ECE2020 Oral Communications Adrenal and Cardiovascular Endocrinology (7 abstracts)
Comparative proteomic analysis of different bilateral adrenocortical hyperplasia
Annabel Berthon 1,2 , Stephanie Cologna 3 , Paul Blank 2 , Fady Hannah-Shmouni 2 , Jerome Bertherat 1 , Forbes Porter 2 & Constantine Stratakis 2
1Institut Cochin , Endocrinology, Metabolism and Diabetes, Paris, France; 2National Institutes of Health, National Institute of Child Health and Development, Bethesda, United States; 3University of Illinois at Chicago, Chicago, United States
Bilateral Adrenal Hyperplasias (BAH) are responsible for approximately 10% of ACTH-independent Cushing syndrome and are classified as either micronodular or macronodular. Whereas Primary Pigmented Nodular Adrenocortical Disease (PPNAD) and isolated Micronodular Adrenal Disease (iMAD) are two types of micronodular hyperplasia, Primary Macronodular Adrenal Hyperplasia (PMAH) is a macronodular BAH. These tumors are classified differently based on clinical, histological and genetic features but they all share a dysregulation of the cyclic AMP/protein kinase (PKA) pathway, a molecular signaling system that is essential for the synthesis and secretion of glucocorticoids. We investigated the molecular differences between the various types of BAHs using a proteomic approach on normal tissue, iMAD, PPNAD and PMAH. In total, we identified 37 proteins differentially expressed between these diagnostic groups. Most of these proteins are involved in metabolism and mitochondrial function, which is consistent with prior transcriptomic data as well as the secretory status of BAH. We are currently comparing all “-omics” for consistency and/or important differences. Interestingly, each BAH (iMAD, PPNAD and PMAH) has its own proteomic signature and can be separated by primary component analysis highlighting differences in molecular pathways. We propose that the 37 proteins identified here may provide new clues for the formation of these neoplasms, how they link to the PKA pathway, and importantly assist in their clinical diagnosis.
Volume 70
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Endocrine Abstracts
ISSN 1470-3947 (print) | ISSN 1479-6848 (online)
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