Genetic and Epigenetic Causes of Pituitary Adenomas
Pituitary adenomas (PAs) can be classified as non-secreting adenomas, somatotroph adenomas, corticotroph adenomas, lactotroph adenomas, and thyrotroph adenomas. Substantial advances have been made in our knowledge of the pathobiology of PAs. To obtain a comprehensive understanding of the molecular b...
Main Authors: | , , , |
---|---|
Format: | Article |
Language: | English |
Published: |
Frontiers Media S.A.
2021-01-01
|
Series: | Frontiers in Endocrinology |
Subjects: | |
Online Access: | https://www.frontiersin.org/articles/10.3389/fendo.2020.596554/full |
id |
doaj-55284d03dbb94d76af7c8c08e08ce7ba |
---|---|
record_format |
Article |
spelling |
doaj-55284d03dbb94d76af7c8c08e08ce7ba2021-01-26T07:22:17ZengFrontiers Media S.A.Frontiers in Endocrinology1664-23922021-01-011110.3389/fendo.2020.596554596554Genetic and Epigenetic Causes of Pituitary AdenomasMengqi ChangChengxian YangXinjie BaoRenzhi WangPituitary adenomas (PAs) can be classified as non-secreting adenomas, somatotroph adenomas, corticotroph adenomas, lactotroph adenomas, and thyrotroph adenomas. Substantial advances have been made in our knowledge of the pathobiology of PAs. To obtain a comprehensive understanding of the molecular biological characteristics of different types of PAs, we reviewed the important advances that have been made involving genetic and epigenetic variation, comprising genetic mutations, chromosome number variations, DNA methylation, microRNA regulation, and transcription factor regulation. Classical tumor predisposition syndromes include multiple endocrine neoplasia type 1 (MEN1) and type 4 (MEN4) syndromes, Carney complex, and X-LAG syndromes. PAs have also been described in association with succinate dehydrogenase-related familial PA, neurofibromatosis type 1, and von Hippel–Lindau, DICER1, and Lynch syndromes. Patients with aryl hydrocarbon receptor-interacting protein (AIP) mutations often present with pituitary gigantism, either in familial or sporadic adenomas. In contrast, guanine nucleotide-binding protein G(s) subunit alpha (GNAS) and G protein-coupled receptor 101 (GPR101) mutations can lead to excess growth hormone. Moreover, the deubiquitinase gene USP8, USP48, and BRAF mutations are associated with adrenocorticotropic hormone production. In this review, we describe the genetic and epigenetic landscape of PAs and summarize novel insights into the regulation of pituitary tumorigenesis.https://www.frontiersin.org/articles/10.3389/fendo.2020.596554/fullpituitary adenomasmolecular markersacromegalyCushing’s diseasenon-secreting adenomas |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Mengqi Chang Chengxian Yang Xinjie Bao Renzhi Wang |
spellingShingle |
Mengqi Chang Chengxian Yang Xinjie Bao Renzhi Wang Genetic and Epigenetic Causes of Pituitary Adenomas Frontiers in Endocrinology pituitary adenomas molecular markers acromegaly Cushing’s disease non-secreting adenomas |
author_facet |
Mengqi Chang Chengxian Yang Xinjie Bao Renzhi Wang |
author_sort |
Mengqi Chang |
title |
Genetic and Epigenetic Causes of Pituitary Adenomas |
title_short |
Genetic and Epigenetic Causes of Pituitary Adenomas |
title_full |
Genetic and Epigenetic Causes of Pituitary Adenomas |
title_fullStr |
Genetic and Epigenetic Causes of Pituitary Adenomas |
title_full_unstemmed |
Genetic and Epigenetic Causes of Pituitary Adenomas |
title_sort |
genetic and epigenetic causes of pituitary adenomas |
publisher |
Frontiers Media S.A. |
series |
Frontiers in Endocrinology |
issn |
1664-2392 |
publishDate |
2021-01-01 |
description |
Pituitary adenomas (PAs) can be classified as non-secreting adenomas, somatotroph adenomas, corticotroph adenomas, lactotroph adenomas, and thyrotroph adenomas. Substantial advances have been made in our knowledge of the pathobiology of PAs. To obtain a comprehensive understanding of the molecular biological characteristics of different types of PAs, we reviewed the important advances that have been made involving genetic and epigenetic variation, comprising genetic mutations, chromosome number variations, DNA methylation, microRNA regulation, and transcription factor regulation. Classical tumor predisposition syndromes include multiple endocrine neoplasia type 1 (MEN1) and type 4 (MEN4) syndromes, Carney complex, and X-LAG syndromes. PAs have also been described in association with succinate dehydrogenase-related familial PA, neurofibromatosis type 1, and von Hippel–Lindau, DICER1, and Lynch syndromes. Patients with aryl hydrocarbon receptor-interacting protein (AIP) mutations often present with pituitary gigantism, either in familial or sporadic adenomas. In contrast, guanine nucleotide-binding protein G(s) subunit alpha (GNAS) and G protein-coupled receptor 101 (GPR101) mutations can lead to excess growth hormone. Moreover, the deubiquitinase gene USP8, USP48, and BRAF mutations are associated with adrenocorticotropic hormone production. In this review, we describe the genetic and epigenetic landscape of PAs and summarize novel insights into the regulation of pituitary tumorigenesis. |
topic |
pituitary adenomas molecular markers acromegaly Cushing’s disease non-secreting adenomas |
url |
https://www.frontiersin.org/articles/10.3389/fendo.2020.596554/full |
work_keys_str_mv |
AT mengqichang geneticandepigeneticcausesofpituitaryadenomas AT chengxianyang geneticandepigeneticcausesofpituitaryadenomas AT xinjiebao geneticandepigeneticcausesofpituitaryadenomas AT renzhiwang geneticandepigeneticcausesofpituitaryadenomas |
_version_ |
1724323337986899968 |