ECE2015 Guided Posters Pituitary–Basic and IGF-1 (9 abstracts)
Molecular classification of pituitary adenomas
Antonio Picó 1 , Laura Sanchez-Tejada 5 , Ruth Sanchez-Ortiga 1 , Rosa Cámara 4 , Cristina Lamas 2 , Javier Abarca 6 , Irene Monjas 7 , Pedro Riesgo 8 & Carmen Fajardo 3
1Endocrinology Department, Hospital General Universitario Alicante, Alicante, Spain; 2Endocrinology Department, Hospital General Universitario Albacete, Albacete, Spain; 3Endocrinology Department, Hospital La Ribera, Alzira, Spain; 4Endocrinology Department, Hospital Universitario La Fe, Valencia, Spain; 5Research Unit, Hospital General Universitario Alicante, Alicante, Spain; 6Neurosurgery Department, Hospital General Universitario Alicante, Alicante, Spain; 7Otorhinolaryngology Department, Hospital General Universitario Alicante, Alicante, Spain; 8Neurosurgery Department, Hospital La Ribera, Alzira, Spain.
Purpose: The 2004 edition of the WHO text ‘Histological typing of endocrine tumors’ classified pituitary adenomas (PA) on the basis of their histological and immunohistochemical characteristics. Recent advances on the knowledge of the molecular patterns of these tumours may allow establishing a molecular classification with higher accuracy and specificity than previous one.
Methods: Within the pale of the multicenter Spanish Molecular Registry of Pituitary Adenomas (REMAH), a multicentre clinical-basic project, we had obtained the molecular phenotype of 172 PA. Expression levels of 26 genes were measured by qRT-PCR, including all pituitary hormones, receptors for somatostatin, dopamine, and others: GH-releasing hormone receptor, gonadotropin-releasing hormone receptor, type 1 corticotropin-releasing hormone receptor, arginine vasopressin receptor 1b and type 1 ghrelin receptor, and three housekeeping genes for normalization. Nine healthy pituitary from autopsies were used as calibrator reference.
Results: Based on the established clinical diagnosis (functioning PA (FPA: somatotroph, corticotroph, tirotroph, and lactotroph adenomas) and non-functioning PA (NFPA)) and immunohistochemical data, we have defined ranges of expression for all hormones and receptors with 25th and 75th percentiles for each subtype. NFPA and FPA presenting expression of several hormonal genes were subclassified depending on the dominant expression, establishing as ‘gold standard’ the p25 expression in the complete sample. On the basis of our study we have been able to define the following molecular classification: somatotroph (pure, mixed, and plurihormonal), functioning corticotroph, tirotroph, lactotroph, gonadotroph (FSHoma, LHoma, and mixed), null cell, and silent corticotroph adenomas with higher accuracy than the immunohistochemical previous classification.
Conclusion: Advances in the molecular knowledge of the pathogenesis of PA may allow a more specific classification of PA, especially in the case of NFPA, helping physicians to better manage these patients.
Disclosure: This work was supported by SEEN (Novartis–REMAH).
Volume 37
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Endocrine Abstracts
ISSN 1470-3947 (print) | ISSN 1479-6848 (online)
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