains poor. We studied the potential role of the microRNA miR-125b in the development of resistance to doxorubicin in NPM-ALK(+) ALCL. Our results show that miR-125b expression is repressed in NPM-ALK(+) cell lines and patient samples through hypermethylation of its promoter. NPM-ALK activity, in cooperation with DNA topoisomerase II (Topo II) and DNA methyltransferase"],"journal":["Oncotarget"],"pagination":["14539-14551"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC5865688"],"repository":["biostudies-literature"],"pubmed_title":["Doxorubicin-induced loss of DNA topoisomerase II and DNMT1- dependent suppression of MiR-125b induces chemoresistance in ALK-positive cells."],"pmcid":["PMC5865688"],"pubmed_authors":["Congras A","Brousset P","Torossian N","Hoareau-Aveilla C","Quelen C","Daugrois C","Lamant L","Meggetto F","Caillet N"],"additional_accession":[]},"is_claimable":false,"name":"Doxorubicin-induced loss of DNA topoisomerase II and DNMT1- dependent suppression of MiR-125b induces chemoresistance in ALK-positive cells.","description":"Systemic anaplastic large-cell lymphoma (ALCL) is a childhood T cell neoplasm defined by the presence or absence of translocations that lead to the ectopic expression of anaplastic lymphoma kinase (ALK), with nucleophosmin-ALK (NPM-ALK) fusions being the most common. Polychemotherapy involving doxorubicin is the standard first-line treatment but for the 25 to 35% of patients who relapse and develop resistance the prognosis remains poor. We studied the potential role of the microRNA miR-125b in the development of resistance to doxorubicin in NPM-ALK(+) ALCL. Our results show that miR-125b expression is repressed in NPM-ALK(+) cell lines and patient samples through hypermethylation of its promoter. NPM-ALK activity, in cooperation with DNA topoisomerase II (Topo II) and DNA methyltransferase","dates":{"release":"2018-01-01T00:00:00Z","publication":"2018 Mar","modification":"2025-04-04T12:55:58.294Z","creation":"2019-03-26T23:47:53Z"},"accession":"S-EPMC5865688","cross_references":{"pubmed":["29581862"],"doi":["10.18632/oncotarget.24465"]}}