{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Gil J"],"funding":["Instituto de Salud Carlos III","Novartis (Spain)"],"pagination":["460"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8962441"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["10(2)"],"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 "],"journal":["Biomedicines"],"pubmed_title":["Implications of Heterogeneity of Epithelial-Mesenchymal States in Acromegaly Therapeutic Pharmacologic Response."],"pmcid":["PMC8962441"],"funding_grant_id":["REMAH","PMP 15/00027"],"pubmed_authors":["Rodriguez-Lloveras H","Lamas C","Hostalot C","Marazuela M","Bernabeu I","Camara R","Webb SM","Fajardo-Montanana C","Serra G","Gil J","Valassi E","Puig-Domingo M","Salinas I","Biagetti B","Carrato C","Marques-Pamies M","Jorda M","Simo-Servat A","Garcia-Martinez A","Pico A"],"additional_accession":[]},"is_claimable":false,"name":"Implications of Heterogeneity of Epithelial-Mesenchymal States in Acromegaly Therapeutic Pharmacologic Response.","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 ","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Feb","modification":"2026-04-08T17:37:26.243Z","creation":"2025-02-19T03:59:04.024Z"},"accession":"S-EPMC8962441","cross_references":{"pubmed":["35203668"],"doi":["10.3390/biomedicines10020460"]}}