<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/GSE330nnn/GSE330658/</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=GSE330658</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>Limited Immune-Mediated Efficacy of Anti-PD-L1/VEGF in EGFR-TKI-Naïve Egfr-Mutant Lung Cancer with Non-Inflamed Tumor Microenvironment</name><description>Patients with EGFR-mutated lung cancer show limited response to immune checkpoint inhibitors. In this study, we found that anti-PD-L1/VEGF combination therapy failed to activate tumor immunity in a syngeneic Egfr-mutant lung cancer mouse model. Unlike the combination of paclitaxel (PTX) and anti-PD-L1, the combination of PTX and anti-VEGF enhanced anti-tumor effects and altered the tumor microenvironment (TME), showing potential to activate anti-tumor immunity. To investigate these mechanisms, we profiled the transcriptomes of tumors treated with PTX and/or anti-VEGF. The data suggested a potential trend where the combination of PTX and anti-VEGF therapy might be associated with a modest increase in natural killer (NK) cell populations within the TME.</description><dates><publication>2026/07/01</publication></dates><accession>GSE330658</accession><cross_references><GSM>GSM9729953</GSM><GSM>GSM9729952</GSM><GSM>GSM9729955</GSM><GSM>GSM9729954</GSM><GSM>GSM9729957</GSM><GSM>GSM9729956</GSM><GSM>GSM9729959</GSM><GSM>GSM9729958</GSM><GPL>28457</GPL><GSE>330658</GSE><taxon>Mus musculus</taxon><PMID>[42346215]</PMID></cross_references></HashMap>