<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Gil J</submitter><funding>Instituto de Salud Carlos III</funding><funding>Novartis (Spain)</funding><pagination>460</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC8962441</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>10(2)</volume><pubmed_abstract>Acromegaly is caused by excess growth hormone (GH) produced by a pituitary tumor. First-generation somatostatin receptor ligands (SRLs) are the first-line treatment. Several studies have linked E-cadherin loss and epithelial-mesenchymal transition (EMT) with resistance to SRLs. Our aim was to study EMT and its relationship with SRLs resistance in GH-producing tumors. We analyzed the expression of EMT-related genes by RT-qPCR in 57 tumors. The postsurgical response to SRLs was categorized as complete response, partial response, or nonresponse if IGF-1 was normal, had decreased more than 30% without normalization, or neither of those, respectively. Most tumors showed a hybrid and variable EMT expression profile not specifically associated with SRL response instead of a defined epithelial or </pubmed_abstract><journal>Biomedicines</journal><pubmed_title>Implications of Heterogeneity of Epithelial-Mesenchymal States in Acromegaly Therapeutic Pharmacologic Response.</pubmed_title><pmcid>PMC8962441</pmcid><funding_grant_id>REMAH</funding_grant_id><funding_grant_id>PMP 15/00027</funding_grant_id><pubmed_authors>Rodriguez-Lloveras H</pubmed_authors><pubmed_authors>Lamas C</pubmed_authors><pubmed_authors>Hostalot C</pubmed_authors><pubmed_authors>Marazuela M</pubmed_authors><pubmed_authors>Bernabeu I</pubmed_authors><pubmed_authors>Camara R</pubmed_authors><pubmed_authors>Webb SM</pubmed_authors><pubmed_authors>Fajardo-Montanana C</pubmed_authors><pubmed_authors>Serra G</pubmed_authors><pubmed_authors>Gil J</pubmed_authors><pubmed_authors>Valassi E</pubmed_authors><pubmed_authors>Puig-Domingo M</pubmed_authors><pubmed_authors>Salinas I</pubmed_authors><pubmed_authors>Biagetti B</pubmed_authors><pubmed_authors>Carrato C</pubmed_authors><pubmed_authors>Marques-Pamies M</pubmed_authors><pubmed_authors>Jorda M</pubmed_authors><pubmed_authors>Simo-Servat A</pubmed_authors><pubmed_authors>Garcia-Martinez A</pubmed_authors><pubmed_authors>Pico A</pubmed_authors></additional><is_claimable>false</is_claimable><name>Implications of Heterogeneity of Epithelial-Mesenchymal States in Acromegaly Therapeutic Pharmacologic Response.</name><description>Acromegaly is caused by excess growth hormone (GH) produced by a pituitary tumor. First-generation somatostatin receptor ligands (SRLs) are the first-line treatment. Several studies have linked E-cadherin loss and epithelial-mesenchymal transition (EMT) with resistance to SRLs. Our aim was to study EMT and its relationship with SRLs resistance in GH-producing tumors. We analyzed the expression of EMT-related genes by RT-qPCR in 57 tumors. The postsurgical response to SRLs was categorized as complete response, partial response, or nonresponse if IGF-1 was normal, had decreased more than 30% without normalization, or neither of those, respectively. Most tumors showed a hybrid and variable EMT expression profile not specifically associated with SRL response instead of a defined epithelial or </description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Feb</publication><modification>2026-04-08T17:37:26.243Z</modification><creation>2025-02-19T03:59:04.024Z</creation></dates><accession>S-EPMC8962441</accession><cross_references><pubmed>35203668</pubmed><doi>10.3390/biomedicines10020460</doi></cross_references></HashMap>