{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["de Sousa GR"],"funding":["NCATS NIH HHS","NCI NIH HHS","NIH HHS"],"pagination":["1597-1610"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12309711"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["27(6)"],"pubmed_abstract":["<h4>Background</h4>Posterior fossa molecular subtype A (PFA) ependymoma occurs in young children and is the deadliest subtype of pediatric ependymoma. High-risk subtypes with chromosome 1q + and/or 6q- exhibit significantly poorer outcomes compared to wild-type PFA. However, 50% of wild-type PFA patients relapse and there is a high risk of gaining chromosome 1q at recurrence. We previously found constitutively active NF-κB, through loss of LDOC1, led to chronic IL-6 secretion and an overall immunosuppressive tumor microenvironment in the higher-risk wild-type PFA ependymoma subset (PFA1).<h4>Methods</h4>In this study, we delineate the mechanistic consequences of LDOC1 loss in PFA1, using our PFA ependymoma in vitro and in vivo models under normoxia and hypoxia conditions.<h4>Results</h4>We"],"journal":["Neuro-oncology"],"pubmed_title":["Loss of LDOC1 by chromatin compaction in mesenchymal tumor cells is required for PFA1 ependymoma growth."],"pmcid":["PMC12309711"],"funding_grant_id":["P30 CA046934","S10 OD023485","R01 CA239302","UM1 TR004399"],"pubmed_authors":["Valera ET","Phang T","Levy JMM","Jones KM","Dahl NA","Grimaldo E","Sobral LM","Liu T","Griesinger AM","Calzadilla AJ","Handler M","Donson AM","Vibhakar R","de Sousa GR","Amani V","Foreman NK","Hankinson T","Venkataraman S"],"additional_accession":[]},"is_claimable":false,"name":"Loss of LDOC1 by chromatin compaction in mesenchymal tumor cells is required for PFA1 ependymoma growth.","description":"<h4>Background</h4>Posterior fossa molecular subtype A (PFA) ependymoma occurs in young children and is the deadliest subtype of pediatric ependymoma. High-risk subtypes with chromosome 1q + and/or 6q- exhibit significantly poorer outcomes compared to wild-type PFA. However, 50% of wild-type PFA patients relapse and there is a high risk of gaining chromosome 1q at recurrence. We previously found constitutively active NF-κB, through loss of LDOC1, led to chronic IL-6 secretion and an overall immunosuppressive tumor microenvironment in the higher-risk wild-type PFA ependymoma subset (PFA1).<h4>Methods</h4>In this study, we delineate the mechanistic consequences of LDOC1 loss in PFA1, using our PFA ependymoma in vitro and in vivo models under normoxia and hypoxia conditions.<h4>Results</h4>We","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Jul","modification":"2026-03-16T05:53:28.471Z","creation":"2025-08-14T03:06:23.763Z"},"accession":"S-EPMC12309711","cross_references":{"pubmed":["39901723"],"doi":["10.1093/neuonc/noaf029"]}}