<HashMap><database>biostudies-literature</database><scores/><additional><submitter>McMiller TL</submitter><funding>Bloomberg~Kimmel Institute for Cancer Immunotherapy, Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University</funding><funding>Clinical Center</funding><funding>Bristol Myers Squibb</funding><funding>Mark Foundation For Cancer Research</funding><pagination>e010201</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC11580252</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>12(11)</volume><pubmed_abstract>&lt;h4>Background&lt;/h4>Gastric carcinomas (GC) are aggressive malignancies, and only ~15% of patients respond to anti-programmed cell death (ligand) 1 (PD-(L)1) monotherapy. However, Epstein-Barr virus (EBV)-associated GCs (~5-10% of GCs) often harbor PD-L1 and PD-L2 chromosomal amplifications and robust CD8+ T cell infiltrates, and respond at a high rate to anti-PD-1. The current study compares the tumor immune microenvironments (TiMEs) of EBV+ versus EBV(-) GCs.&lt;h4>Methods&lt;/h4>Over 1000 cases of primary invasive GCs were screened to identify 25 treatment-naïve specimens for study (11 EBV+, 14 EBV(-)). Quantitative immunohistochemistry (IHC) was conducted for markers of immune cell subsets and co-regulatory molecules. Gene expression profiling (GEP) was performed on RNAs isolated from macrodi</pubmed_abstract><journal>Journal for immunotherapy of cancer</journal><pubmed_title>Immune microenvironment of Epstein-Barr virus (EBV)-negative compared to EBV-associated gastric cancers: implications for immunotherapy.</pubmed_title><pmcid>PMC11580252</pmcid><funding_grant_id>N/A</funding_grant_id><funding_grant_id>NCI R01CA142779</funding_grant_id><pubmed_authors>Xu K</pubmed_authors><pubmed_authors>Taube JM</pubmed_authors><pubmed_authors>Anders RA</pubmed_authors><pubmed_authors>McMiller TL</pubmed_authors><pubmed_authors>Lee J</pubmed_authors><pubmed_authors>Engle LL</pubmed_authors><pubmed_authors>Bhaijee F</pubmed_authors><pubmed_authors>Unsal-Kacmaz K</pubmed_authors><pubmed_authors>Berger AE</pubmed_authors><pubmed_authors>Besharati S</pubmed_authors><pubmed_authors>Yarchoan M</pubmed_authors><pubmed_authors>Zhu Q</pubmed_authors><pubmed_authors>Topalian SL</pubmed_authors></additional><is_claimable>false</is_claimable><name>Immune microenvironment of Epstein-Barr virus (EBV)-negative compared to EBV-associated gastric cancers: implications for immunotherapy.</name><description>&lt;h4>Background&lt;/h4>Gastric carcinomas (GC) are aggressive malignancies, and only ~15% of patients respond to anti-programmed cell death (ligand) 1 (PD-(L)1) monotherapy. However, Epstein-Barr virus (EBV)-associated GCs (~5-10% of GCs) often harbor PD-L1 and PD-L2 chromosomal amplifications and robust CD8+ T cell infiltrates, and respond at a high rate to anti-PD-1. The current study compares the tumor immune microenvironments (TiMEs) of EBV+ versus EBV(-) GCs.&lt;h4>Methods&lt;/h4>Over 1000 cases of primary invasive GCs were screened to identify 25 treatment-naïve specimens for study (11 EBV+, 14 EBV(-)). Quantitative immunohistochemistry (IHC) was conducted for markers of immune cell subsets and co-regulatory molecules. Gene expression profiling (GEP) was performed on RNAs isolated from macrodi</description><dates><release>2024-01-01T00:00:00Z</release><publication>2024 Nov</publication><modification>2025-04-04T01:20:51.643Z</modification><creation>2025-04-04T01:20:51.643Z</creation></dates><accession>S-EPMC11580252</accession><cross_references><pubmed>39572160</pubmed><doi>10.1136/jitc-2024-010201</doi></cross_references></HashMap>