<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/GSE306nnn/GSE306038/</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>Expression profiling by high throughput sequencing</gds_type><full_dataset_link>https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE306038</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>Intratumoral plasma cells are required for immune checkpoint blockade therapy in de novo MPNSTs</name><description>In most human cancers, intratumoral plasma cells connote improved patient survival and heightened anti-tumor response to immune checkpoint blockade (ICB) therapies, such as those targeting programmed death-ligand 1 (PD-L1) or programmed death 1 (PD1). Using an immunocompetent mouse model of de novo malignant peripheral nerve sheath tumors (MPNSTs), we found that plasma cells are required for successful anti-PD-L1 therapy and extended survival. In order to uncover the role of plasma cells in this response, we performed scRNA-seq of de novo MPNSTs within wild-type controls versus plasma cell-deficient AID-/-; µS-/- mice following CDK4/6-MEK inhibition. These results support our hypothesis that response to anti-PD-L1 is influenced by plasma cell infiltration into MPNSTs following CDK4/6-MEK inhibition.</description><dates><publication>2026/08/19</publication></dates><accession>GSE306038</accession><cross_references><GSM>GSM9191981</GSM><GSM>GSM9191980</GSM><GSM>GSM9191976</GSM><GSM>GSM9191979</GSM><GSM>GSM9191978</GSM><GSM>GSM9191977</GSM><GPL>24247</GPL><GSE>306038</GSE><taxon>Mus musculus</taxon><PMID>[42541926]</PMID></cross_references></HashMap>