<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>12(15)</volume><submitter>Wang C</submitter><pubmed_abstract>&lt;h4>Background&lt;/h4>Breast cancer (BC) is the leading cause of cancer-related death among women. One of the hallmarks of cancer is sustained angiogenesis. YAP/STAT3 may promote angiogenesis and driving BC progression. This study aimed to investigate how YAP/STAT3 affects the immune microenvironment in BC and understand the underlying mechanism.&lt;h4>Methods&lt;/h4>To establish a tumor-associated macrophages (TAMs) model, macrophages were cultured in the 4T1 cell culture medium. A BC mouse model was created by injecting 4T1 cells. The expression of YAP, STAT3, p-STAT3, VEGF, VEGFR-2, and PD-L1 was analyzed using immunofluorescence, western blotting, and quantitative real-time PCR. Flow cytometry was used to identify M1 and M2 macrophages, CD4&lt;sup>+&lt;/sup> T, CD8&lt;sup>+&lt;/sup> T, and Treg cells. Leve</pubmed_abstract><journal>Cancer medicine</journal><pagination>16295-16309</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC10469732</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>YAP/STAT3 inhibited CD8&lt;sup>+&lt;/sup> T cells activity in the breast cancer immune microenvironment by inducing M2 polarization of tumor-associated macrophages.</pubmed_title><pmcid>PMC10469732</pmcid><pubmed_authors>He S</pubmed_authors><pubmed_authors>Tan X</pubmed_authors><pubmed_authors>Wang C</pubmed_authors><pubmed_authors>Shen N</pubmed_authors><pubmed_authors>Guo Q</pubmed_authors></additional><is_claimable>false</is_claimable><name>YAP/STAT3 inhibited CD8&lt;sup>+&lt;/sup> T cells activity in the breast cancer immune microenvironment by inducing M2 polarization of tumor-associated macrophages.</name><description>&lt;h4>Background&lt;/h4>Breast cancer (BC) is the leading cause of cancer-related death among women. One of the hallmarks of cancer is sustained angiogenesis. YAP/STAT3 may promote angiogenesis and driving BC progression. This study aimed to investigate how YAP/STAT3 affects the immune microenvironment in BC and understand the underlying mechanism.&lt;h4>Methods&lt;/h4>To establish a tumor-associated macrophages (TAMs) model, macrophages were cultured in the 4T1 cell culture medium. A BC mouse model was created by injecting 4T1 cells. The expression of YAP, STAT3, p-STAT3, VEGF, VEGFR-2, and PD-L1 was analyzed using immunofluorescence, western blotting, and quantitative real-time PCR. Flow cytometry was used to identify M1 and M2 macrophages, CD4&lt;sup>+&lt;/sup> T, CD8&lt;sup>+&lt;/sup> T, and Treg cells. Leve</description><dates><release>2023-01-01T00:00:00Z</release><publication>2023 Aug</publication><modification>2025-04-19T20:04:26.175Z</modification><creation>2025-04-19T20:04:26.175Z</creation></dates><accession>S-EPMC10469732</accession><cross_references><pubmed>37329188</pubmed><doi>10.1002/cam4.6242</doi></cross_references></HashMap>