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p27 variant and corticotropinoma susceptibility: a genetic and in vitro study. | LitMetric

p27 variant and corticotropinoma susceptibility: a genetic and in vitro study.

Endocr Relat Cancer

Endocrine Genetics Unit LIM-25 Neuroendocrinology Unit Adrenal Unit (LIM-42) Experimental Oncology Laboratory (LIM-24), School of Medicine, Hospital das Clinicas, University of Sao Paulo, Sao Paulo, Brazil Nursing School School of Public Health, University of Sao Paulo, Sao Paulo, Brazil Endocrinology Division, Santa Casa Hospital, Sao Paulo, Brazil Brigadeiro Hospital, Sao Paulo, Brazil Federal University of Sao Paulo, Sao Paulo, Brazil Human Genome Research Center Department of Cell and Developmental Biology, Institute of Biomedical Sciences, University of São Paulo, Sao Paulo, Brazil Instituto do Cérebro, Instituto Israelita de Ensino e Pesquisa Albert Einstein, Sao Paulo, Brazil National Institute of Aging, National Institutes of Health (NIH), Bethesda, Maryland, USA Institute of Pathology, Helmholtz Zentrum München, Neuherberg, Germany.

Published: June 2014

AI Article Synopsis

  • Germline mutations in the p27(kip1) gene increase the risk of multiple endocrine neoplasias (MEN) in both rats and humans, but the impact of common genetic variations like p27-V109G is still unclear.
  • A study of Brazilian patients with various endocrine tumors found a significant association of the p27-V109G polymorphism with pituitary adenomas, especially those secreting ACTH, but not with GH-secreting tumors or MEN2.
  • Laboratory tests showed that cells with the p27-V109G variant had higher growth rates, indicating a potential link to tumor development, but results were inconsistent across different cell types.

Article Abstract

Germline mutations in p27(kip1) are associated with increased susceptibility to multiple endocrine neoplasias (MEN) both in rats and humans; however, the potential role of common polymorphisms of this gene in endocrine tumor susceptibility and tumorigenesis remains mostly unrecognized. To assess the risk associated with polymorphism rs2066827 (p27-V109G), we genotyped a large cohort of Brazilian patients with sporadic endocrine tumors (pituitary adenomas, n=252; pheochromocytomas, n=125; medullary thyroid carcinoma, n=51; and parathyroid adenomas, n=19) and 885 population-matched healthy controls and determined the odds ratios and 95% CIs. Significant associations were found for the group of patients with pituitary adenomas (P=0.01), particularly for those with ACTH-secreting pituitary adenomas (P=0.005). In contrast, no association was found with GH-secreting pituitary tumors alone or with the sporadic counterpart of MEN2-component neoplasias. Our in vitro analyses revealed increased colony formation and cell growth rate for an AtT20 corticotropin mouse cell line overexpressing the p27-V109G variant compared with cells transfected with the WT p27. However, the genotypic effects in genetic and in vitro approaches were divergent. In accordance with our genetic data showing specificity for ACTH-secreting pituitary tissues, the overexpression of p27-V109G in a GH3 somatotropin rat cell line resulted in no difference compared with the WT. Pituitary tumors are one of the major clinical components of syndromes associated with the p27 pathogenic mutations MENX and MEN4. Our genetic and in vitro data indicate that the common polymorphism rs2066827 may play a role in corticotropinoma susceptibility and tumorigenesis through a molecular mechanism not fully understood thus far.

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Source
http://dx.doi.org/10.1530/ERC-13-0486DOI Listing

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