{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Murray JE"],"funding":["Associazione Italiana per la Ricerca sul Cancro","Cancer Council NSW","Profield Foundation Australia Tour de Cure Australia Neuroblastoma Australia","Università di Bologna (University of Bologna)","Università di Bologna","Department of Health | National Health and Medical Research Council (NHMRC)","Associazione Italiana per la Ricerca sul Cancro (Italian Association for Cancer Research)","Department of Health | National Health and Medical Research Council"],"pagination":["5585"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11239676"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["15(1)"],"pubmed_abstract":["MYCN oncogene amplification is frequently observed in aggressive childhood neuroblastoma. Using an unbiased large-scale mutagenesis screen in neuroblastoma-prone transgenic mice, we identify a single germline point mutation in the transcriptional corepressor Runx1t1, which abolishes MYCN-driven tumorigenesis. This loss-of-function mutation disrupts a highly conserved zinc finger domain within Runx1t1. Deletion of one Runx1t1 allele in an independent Runx1t1 knockout mouse model is also sufficient to prevent MYCN-driven neuroblastoma development, and reverse ganglia hyperplasia, a known pre-requisite for tumorigenesis. Silencing RUNX1T1 in human neuroblastoma cells decreases colony formation in vitro, and inhibits tumor growth in vivo. Moreover, RUNX1T1 knockdown inhibits the viability of P"],"journal":["Nature communications"],"pubmed_title":["The transcriptional co-repressor Runx1t1 is essential for MYCN-driven neuroblastoma tumorigenesis."],"pmcid":["PMC11239676"],"funding_grant_id":["IG15182","APP1132608","IG24341","RFO","APP1016699","APP1083938"],"pubmed_authors":["Salehzadeh F","Allan S","Xue C","Fleuren EDG","Murray JE","Mackay JP","Fletcher JI","Gifford AJ","Clark A","Norris MD","Milazzo G","Wilkinson-White L","Giorgi FM","Kusuma FK","Carter DR","Forgham H","Haber M","Perini G","Russell AJ","Kile BT","Low JKK","Sekyere EO","Eden G","Valli E","Mayoh C","Rouaen JRC","Hilton DJ","Koster J","Webber H","Santulli M","De Rosa P","Keating J","Marshall GM","Alfred S","de Weck A","Gao W","Jayatilleke N","Gamble LD"],"additional_accession":[]},"is_claimable":false,"name":"The transcriptional co-repressor Runx1t1 is essential for MYCN-driven neuroblastoma tumorigenesis.","description":"MYCN oncogene amplification is frequently observed in aggressive childhood neuroblastoma. Using an unbiased large-scale mutagenesis screen in neuroblastoma-prone transgenic mice, we identify a single germline point mutation in the transcriptional corepressor Runx1t1, which abolishes MYCN-driven tumorigenesis. This loss-of-function mutation disrupts a highly conserved zinc finger domain within Runx1t1. Deletion of one Runx1t1 allele in an independent Runx1t1 knockout mouse model is also sufficient to prevent MYCN-driven neuroblastoma development, and reverse ganglia hyperplasia, a known pre-requisite for tumorigenesis. Silencing RUNX1T1 in human neuroblastoma cells decreases colony formation in vitro, and inhibits tumor growth in vivo. Moreover, RUNX1T1 knockdown inhibits the viability of P","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Jul","modification":"2026-07-15T05:14:15.438Z","creation":"2025-04-05T15:48:05.276Z"},"accession":"S-EPMC11239676","cross_references":{"pubmed":["38992040"],"doi":["10.1038/s41467-024-49871-0"]}}