<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Wang J</submitter><funding>S&amp;T program of Hebei</funding><funding>Clinical Research and Innovation Team Support Program of Hebei Medical University</funding><funding>Medical Science Research Project of Hebei</funding><funding>S&amp;amp;T program of Hebei</funding><pagination>141</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC12063428</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>44(1)</volume><pubmed_abstract>&lt;h4>Background&lt;/h4>Tumors often evade immune surveillance by limiting T cell infiltration. In non-small cell lung cancer (NSCLC), increased infiltration of CD8&lt;sup>+&lt;/sup> T cells is associated with a favorable response to immunotherapy. While BIN1 is recognized as a tumor suppressor gene, its role in shaping the tumor microenvironment in NSCLC has yet to be fully clarified.&lt;h4>Methods&lt;/h4>To investigate the relationship between BIN1 expression and CD8&lt;sup>+&lt;/sup>T cell infiltration in NSCLC, we performed a comprehensive data analysis utilizing clinical information from NSCLC patients. BIN1 expression levels in NSCLC tissues were evaluated, and their correlation with CD8&lt;sup>+&lt;/sup>T cells infiltration and patient survival outcomes was examined. Loss-of-function strategies targeting BIN1 w</pubmed_abstract><journal>Journal of experimental &amp; clinical cancer research : CR</journal><pubmed_title>Tumor cell-intrinsic BIN1 deficiency promotes the immunosuppression and impedes ferroptosis of non-small cell lung cancer via G3BP1-mediated degradation of STAT1.</pubmed_title><pmcid>PMC12063428</pmcid><funding_grant_id>20210168</funding_grant_id><funding_grant_id>2022LCTD-A11</funding_grant_id><funding_grant_id>H2024206222</funding_grant_id><pubmed_authors>Liu X</pubmed_authors><pubmed_authors>Liu L</pubmed_authors><pubmed_authors>Chen J</pubmed_authors><pubmed_authors>Yin S</pubmed_authors><pubmed_authors>Zhang Y</pubmed_authors><pubmed_authors>Jia Y</pubmed_authors><pubmed_authors>Liu T</pubmed_authors><pubmed_authors>Xu X</pubmed_authors><pubmed_authors>Wang J</pubmed_authors></additional><is_claimable>false</is_claimable><name>Tumor cell-intrinsic BIN1 deficiency promotes the immunosuppression and impedes ferroptosis of non-small cell lung cancer via G3BP1-mediated degradation of STAT1.</name><description>&lt;h4>Background&lt;/h4>Tumors often evade immune surveillance by limiting T cell infiltration. In non-small cell lung cancer (NSCLC), increased infiltration of CD8&lt;sup>+&lt;/sup> T cells is associated with a favorable response to immunotherapy. While BIN1 is recognized as a tumor suppressor gene, its role in shaping the tumor microenvironment in NSCLC has yet to be fully clarified.&lt;h4>Methods&lt;/h4>To investigate the relationship between BIN1 expression and CD8&lt;sup>+&lt;/sup>T cell infiltration in NSCLC, we performed a comprehensive data analysis utilizing clinical information from NSCLC patients. BIN1 expression levels in NSCLC tissues were evaluated, and their correlation with CD8&lt;sup>+&lt;/sup>T cells infiltration and patient survival outcomes was examined. Loss-of-function strategies targeting BIN1 w</description><dates><release>2025-01-01T00:00:00Z</release><publication>2025 May</publication><modification>2026-06-02T13:12:00.814Z</modification><creation>2026-04-18T03:11:30.898Z</creation></dates><accession>S-EPMC12063428</accession><cross_references><pubmed>40346580</pubmed><doi>10.1186/s13046-025-03404-9</doi></cross_references></HashMap>