<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/GSE307120/</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> Genome binding/occupancy profiling by high throughput sequencing</gds_type><gds_type>Expression profiling by high throughput sequencing</gds_type><full_dataset_link>https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE307120</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>Fusion-driven oncogenic programs shape the immune landscape in translocation renal cell carcinoma</name><description>Renal cell carcinomas comprise multiple molecularly distinct cancers but most are treated empirically with therapies designed for clear cell RCC (ccRCC), the most common subtype, due to incomplete understanding of subtype-specific biology. We analyzed single-cell transcriptomes and chromatin accessibility profiles from translocation renal cell carcinoma (tRCC), an aggressive RCC defined by oncogenic TFE3 gene fusions.</description><dates><publication>2026/08/06</publication></dates><accession>GSE307120</accession><cross_references><GSM>GSM9485536</GSM><GSM>GSM9485534</GSM><GSM>GSM9485531</GSM><GSM>GSM9485532</GSM><GSM>GSM9216856</GSM><GSM>GSM9216857</GSM><GSM>GSM9216854</GSM><GSM>GSM9216855</GSM><GSM>GSM9485528</GSM><GSM>GSM9216858</GSM><GSM>GSM9216859</GSM><GSM>GSM9485538</GSM><GSM>GSM9216860</GSM><GSM>GSM9216863</GSM><GSM>GSM9216852</GSM><GSM>GSM9216864</GSM><GSM>GSM9216853</GSM><GSM>GSM9216861</GSM><GSM>GSM9216850</GSM><GSM>GSM9216851</GSM><GSM>GSM9216862</GSM><GPL>24676</GPL><GSE>307120</GSE><taxon>Homo sapiens</taxon></cross_references></HashMap>