Epigenetic Control in Pituitary Tumors

Ezzat, Shereen

doi:10.1507/endocrj.k08e-082

Cited by 30 publications

(31 citation statements)

References 51 publications

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“…These types of studies on testicular (Cheung et al 2010) and ovarian cancer (Michaelson--Cohen et al 2011) have utilised MeDIP enrichment and on pancreatic tumours and ovarian cancer have used pharmacologic unmasking approaches (Kang et al 2010, Shimizu et al 2011. Still other studies on pituitary and thyroid tumours have described drug-induced unmasking techniques of histone tail modification that impact upon gene expression in these tumour types (reviewed in Farrell (2006), Ezzat (2008) and Yacqub-Usman et al (2012)). …”

Section: Endocrine Cells and Epigeneticsmentioning

confidence: 99%

Make way for the ‘next generation’: application and prospects for genome-wide, epigenome-specific technologies in endocrine research

Emes

Farrell²

2012

Journal of Molecular Endocrinology

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Epigenetic changes, which target DNA and associated histones, can be described as a pivotal mechanism of interaction between genes and the environment. The field of epigenomics aims to detect and interpret epigenetic modifications at the whole genome level. These approaches have the potential to increase resolution of epigenetic changes to the single base level in multiple disease states or across a population of individuals. Identification and comparison of the epigenomic landscape has challenged our understanding of the regulation of phenotype. Additionally, inclusion of these marks as biomarkers in the early detection or progression monitoring of disease is providing novel avenues for future biomedical research. Cells of the endocrine organs, which include pituitary, thyroid, thymus, pancreas ovary and testes, have been shown to be susceptible to epigenetic alteration, leading to both local and systemic changes often resulting in lifethreatening metabolic disease. As with other cell types and populations, endocrine cells are susceptible to tumour development, which in turn may have resulted from aberration of epigenetic control. Techniques including highthroughput sequencing and array-based analysis to investigate these changes have rapidly emerged and are continually evolving. Here, we present a review of these methods and their promise to influence our studies on the epigenome for endocrine research and perhaps to uncover novel therapeutic options in disease states.

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Section: Endocrine Cells and Epigeneticsmentioning

confidence: 99%

Make way for the ‘next generation’: application and prospects for genome-wide, epigenome-specific technologies in endocrine research

Emes

Farrell²

2012

Journal of Molecular Endocrinology

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“…38 Thus, epigenetically mediated gene dysregulation is implicated in pituitary tumorigenesis. 39,40 Prolactinomas in men tend to exhibit a more aggressive course. 18 It has been suggested that although men have lower estrogen levels, as expected, compared to women, their tumors express more estrogen receptors than those in women, this making them more vulnerable to the biological effect of the latter.…”

Section: Casementioning

confidence: 99%

Clinical Case Seminar. Peculiar prolactinomas in patients with pituitary developmental gene mutations: from an adult endocrinologist perspective

Doknic¹,

Pekić²,

Civcic³

et al. 2012

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We report a female with combined pituitary hormone deficiencies (GH, tsH, gonadotropin and ActH), except for prolactin, as a consequence of PrOP1 mutation, and a male with Ks (anosmia and IHH) due to Kal 2 gene (fibroblast growth factor receptor 1-FGFr1) mutation, both of whom in adulthood presented with prolactinomas. cONcLUsION: both patients with developmental gene mutations, after long-term correction of their sex steroid status, developed prolactinomas. Although the exact mechanism of pituitary tumorigenesis is not known, we speculate that sex steroids may have facilitated prolactinoma development from the prolactin cell pool which underwent uncontrolled proliferation in the setting of a developmental disorder.

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“…Acetylation of lysine (K) residues associated with H4 and methylation of lysine 9 (K9) in H3 may be present at inactive gene loci. Alternatively, acetylation on K9, K14 and methylation on K4 of H3, or acetylation on K5 of H4 can be found both at active or activating gene loci, reviewed by Tateno et al, 2010(Tateno et al, 2010Ezzat, 2008). …”

Section: Histone Modificationmentioning

confidence: 99%

Epigenetic and Posttranscriptional Alterations of Tumor Suppressor Genes in Sporadic Pituitary Adenomas

Butz¹,

Rácz²,

Patócs³

2012

Tumor Suppressor Genes

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Epigenetic Control in Pituitary Tumors

Cited by 30 publications

References 51 publications

Make way for the ‘next generation’: application and prospects for genome-wide, epigenome-specific technologies in endocrine research

Make way for the ‘next generation’: application and prospects for genome-wide, epigenome-specific technologies in endocrine research

Clinical Case Seminar. Peculiar prolactinomas in patients with pituitary developmental gene mutations: from an adult endocrinologist perspective

Epigenetic and Posttranscriptional Alterations of Tumor Suppressor Genes in Sporadic Pituitary Adenomas

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