<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/GSE331nnn/GSE331042/</Other></files><type>primary</type></body><statusCodeValue>200</statusCodeValue><statusCode>OK</statusCode></file_versions><scores/><additional><omics_type>Transcriptomics</omics_type><species>Mus musculus</species><gds_type> Other</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=GSE331042</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>Mechanoimmunological Control of Metastatic Site Selection</name><description>To explore the molecular mechanisms underlying stiffness modulation in vivo, GFP+ B16F10 MTCs from the lungs of wild type mice and from the lungs and bones of Prf1-/- mice were subjected to single cell RNA-sequencing (scRNA-seq). Uniform manifold approximation and projection (UMAP) analysis of the resulting data revealed 9 distinguishable populations of cancer cells. Lung metastases from wild type and Prf1-/- animals contained all 9 populations, implying that cellular cytotoxicity does not drastically alter tumor composition in this organ. Nevertheless, subtle shifts in the size and make-up of certain clusters were apparent, consistent with some degree of immune pressure. B16F10 composition differed dramatically in Prf1-/- bone, with several clusters shifting substantially in the UMAP plot or disappearing altogether.</description><dates><publication>2026/07/28</publication></dates><accession>GSE331042</accession><cross_references><GSM>GSM9738019</GSM><GSM>GSM9738018</GSM><GPL>24247</GPL><GSE>331042</GSE><taxon>Mus musculus</taxon></cross_references></HashMap>