<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Wescott EC</submitter><funding>U.S. Department of Defense (DOD)</funding><funding>NCI NIH HHS</funding><funding>HHS | NIH | National Cancer Institute (NCI)</funding><pagination>1120-1134</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC11041871</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>4(4)</volume><pubmed_abstract>Combinations of immune checkpoint inhibitors (ICI, including anti-PD-1/PD-L1) and chemotherapy have been FDA approved for metastatic and early-stage triple-negative breast cancer (TNBC), but most patients do not benefit. B7-H4 is a B7 family ligand with proposed immunosuppressive functions being explored as a cancer immunotherapy target and may be associated with anti-PD-L1 resistance. However, little is known about its regulation and effect on immune cell function in breast cancers. We assessed murine and human breast cancer cells to identify regulation mechanisms of B7-H4 in vitro. We used an immunocompetent anti-PD-L1-sensitive orthotopic mammary cancer model and induced ectopic expression of B7-H4. We assessed therapy response and transcriptional changes at baseline and under treatment</pubmed_abstract><journal>Cancer research communications</journal><pubmed_title>Epithelial Expressed B7-H4 Drives Differential Immunotherapy Response in Murine and Human Breast Cancer.</pubmed_title><pmcid>PMC11041871</pmcid><funding_grant_id>5P30CA068485</funding_grant_id><funding_grant_id>P01 CA210961</funding_grant_id><funding_grant_id>BC170037</funding_grant_id><funding_grant_id>5P50CA098131</funding_grant_id><pubmed_authors>Hanna A</pubmed_authors><pubmed_authors>Bronzini J</pubmed_authors><pubmed_authors>Wulfkuhle J</pubmed_authors><pubmed_authors>Wescott EC</pubmed_authors><pubmed_authors>Taylor BC</pubmed_authors><pubmed_authors>Dees EC</pubmed_authors><pubmed_authors>Opalenik SR</pubmed_authors><pubmed_authors>Esserman LJ</pubmed_authors><pubmed_authors>Isaacs C</pubmed_authors><pubmed_authors>Sanchez V</pubmed_authors><pubmed_authors>Wilson JT</pubmed_authors><pubmed_authors>Ballinger TJ</pubmed_authors><pubmed_authors>Bharti V</pubmed_authors><pubmed_authors>Santa-Maria CA</pubmed_authors><pubmed_authors>Shah PD</pubmed_authors><pubmed_authors>Petricoin EF</pubmed_authors><pubmed_authors>Balko JM</pubmed_authors><pubmed_authors>van ˈt Veer LJ</pubmed_authors><pubmed_authors>Hirst GL</pubmed_authors><pubmed_authors>Brown Swigart L</pubmed_authors><pubmed_authors>Pietenpol JA</pubmed_authors><pubmed_authors>Lehmann BD</pubmed_authors><pubmed_authors>Sun X</pubmed_authors><pubmed_authors>Abramson VG</pubmed_authors><pubmed_authors>Sanders ME</pubmed_authors><pubmed_authors>Gallagher RI</pubmed_authors><pubmed_authors>Gomez H</pubmed_authors><pubmed_authors>Gonzalez-Ericsson P</pubmed_authors></additional><is_claimable>false</is_claimable><name>Epithelial Expressed B7-H4 Drives Differential Immunotherapy Response in Murine and Human Breast Cancer.</name><description>Combinations of immune checkpoint inhibitors (ICI, including anti-PD-1/PD-L1) and chemotherapy have been FDA approved for metastatic and early-stage triple-negative breast cancer (TNBC), but most patients do not benefit. B7-H4 is a B7 family ligand with proposed immunosuppressive functions being explored as a cancer immunotherapy target and may be associated with anti-PD-L1 resistance. However, little is known about its regulation and effect on immune cell function in breast cancers. We assessed murine and human breast cancer cells to identify regulation mechanisms of B7-H4 in vitro. We used an immunocompetent anti-PD-L1-sensitive orthotopic mammary cancer model and induced ectopic expression of B7-H4. We assessed therapy response and transcriptional changes at baseline and under treatment</description><dates><release>2024-01-01T00:00:00Z</release><publication>2024 Apr</publication><modification>2026-05-29T12:38:47.411Z</modification><creation>2026-04-08T04:47:55.508Z</creation></dates><accession>S-EPMC11041871</accession><cross_references><pubmed>38687247</pubmed><doi>10.1158/2767-9764.CRC-23-0468</doi></cross_references></HashMap>