<HashMap><database>GEO</database><file_versions><headers><Content-Type>application/xml</Content-Type></headers><body><files><Other>ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE336nnn/GSE336546/</Other></files><type>primary</type></body><statusCode>OK</statusCode><statusCodeValue>200</statusCodeValue></file_versions><scores/><additional><omics_type>Transcriptomics</omics_type><species>Homo sapiens</species><gds_type>Expression profiling by high throughput sequencing</gds_type><full_dataset_link>https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE336546</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>CpG Hypermethylation and WNT/AP-1 cooperativity Define the Epigenetic Landscape and a Clinical Subgroup of High-Risk Pediatric Adrenocortical Carcinoma [cell line]</name><description>Treatment of two adult ACC cell lines (H295R and CU-ACC1) with the HDAC inhibitor entinostat led to consistent dose-dependent reductions in viability, outperforming the DNA demethylating agent decitabine. scRNA-seq analyses revealed global transcriptional reprogramming. This included downregulation of AP-1 transcription factors (FOS, JUND, JUNB), suppression of oxidative phosphorylation and steroidogenic pathways, and increased expression of pro-apoptotic genes. These findings support entinostat's potential to reverse high-risk epigenetic programs in pACT and highlight HDAC inhibition as a promising therapeutic avenue, particularly when combined with established treatments.</description><dates><publication>2026/08/12</publication></dates><accession>GSE336546</accession><cross_references><GSM>GSM9837159</GSM><GSM>GSM9837158</GSM><GSM>GSM9837160</GSM><GSM>GSM9837157</GSM><GSM>GSM9837156</GSM><GSM>GSM9837155</GSM><GPL>34284</GPL><GSE>336546</GSE><taxon>Homo sapiens</taxon></cross_references></HashMap>