Hypermethylation of the CDKN2A gene promoter is a frequent epigenetic change in periocular sebaceous carcinoma and is associated with younger patient age

Liau, Jau–Yu; Liao, Shu‐Lang; Hsiao, Cheng–Hsiang; Lin, Ming-Chieh; Chang, Hsiao-Ching; Kuo, Kuan-Ting

doi:10.1016/j.humpath.2013.10.019

Cited by 35 publications

(25 citation statements)

References 32 publications

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“…Another group reported overexpression of this protein in 10 of 14 cases (71%) and noted that this was higher than in other types of eyelid tumors [9]. In contrast, Liau et al [10] found diffuse and strong p16 expression in only 1 of 24 periocular carcinoma cases (4%). They do not show an example of what they considered positive or negative p16 immunostaining, and it is unclear why the results of this group differ from ours and those listed above, although the fact that they score only nuclear protein may have played a role.…”

Section: Discussionmentioning

confidence: 99%

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Expression of p16 and p53 in Intraepithelial Periocular Sebaceous Carcinoma

Bell

Singh

et al. 2015

Ocul Oncol Pathol

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Purpose: Identifying intraepithelial sebaceous carcinoma cells in small periocular biopsies can be difficult, particularly in the conjunctiva. The goal of this study was to evaluate p53 and p16 immunohistochemistry as potential markers of intraepithelial sebaceous carcinoma. Procedures: A total of 25 tumors, including 4 recurrent lesions, were stained for p16 and p53, with intensity scored as negative, weak, moderate or strong. Results: Expression of p16 was detected in intraepithelial sebaceous carcinoma cells in 24 of the 25 cases (96%), with only 1 case showing weak immunoreactivity. Intraepithelial p53 immunoreactivity was present in 17 of 25 tumors (68%), but was weak in 3 cases. Expression levels remained relatively stable in primary and recurrent tumors, but varied in a few cases between intraepithelial and subepithelial sites. Conclusions: Intraepithelial sebaceous carcinomas stained for p53 and p16 demonstrated moderate to strong immunoreactivity in 100% of cases for at least one of these proteins, suggesting that together they are useful markers for determining the extent of tumor spread. Of the two, p16 was immunoreactive in more cases than p53.

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Section: Discussionmentioning

confidence: 99%

“…In carcinomas at other sites, p16 expression is often used as a surrogate marker of human papilloma virus (HPV) infection. However, no HPV was detected in SC in the two studies which sought to correlate it with p16 immunoreactivity [9,10]. …”

Section: Discussionmentioning

confidence: 99%

Expression of p16 and p53 in Intraepithelial Periocular Sebaceous Carcinoma

Bell

Singh

et al. 2015

Ocul Oncol Pathol

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“…IHC of MMR proteins (MLH1, PMS2, MSH6, and MSH2) was performed in MSI‐H cases. Detailed information on these antibodies and protocols for immunohistochemical stains have been described in previous reports …”

Section: Methodsmentioning

confidence: 99%

Ovarian and endometrial endometrioid adenocarcinomas have distinct profiles of microsatellite instability, PTEN expression, and ARID1A expression

et al. 2014

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“…For instance, hypermethylation of the promoter of the DNA repair gene hMLH1 is associated with early stages of endometrial and colon cancer, and microsatellite instability phenotype (Esteller et al, 1999). Epigenetically mediated silencing of cyclin-dependent kinase inhibitor 2A, which is crucial for control of cell cycle has been reported in several cancers (Brock et al, 2008; Liau et al, 2014). Additionally, pathways regulated by microRNAs have been associated with DNA hypermethylation-dependent silencing (Saito et al, 2006).…”

Section: Epigenetic Changes Mediated By the Vitamin D Receptor And Itmentioning

confidence: 99%

Vitamin D and the epigenome

2014

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Epigenetic mechanisms play a crucial role in regulating gene expression. The main mechanisms involve methylation of DNA and covalent modifications of histones by methylation, acetylation, phosphorylation, or ubiquitination. The complex interplay of different epigenetic mechanisms is mediated by enzymes acting in the nucleus. Modifications in DNA methylation are performed mainly by DNA methyltransferases (DNMTs) and ten-eleven translocation (TET) proteins, while a plethora of enzymes, such as histone acetyltransferases (HATs), histone deacetylases (HDACs), histone methyltransferases (HMTs), and histone demethylases (HDMs) regulate covalent histone modifications. In many diseases, such as cancer, the epigenetic regulatory system is often disturbed. Vitamin D interacts with the epigenome on multiple levels. Firstly, critical genes in the vitamin D signaling system, such as those coding for vitamin D receptor (VDR) and the enzymes 25-hydroxylase (CYP2R1), 1α-hydroxylase (CYP27B1), and 24-hydroxylase (CYP24A1) have large CpG islands in their promoter regions and therefore can be silenced by DNA methylation. Secondly, VDR protein physically interacts with coactivator and corepressor proteins, which in turn are in contact with chromatin modifiers, such as HATs, HDACs, HMTs, and with chromatin remodelers. Thirdly, a number of genes encoding for chromatin modifiers and remodelers, such as HDMs of the Jumonji C (JmjC)-domain containing proteins and lysine-specific demethylase (LSD) families are primary targets of VDR and its ligands. Finally, there is evidence that certain VDR ligands have DNA demethylating effects. In this review we will discuss regulation of the vitamin D system by epigenetic modifications and how vitamin D contributes to the maintenance of the epigenome, and evaluate its impact in health and disease.

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Hypermethylation of the CDKN2A gene promoter is a frequent epigenetic change in periocular sebaceous carcinoma and is associated with younger patient age

Cited by 35 publications

References 32 publications

Expression of p16 and p53 in Intraepithelial Periocular Sebaceous Carcinoma

Expression of p16 and p53 in Intraepithelial Periocular Sebaceous Carcinoma

Ovarian and endometrial endometrioid adenocarcinomas have distinct profiles of microsatellite instability, PTEN expression, and ARID1A expression

Vitamin D and the epigenome

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