<HashMap><database>biostudies-literature</database><scores/><additional><submitter>You R</submitter><funding>BLRD VA</funding><funding>Intramural NIH HHS</funding><funding>NCRR NIH HHS</funding><funding>NIAID NIH HHS</funding><funding>NHLBI NIH HHS</funding><funding>NHGRI NIH HHS</funding><funding>NCI NIH HHS</funding><funding>VA</funding><funding>NIH</funding><funding>Cancer Prevention and Research Institute of Texas</funding><funding>CSRD VA</funding><pagination>645-657</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC6342490</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>6(6)</volume><pubmed_abstract>Somatic mutations can promote malignant transformation of airway epithelial cells and induce inflammatory responses directed against resultant tumors. Tumor-infiltrating T lymphocytes (TIL) in early-stage non-small cell lung cancer (NSCLC) secrete distinct proinflammatory cytokines, but the contribution of these TILs to tumor development and metastasis remains unknown. We show here that TILs in early-stage NSCLC are biased toward IL17A expression (Th17) when compared with adjacent tumor-free tissue, whereas Th17 cells are decreased in tumor infiltrating locoregional lymph nodes in advanced NSCLC. Mice in which &lt;i>Pten&lt;/i> and &lt;i>Smad4&lt;/i> (&lt;i>Pts4&lt;sup>d/d&lt;/sup>&lt;/i> ) are deleted from airway epithelial cells develop spontaneous tumors, that share genetic signatures with squamous- (SQ.2b), a</pubmed_abstract><journal>Cancer immunology research</journal><pubmed_title>IL17A Regulates Tumor Latency and Metastasis in Lung Adeno and Squamous SQ.2b and AD.1 Cancer.</pubmed_title><pmcid>PMC6342490</pmcid><funding_grant_id>BX002221</funding_grant_id><funding_grant_id>CA125123</funding_grant_id><funding_grant_id>AI036211, CA125123, and RR024574</funding_grant_id><funding_grant_id>R01HL117181-01</funding_grant_id><funding_grant_id>I01 CX000104</funding_grant_id><funding_grant_id>UM1HG006348</funding_grant_id><funding_grant_id>CX000104</funding_grant_id><funding_grant_id>R01 HL110883</funding_grant_id><funding_grant_id>P30 CA125123</funding_grant_id><funding_grant_id>RP120713</funding_grant_id><funding_grant_id>P30 AI036211</funding_grant_id><funding_grant_id>UM1 HG006348</funding_grant_id><funding_grant_id>ZIA ES103311</funding_grant_id><funding_grant_id>I01 BX002221</funding_grant_id><funding_grant_id>R01 HL117181</funding_grant_id><funding_grant_id>S10 RR024574</funding_grant_id><funding_grant_id>R01 AI125264</funding_grant_id><pubmed_authors>Liu J</pubmed_authors><pubmed_authors>Perusich S</pubmed_authors><pubmed_authors>Lu W</pubmed_authors><pubmed_authors>Casal RF</pubmed_authors><pubmed_authors>Paust S</pubmed_authors><pubmed_authors>Cornwell L</pubmed_authors><pubmed_authors>You R</pubmed_authors><pubmed_authors>Burt BM</pubmed_authors><pubmed_authors>Creighton CJ</pubmed_authors><pubmed_authors>Hill-McAlester A</pubmed_authors><pubmed_authors>Kim M</pubmed_authors><pubmed_authors>Rosen D</pubmed_authors><pubmed_authors>Lazarus DR</pubmed_authors><pubmed_authors>Kheradmand F</pubmed_authors><pubmed_authors>Cho SN</pubmed_authors><pubmed_authors>Song LZ</pubmed_authors><pubmed_authors>Corry D</pubmed_authors><pubmed_authors>Tung HY</pubmed_authors><pubmed_authors>Yuan X</pubmed_authors><pubmed_authors>DeMayo FJ</pubmed_authors><pubmed_authors>Diehl G</pubmed_authors></additional><is_claimable>false</is_claimable><name>IL17A Regulates Tumor Latency and Metastasis in Lung Adeno and Squamous SQ.2b and AD.1 Cancer.</name><description>Somatic mutations can promote malignant transformation of airway epithelial cells and induce inflammatory responses directed against resultant tumors. Tumor-infiltrating T lymphocytes (TIL) in early-stage non-small cell lung cancer (NSCLC) secrete distinct proinflammatory cytokines, but the contribution of these TILs to tumor development and metastasis remains unknown. We show here that TILs in early-stage NSCLC are biased toward IL17A expression (Th17) when compared with adjacent tumor-free tissue, whereas Th17 cells are decreased in tumor infiltrating locoregional lymph nodes in advanced NSCLC. Mice in which &lt;i>Pten&lt;/i> and &lt;i>Smad4&lt;/i> (&lt;i>Pts4&lt;sup>d/d&lt;/sup>&lt;/i> ) are deleted from airway epithelial cells develop spontaneous tumors, that share genetic signatures with squamous- (SQ.2b), a</description><dates><release>2018-01-01T00:00:00Z</release><publication>2018 Jun</publication><modification>2026-04-15T13:05:11.699Z</modification><creation>2019-03-26T22:39:12Z</creation></dates><accession>S-EPMC6342490</accession><cross_references><pubmed>29653981</pubmed><doi>10.1158/2326-6066.cir-17-0554</doi><doi>10.1158/2326-6066.CIR-17-0554</doi></cross_references></HashMap>