<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/GSE307906/</Other></files><type>primary</type></body><statusCode>OK</statusCode><statusCodeValue>200</statusCodeValue></file_versions><scores/><additional><omics_type>Transcriptomics</omics_type><species>Mus musculus</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=GSE307906</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>Effect of Ttyh2 Knockout on Tumor Growth Control [scRNA-Seq]</name><description>We employed single-cell RNA sequencing (scRNA-seq) using the 10x Genomics platform to investigate the role of Ttyh2 in tumor growth control. Ttyh2 knockout (KO) mice exhibited impaired tumor growth. In wild-type (WT) mice, Ttyh2 expression was enriched in Cd206⁺ tumor-associated macrophages (TAMs) and a subset of dendritic cells (DCs). In Ttyh2 KO tumors, the Nos2⁺/Cd206⁺ TAM ratio was elevated, accompanied by a compensatory expansion of monocytes. Pathway analysis revealed upregulation of type I interferon and NF-κB signaling signatures in both TAM subsets and cDC1 cells. Additionally, Ttyh2 KO tumors displayed increased infiltration of CD8⁺ T cells and a reduction in regulatory T cells (Tregs). These findings suggest that Ttyh2 deficiency remodels both the myeloid and lymphoid compartments toward a pro-inflammatory, antitumor immune state.</description><dates><publication>2026/09/09</publication></dates><accession>GSE307906</accession><cross_references><GSM>GSM9233788</GSM><GSM>GSM9233789</GSM><GPL>34290</GPL><GSE>307906</GSE><taxon>Mus musculus</taxon></cross_references></HashMap>