<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/GSE307nnn/GSE307571/</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=GSE307571</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>RNA sequencing analysis of BTN3A-deficient osteosarcoma MNNG-HOS cells</name><description>Butyrophilins (BTN) belong to the B7 receptors family and mediate complex interactions within the immune response. Several studies have shown that the BTN3A family may play an important role in some types of cancer. We detected a high overexpression of BTN3A proteins in human osteosarcoma (OS), the most common primary malignant bone tumor in children and adolescents. To investigate the molecular mechanisms altered in BTN3A-deficient cells we performed RNA‑Seq to identify changes in gene expression after BTN3A knockdown or knockout in OS cells.</description><dates><publication>2026/09/09</publication></dates><accession>GSE307571</accession><cross_references><GSM>GSM9227018</GSM><GSM>GSM9227007</GSM><GSM>GSM9227008</GSM><GSM>GSM9227009</GSM><GSM>GSM9227010</GSM><GSM>GSM9227011</GSM><GSM>GSM9227012</GSM><GSM>GSM9227013</GSM><GSM>GSM9227014</GSM><GSM>GSM9227015</GSM><GSM>GSM9227016</GSM><GSM>GSM9227017</GSM><GPL>34281</GPL><GSE>307571</GSE><taxon>Homo sapiens</taxon></cross_references></HashMap>