<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/GSE344nnn/GSE344585/</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=GSE344585</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>Gene expression analysis of HSD17B4 knock-out breast cancer cells</name><description>HER2-positive breast cancer has a high chance of achieving pathological complete response when HSD17B4, responsible for peroxisomal β-oxidation of very long-chain fatty acids and estradiol, is methylation-silenced. Here, we aimed to identify the underlying molecular mechanism. We conducted RNA-seq analysis and Gene Set Enrichment Analysis to make an unbiased search for genes driven by HSD17B4 KO. Analysis of the pathways upregulated by HSD17B4 depletion revealed a gene network associated with oxidative phosphorylation, using the KEGG database, and that associated with the mitochondrial respiratory chain, using the GOBP terms.</description><dates><publication>2026/09/01</publication></dates><accession>GSE344585</accession><cross_references><GSM>GSM9981864</GSM><GSM>GSM9981865</GSM><GSM>GSM9981862</GSM><GSM>GSM9981863</GSM><GPL>29480</GPL><GSE>344585</GSE><taxon>Homo sapiens</taxon></cross_references></HashMap>