Alterations of DNA methylation in parathyroid tumors

Research output: Contribution to journalArticle

4 Citations (Scopus)

Abstract

Parathyroid tumors are common endocrine neoplasias associated with primary hyperparathyroidism, a metabolic disorder characterized by parathormone hypersecretion. Parathyroid neoplasia are frequently benign adenomas or multiple glands hyperplasia, while malignancies are rare. The epigenetic scenario in parathyroid tumors has just begun to be decoded: DNA methylation, histones and chromatin modifiers expression have been investigated so far. The main findings suggest that DNA methylation and chromatin remodeling are active and deregulated in parathyroid tumors, cooperating with genetic alterations to drive the tumor phenotype: the tumor suppressors menin and parafibromin, involved in parathyroid tumorigenesis, interact with chromatin modifiers, defining distinct epigenetic derangements. Many epigenetic alterations identified in parathyroid tumors are common to those in human cancers; moreover, some aspects of the epigenetic profile resemble epigenetic features of embryonic stem cells. Epigenetic profile may contribute to define the heterogeneity of parathyroid tumors and to provide targets for new therapeutic approaches.

Original languageEnglish
JournalMolecular and Cellular Endocrinology
DOIs
Publication statusAccepted/In press - Jan 8 2017

Fingerprint

DNA Methylation
Tumors
Epigenomics
Neoplasms
Chromatin
Stem cells
Parathyroid Hormone
Histones
Chromatin Assembly and Disassembly
Primary Hyperparathyroidism
Embryonic Stem Cells
Adenoma
Hyperplasia
Carcinogenesis
Phenotype

Keywords

  • Chromatin modifiers
  • Histones
  • Hyperparathyroidism
  • Methylation
  • Parathyroid tumors
  • PTH

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology
  • Endocrinology

Cite this

@article{2e86b0f0c2454d12a965c3cd649e614c,
title = "Alterations of DNA methylation in parathyroid tumors",
abstract = "Parathyroid tumors are common endocrine neoplasias associated with primary hyperparathyroidism, a metabolic disorder characterized by parathormone hypersecretion. Parathyroid neoplasia are frequently benign adenomas or multiple glands hyperplasia, while malignancies are rare. The epigenetic scenario in parathyroid tumors has just begun to be decoded: DNA methylation, histones and chromatin modifiers expression have been investigated so far. The main findings suggest that DNA methylation and chromatin remodeling are active and deregulated in parathyroid tumors, cooperating with genetic alterations to drive the tumor phenotype: the tumor suppressors menin and parafibromin, involved in parathyroid tumorigenesis, interact with chromatin modifiers, defining distinct epigenetic derangements. Many epigenetic alterations identified in parathyroid tumors are common to those in human cancers; moreover, some aspects of the epigenetic profile resemble epigenetic features of embryonic stem cells. Epigenetic profile may contribute to define the heterogeneity of parathyroid tumors and to provide targets for new therapeutic approaches.",
keywords = "Chromatin modifiers, Histones, Hyperparathyroidism, Methylation, Parathyroid tumors, PTH",
author = "Vito Guarnieri and Muscarella, {Lucia Anna} and Chiara Verdelli and Sabrina Corbetta",
year = "2017",
month = "1",
day = "8",
doi = "10.1016/j.mce.2017.05.010",
language = "English",
journal = "Molecular and Cellular Endocrinology",
issn = "0303-7207",
publisher = "Elsevier Ireland Ltd",

}

TY - JOUR

T1 - Alterations of DNA methylation in parathyroid tumors

AU - Guarnieri, Vito

AU - Muscarella, Lucia Anna

AU - Verdelli, Chiara

AU - Corbetta, Sabrina

PY - 2017/1/8

Y1 - 2017/1/8

N2 - Parathyroid tumors are common endocrine neoplasias associated with primary hyperparathyroidism, a metabolic disorder characterized by parathormone hypersecretion. Parathyroid neoplasia are frequently benign adenomas or multiple glands hyperplasia, while malignancies are rare. The epigenetic scenario in parathyroid tumors has just begun to be decoded: DNA methylation, histones and chromatin modifiers expression have been investigated so far. The main findings suggest that DNA methylation and chromatin remodeling are active and deregulated in parathyroid tumors, cooperating with genetic alterations to drive the tumor phenotype: the tumor suppressors menin and parafibromin, involved in parathyroid tumorigenesis, interact with chromatin modifiers, defining distinct epigenetic derangements. Many epigenetic alterations identified in parathyroid tumors are common to those in human cancers; moreover, some aspects of the epigenetic profile resemble epigenetic features of embryonic stem cells. Epigenetic profile may contribute to define the heterogeneity of parathyroid tumors and to provide targets for new therapeutic approaches.

AB - Parathyroid tumors are common endocrine neoplasias associated with primary hyperparathyroidism, a metabolic disorder characterized by parathormone hypersecretion. Parathyroid neoplasia are frequently benign adenomas or multiple glands hyperplasia, while malignancies are rare. The epigenetic scenario in parathyroid tumors has just begun to be decoded: DNA methylation, histones and chromatin modifiers expression have been investigated so far. The main findings suggest that DNA methylation and chromatin remodeling are active and deregulated in parathyroid tumors, cooperating with genetic alterations to drive the tumor phenotype: the tumor suppressors menin and parafibromin, involved in parathyroid tumorigenesis, interact with chromatin modifiers, defining distinct epigenetic derangements. Many epigenetic alterations identified in parathyroid tumors are common to those in human cancers; moreover, some aspects of the epigenetic profile resemble epigenetic features of embryonic stem cells. Epigenetic profile may contribute to define the heterogeneity of parathyroid tumors and to provide targets for new therapeutic approaches.

KW - Chromatin modifiers

KW - Histones

KW - Hyperparathyroidism

KW - Methylation

KW - Parathyroid tumors

KW - PTH

UR - http://www.scopus.com/inward/record.url?scp=85019478079&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85019478079&partnerID=8YFLogxK

U2 - 10.1016/j.mce.2017.05.010

DO - 10.1016/j.mce.2017.05.010

M3 - Article

AN - SCOPUS:85019478079

JO - Molecular and Cellular Endocrinology

JF - Molecular and Cellular Endocrinology

SN - 0303-7207

ER -