<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Kawai H</submitter><funding>Japan Society for the Promotion of Science</funding><pagination>343-354</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC11876232</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>486(2)</volume><pubmed_abstract>&lt;h4>Introduction&lt;/h4>HNF4α expression and SMARCA4 loss were thought to be features of non-terminal respiratory unit (TRU)-type lung adenocarcinomas, but their relationships remained unclear.&lt;h4>Materials and methods&lt;/h4>HNF4α-positive cases among 241 lung adenocarcinomas were stratified based on TTF-1 and SMARCA4 expressions, histological subtypes, and driver mutations. Immunohistochemical analysis was performed using xenograft tumors of lung adenocarcinoma cell lines with high HNF4A expression.&lt;h4>Result&lt;/h4>HNF4α-positive adenocarcinomas(n = 33) were divided into two groups: the variant group(15 mucinous, 2 enteric, and 1 colloid), where SMARCA4 was retained in all cases, and the conventional non-mucinous group(6 papillary, 5 solid, and 4 acinar), where SMARCA4 was lost in 3/15 cases(20%</pubmed_abstract><journal>Virchows Archiv : an international journal of pathology</journal><pubmed_title>Expression patterns of HNF4α, TTF-1, and SMARCA4 in lung adenocarcinomas: impacts on clinicopathological and genetic features.</pubmed_title><pmcid>PMC11876232</pmcid><funding_grant_id>22H02840</funding_grant_id><funding_grant_id>19K07441</funding_grant_id><funding_grant_id>23K14469</funding_grant_id><funding_grant_id>18H02634</funding_grant_id><funding_grant_id>23K06470</funding_grant_id><funding_grant_id>17K15652</funding_grant_id><pubmed_authors>Ishikawa S</pubmed_authors><pubmed_authors>Kawai H</pubmed_authors><pubmed_authors>Hagiwara K</pubmed_authors><pubmed_authors>Shiba-Ishii A</pubmed_authors><pubmed_authors>Kawamatsu N</pubmed_authors><pubmed_authors>Fujita K</pubmed_authors><pubmed_authors>Kihara A</pubmed_authors><pubmed_authors>Miura T</pubmed_authors><pubmed_authors>Amano Y</pubmed_authors><pubmed_authors>Matsubara D</pubmed_authors><pubmed_authors>Fukayama M</pubmed_authors><pubmed_authors>Shibano T</pubmed_authors><pubmed_authors>Tsubochi H</pubmed_authors><pubmed_authors>Nakagawa T</pubmed_authors><pubmed_authors>Yoshimoto T</pubmed_authors><pubmed_authors>Endo S</pubmed_authors><pubmed_authors>Sakuma Y</pubmed_authors><pubmed_authors>Niki T</pubmed_authors><pubmed_authors>Ushiku T</pubmed_authors></additional><is_claimable>false</is_claimable><name>Expression patterns of HNF4α, TTF-1, and SMARCA4 in lung adenocarcinomas: impacts on clinicopathological and genetic features.</name><description>&lt;h4>Introduction&lt;/h4>HNF4α expression and SMARCA4 loss were thought to be features of non-terminal respiratory unit (TRU)-type lung adenocarcinomas, but their relationships remained unclear.&lt;h4>Materials and methods&lt;/h4>HNF4α-positive cases among 241 lung adenocarcinomas were stratified based on TTF-1 and SMARCA4 expressions, histological subtypes, and driver mutations. Immunohistochemical analysis was performed using xenograft tumors of lung adenocarcinoma cell lines with high HNF4A expression.&lt;h4>Result&lt;/h4>HNF4α-positive adenocarcinomas(n = 33) were divided into two groups: the variant group(15 mucinous, 2 enteric, and 1 colloid), where SMARCA4 was retained in all cases, and the conventional non-mucinous group(6 papillary, 5 solid, and 4 acinar), where SMARCA4 was lost in 3/15 cases(20%</description><dates><release>2025-01-01T00:00:00Z</release><publication>2025 Feb</publication><modification>2025-04-04T09:10:07.179Z</modification><creation>2025-04-04T09:10:07.179Z</creation></dates><accession>S-EPMC11876232</accession><cross_references><pubmed>38710944</pubmed><doi>10.1007/s00428-024-03816-6</doi></cross_references></HashMap>