<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Camp FA</submitter><funding>National Institutes of Health/National Cancer Institute</funding><funding>Cancer Center Support Grant</funding><funding>NCI NIH HHS</funding><funding>Men for the Cure and the Department of Immunology and Microbiology at CU|AMC</funding><pagination>4397</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9496737</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>14(18)</volume><pubmed_abstract>Antigenic differences formed by alterations in gene expression and alternative splicing are predicted in breast cancer cells undergoing epithelial to mesenchymal transition (EMT) and the reverse plasticity known as MET. How these antigenic differences impact immune interactions and the degree to which they can be exploited to enhance immune responses against mesenchymal cells is not fully understood. We utilized a master microRNA regulator of EMT to alter mesenchymal-like EO771 mammary carcinoma cells to a more epithelial phenotype. A computational approach was used to identify neoantigens derived from the resultant differentially expressed somatic variants (SNV) and alternative splicing events (neojunctions). Using whole cell vaccines and peptide-based vaccines, we find superior cytotoxic</pubmed_abstract><journal>Cancers</journal><pubmed_title>Antigens Expressed by Breast Cancer Cells Undergoing EMT Stimulate Cytotoxic CD8&lt;sup>+&lt;/sup> T Cell Immunity.</pubmed_title><pmcid>PMC9496737</pmcid><funding_grant_id>T32 CA190216</funding_grant_id><funding_grant_id>F32 CA239436</funding_grant_id><funding_grant_id>P30 CA046934</funding_grant_id><funding_grant_id>CA226879</funding_grant_id><funding_grant_id>P30CA046934</funding_grant_id><funding_grant_id>CA226879-04</funding_grant_id><funding_grant_id>R01 CA226879</funding_grant_id><pubmed_authors>Brunetti TM</pubmed_authors><pubmed_authors>Camp FA</pubmed_authors><pubmed_authors>Richer JK</pubmed_authors><pubmed_authors>Sreekanth V</pubmed_authors><pubmed_authors>Kedl RM</pubmed_authors><pubmed_authors>Slansky JE</pubmed_authors><pubmed_authors>Hay ZLZ</pubmed_authors><pubmed_authors>Christenson JL</pubmed_authors><pubmed_authors>Costello JC</pubmed_authors><pubmed_authors>Williams MM</pubmed_authors></additional><is_claimable>false</is_claimable><name>Antigens Expressed by Breast Cancer Cells Undergoing EMT Stimulate Cytotoxic CD8&lt;sup>+&lt;/sup> T Cell Immunity.</name><description>Antigenic differences formed by alterations in gene expression and alternative splicing are predicted in breast cancer cells undergoing epithelial to mesenchymal transition (EMT) and the reverse plasticity known as MET. How these antigenic differences impact immune interactions and the degree to which they can be exploited to enhance immune responses against mesenchymal cells is not fully understood. We utilized a master microRNA regulator of EMT to alter mesenchymal-like EO771 mammary carcinoma cells to a more epithelial phenotype. A computational approach was used to identify neoantigens derived from the resultant differentially expressed somatic variants (SNV) and alternative splicing events (neojunctions). Using whole cell vaccines and peptide-based vaccines, we find superior cytotoxic</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Sep</publication><modification>2026-06-20T03:24:34.655Z</modification><creation>2025-02-19T00:44:08.172Z</creation></dates><accession>S-EPMC9496737</accession><cross_references><pubmed>36139558</pubmed><doi>10.3390/cancers14184397</doi></cross_references></HashMap>