{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Wei SJ"],"funding":["Alex's Lemonade Stand Foundation for Childhood Cancer","U.S. Department of Health & Human Services | NIH | National Cancer Institute","NCI NIH HHS","Cancer Prevention and Research Institute of Texas"],"pagination":["368"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC7224192"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["11(5)"],"pubmed_abstract":["Despite the improvement in clinical outcome with 13-cis-retinoic acid (13-cisRA) + anti-GD2 antibody + cytokine immunotherapy given in first response ~40% of high-risk neuroblastoma patients die of recurrent disease. MYCN genomic amplification is a biomarker of aggressive tumors in the childhood cancer neuroblastoma. MYCN expression is downregulated by 13-cisRA, a differentiating agent that is a component of neuroblastoma therapy. Although MYC amplification is rare in neuroblastoma at diagnosis, we report transcriptional activation of MYC medicated by the transcription factor OCT4, functionally replacing MYCN in 13-cisRA-resistant progressive disease neuroblastoma in large panels of patient-derived cell lines and xenograft models. We identified novel OCT4-binding sites in the MYC promoter/"],"journal":["Cell death & disease"],"pubmed_title":["MYC transcription activation mediated by OCT4 as a mechanism of resistance to 13-cisRA-mediated differentiation in neuroblastoma."],"pmcid":["PMC7224192"],"funding_grant_id":["R01 CA232591","R01 CA221957","R01 CA168699","RP130547","RP170470"],"pubmed_authors":["Yang IH","Reynolds CP","Mook DG","Makena MR","Shimada H","Nguyen TH","Wei SJ","Verlekar D","Hindle A","Kang MH","Martinez GM","Yang S"],"additional_accession":[]},"is_claimable":false,"name":"MYC transcription activation mediated by OCT4 as a mechanism of resistance to 13-cisRA-mediated differentiation in neuroblastoma.","description":"Despite the improvement in clinical outcome with 13-cis-retinoic acid (13-cisRA) + anti-GD2 antibody + cytokine immunotherapy given in first response ~40% of high-risk neuroblastoma patients die of recurrent disease. MYCN genomic amplification is a biomarker of aggressive tumors in the childhood cancer neuroblastoma. MYCN expression is downregulated by 13-cisRA, a differentiating agent that is a component of neuroblastoma therapy. Although MYC amplification is rare in neuroblastoma at diagnosis, we report transcriptional activation of MYC medicated by the transcription factor OCT4, functionally replacing MYCN in 13-cisRA-resistant progressive disease neuroblastoma in large panels of patient-derived cell lines and xenograft models. We identified novel OCT4-binding sites in the MYC promoter/","dates":{"release":"2020-01-01T00:00:00Z","publication":"2020 May","modification":"2025-04-19T01:47:35.994Z","creation":"2020-05-22T20:21:19Z"},"accession":"S-EPMC7224192","cross_references":{"pubmed":["32409685"],"doi":["10.1038/s41419-020-2563-4"]}}