<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Iorgulescu JB</submitter><funding>NCI NIH HHS</funding><funding>NINDS NIH HHS</funding><pagination>1297932</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC10782385</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>14</volume><pubmed_abstract>&lt;h4>Background&lt;/h4>The GL261 and CT2A syngeneic tumor lines are frequently used as immunocompetent orthotopic mouse models of human glioblastoma (huGBM) but demonstrate distinct differences in their responses to immunotherapy.&lt;h4>Methods&lt;/h4>To decipher the cell-intrinsic mechanisms that drive immunotherapy resistance in CT2A-luc and to define the aspects of human cancer biology that these lines can best model, we systematically compared their characteristics using whole exome and transcriptome sequencing, and protein analysis through immunohistochemistry, Western blot, flow cytometry, immunopeptidomics, and phosphopeptidomics.&lt;h4>Results&lt;/h4>The transcriptional profiles of GL261-luc2 and CT2A-luc tumors resembled those of some huGBMs, despite neither line sharing the essential genetic or </pubmed_abstract><journal>Frontiers in immunology</journal><pubmed_title>Antigen presentation deficiency, mesenchymal differentiation, and resistance to immunotherapy in the murine syngeneic CT2A tumor model.</pubmed_title><pmcid>PMC10782385</pmcid><funding_grant_id>K12 CA090354</funding_grant_id><funding_grant_id>R01 CA208205</funding_grant_id><funding_grant_id>U01 CA261842</funding_grant_id><funding_grant_id>P01 CA080124</funding_grant_id><funding_grant_id>U01 CA224348</funding_grant_id><funding_grant_id>R01 NS110942</funding_grant_id><funding_grant_id>P01 CA163205</funding_grant_id><funding_grant_id>R01 CA259253</funding_grant_id><funding_grant_id>K22 CA258410</funding_grant_id><funding_grant_id>R35 CA197743</funding_grant_id><funding_grant_id>R01 CA269672</funding_grant_id><funding_grant_id>P01 CA236749</funding_grant_id><pubmed_authors>Piranlioglu R</pubmed_authors><pubmed_authors>Chiocca EA</pubmed_authors><pubmed_authors>Neagu M</pubmed_authors><pubmed_authors>Panagioti E</pubmed_authors><pubmed_authors>Suva ML</pubmed_authors><pubmed_authors>Yates KB</pubmed_authors><pubmed_authors>Eschle BK</pubmed_authors><pubmed_authors>Gokhale PC</pubmed_authors><pubmed_authors>Sharpe AH</pubmed_authors><pubmed_authors>Iorgulescu JB</pubmed_authors><pubmed_authors>Krishnan S</pubmed_authors><pubmed_authors>Baker GJ</pubmed_authors><pubmed_authors>Reardon DA</pubmed_authors><pubmed_authors>Jain RK</pubmed_authors><pubmed_authors>Freeman GJ</pubmed_authors><pubmed_authors>White FM</pubmed_authors><pubmed_authors>Neuberg D</pubmed_authors><pubmed_authors>Wu CJ</pubmed_authors><pubmed_authors>Datta M</pubmed_authors><pubmed_authors>Ruthen N</pubmed_authors><pubmed_authors>Speranza MC</pubmed_authors><pubmed_authors>Soroko KM</pubmed_authors><pubmed_authors>Ahn R</pubmed_authors></additional><is_claimable>false</is_claimable><name>Antigen presentation deficiency, mesenchymal differentiation, and resistance to immunotherapy in the murine syngeneic CT2A tumor model.</name><description>&lt;h4>Background&lt;/h4>The GL261 and CT2A syngeneic tumor lines are frequently used as immunocompetent orthotopic mouse models of human glioblastoma (huGBM) but demonstrate distinct differences in their responses to immunotherapy.&lt;h4>Methods&lt;/h4>To decipher the cell-intrinsic mechanisms that drive immunotherapy resistance in CT2A-luc and to define the aspects of human cancer biology that these lines can best model, we systematically compared their characteristics using whole exome and transcriptome sequencing, and protein analysis through immunohistochemistry, Western blot, flow cytometry, immunopeptidomics, and phosphopeptidomics.&lt;h4>Results&lt;/h4>The transcriptional profiles of GL261-luc2 and CT2A-luc tumors resembled those of some huGBMs, despite neither line sharing the essential genetic or </description><dates><release>2023-01-01T00:00:00Z</release><publication>2023</publication><modification>2026-06-01T20:19:02.603Z</modification><creation>2025-04-04T20:48:12.111Z</creation></dates><accession>S-EPMC10782385</accession><cross_references><pubmed>38213329</pubmed><doi>10.3389/fimmu.2023.1297932</doi></cross_references></HashMap>