ECE2020 Audio ePoster Presentations Pituitary and Neuroendocrinology (217 abstracts)
Characterization of epithelial-mesenchymal transition in growth hormone-secreting adenomas
Joan Gil 1 , Montserrat Marques-Pamies 2 , Araceli García-Martínez 3 , Guillermo Serra 4 , Susan Webb 5 , Miguel Antonio Sampedro-Nunez 6 , Antonio Pico 3 , Monica Marazuela 6 , Mireia Jorda 1 & Manel Puig-Domingo 1,2
1Germans Trias i Pujol Research Institute, Endocrinology and Nutrition, Badalona, Spain; 2Germans Trias i Pujol University Hospital, Endocrinology and Nutrition, Badalona, Spain; 3Hospital General Universitario de Alicante-Institute for Health and Biomedical Research (ISABIAL), Alicante (Alacant), Spain; 4Son Espases University Hospital, Departament of Endocrinology, Palma, Spain; 5CIBERER U747, ISCIII, Research Center for Pituitary Diseases, Hospital Sant Pau, IIB-SPau, Universitat Autònoma de Barcelona, Department of Endocrinology/Medicine, Barcelona, Spain; 6Hospital de La Princesa, Departament of Endocrinology, Madrid, Spain
First generation somatostatin receptor ligands (SRL) are the first-line drugs in primary acromegaly treatment or after surgical failure in patients with active acromegaly. In previous studies we confirmed the association of the expression of SSTR2, Ki67 and E-cadherin (CDH1) in responsive GH-secreting adenomas response to SRL. Moreover, E-cadherin showed a greater predictive capacity than most of the markers described. Loss of E-cadherin is a typical mark of epithelial-mesenchymal transition (EMT) in solid tumors. Then, the objective of the subsequent work was to study the association of the EMT with the somatotropinomas response to SRL. We analyzed the expression of 8 genes related to EMT (CDH1, CDH2, SNAI1, SNAI2, ESRP1, RORC, VIM and TWIST) and other SRL response genes such as SSTR2 and Ki-67 in 57 somatotropinomas (80% treated with SRL before surgery), using RT-qPCR. The results showed an expression pattern compatible with a EMT in 14% of tumors. When a cluster analysis was performed, epithelial markers (CDH1, RORC, ESRP1) clustered with SSTR2 on one hand, and mesenchymal markers (CDH2, SNAI1, SNAI2, VIM, TWIST) with Ki-67. However, no clusterization of the tumors depending SRL response was found. The values of CDH2 and RORC were higher in patients treated with SRL before surgery (F.C. = 3.14, P = 0.02, and F.C. = 2.39, P < 0.01, respectively). SNAI1 and RORC showed differences, the latter only in SRL pretreated patients, between responding patients and resistant to SRL (HR = 2.03, P = 0.05 and HR = 0.59, P = 0.01, respectively). In addition, RORC levels correlated with the percentage decrease in IGF-1 after therapy with SRL (Pearson r = 0.40, P = 0.03).
Therefore, we conclude thatEMT occurs in some somatotropinomas, but it does not seem to explain their response to SRL in this subset of tumors. However, in the rest of somatotropinoma SNAI1 and RORC may predict the response to SRL treatment.
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Endocrine Abstracts
ISSN 1470-3947 (print) | ISSN 1479-6848 (online)
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