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The PI3K/Akt Pathway in Tumors of Endocrine Tissues

The phosphatidylinositol 3-kinase (PI3K)/Akt pathway is a key driver in carcinogenesis. Defects in this pathway in human cancer syndromes such as Cowden’s disease and Multiple Endocrine Neoplasia result in tumors of endocrine tissues, highlighting its importance in these cancer types. This review ex...

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Autores principales: Robbins, Helen Louise, Hague, Angela
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4707207/
https://www.ncbi.nlm.nih.gov/pubmed/26793165
http://dx.doi.org/10.3389/fendo.2015.00188
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author Robbins, Helen Louise
Hague, Angela
author_facet Robbins, Helen Louise
Hague, Angela
author_sort Robbins, Helen Louise
collection PubMed
description The phosphatidylinositol 3-kinase (PI3K)/Akt pathway is a key driver in carcinogenesis. Defects in this pathway in human cancer syndromes such as Cowden’s disease and Multiple Endocrine Neoplasia result in tumors of endocrine tissues, highlighting its importance in these cancer types. This review explores the growing evidence from multiple animal and in vitro models and from analysis of human tumors for the involvement of this pathway in the following: thyroid carcinoma subtypes, parathyroid carcinoma, pituitary tumors, adrenocortical carcinoma, phaeochromocytoma, neuroblastoma, and gastroenteropancreatic neuroendocrine tumors. While data are not always consistent, immunohistochemistry performed on human tumor tissue has been used alongside other techniques to demonstrate Akt overactivation. We review active Akt as a potential prognostic marker and the PI3K pathway as a therapeutic target in endocrine neoplasia.
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spelling pubmed-47072072016-01-20 The PI3K/Akt Pathway in Tumors of Endocrine Tissues Robbins, Helen Louise Hague, Angela Front Endocrinol (Lausanne) Endocrinology The phosphatidylinositol 3-kinase (PI3K)/Akt pathway is a key driver in carcinogenesis. Defects in this pathway in human cancer syndromes such as Cowden’s disease and Multiple Endocrine Neoplasia result in tumors of endocrine tissues, highlighting its importance in these cancer types. This review explores the growing evidence from multiple animal and in vitro models and from analysis of human tumors for the involvement of this pathway in the following: thyroid carcinoma subtypes, parathyroid carcinoma, pituitary tumors, adrenocortical carcinoma, phaeochromocytoma, neuroblastoma, and gastroenteropancreatic neuroendocrine tumors. While data are not always consistent, immunohistochemistry performed on human tumor tissue has been used alongside other techniques to demonstrate Akt overactivation. We review active Akt as a potential prognostic marker and the PI3K pathway as a therapeutic target in endocrine neoplasia. Frontiers Media S.A. 2016-01-11 /pmc/articles/PMC4707207/ /pubmed/26793165 http://dx.doi.org/10.3389/fendo.2015.00188 Text en Copyright © 2016 Robbins and Hague. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Endocrinology
Robbins, Helen Louise
Hague, Angela
The PI3K/Akt Pathway in Tumors of Endocrine Tissues
title The PI3K/Akt Pathway in Tumors of Endocrine Tissues
title_full The PI3K/Akt Pathway in Tumors of Endocrine Tissues
title_fullStr The PI3K/Akt Pathway in Tumors of Endocrine Tissues
title_full_unstemmed The PI3K/Akt Pathway in Tumors of Endocrine Tissues
title_short The PI3K/Akt Pathway in Tumors of Endocrine Tissues
title_sort pi3k/akt pathway in tumors of endocrine tissues
topic Endocrinology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4707207/
https://www.ncbi.nlm.nih.gov/pubmed/26793165
http://dx.doi.org/10.3389/fendo.2015.00188
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