Methylation status of ANAPC1, CDKN2A and TP53 promoter genes in individuals with gastric cancer

Lima, Eleonidas Moura; Leal, Mariana Ferreira; Burbano, Rommel Rodrı́guez; Khayat, André Salim; Assumpção, Paulo Pimentel de; Bello, M. Josefa; Rey, Juan A.; Smith, Marília de Arruda Cardoso; Casartelli, Cacilda

doi:10.1590/s0100-879x2008000600017

Cited by 29 publications

(16 citation statements)

References 26 publications

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“…While the promoter region of TP53 does not contain a classic CpG island, methylation of one or two sites may produce a proportionately greater effect in downregulation of transcription compared to a tumor suppressor gene with a classic CpG island in the promoter (Sidhu et al, 2005). The methylation of TP53 was reported as a mechanism for its inactivation in some neoplasms, such as acute lymphoblastic leukemia, multiple myeloma, malignant glioma cells, and brain metastases of solid tumors (Lima et al, 2008). Kang et al (2001) showed TP53 methylation in 3 of 19 (16%) breast carcinomas.…”

Section: Discussionmentioning

confidence: 99%

Polymorphisms and DNA methylation of gene TP53 associated with extra-axial brain tumors

Almeida

Custódio²,

Pinto³

et al. 2009

Genet. Mol. Res.

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AbSTRACT. The p53 tumor suppressor gene is the most frequently mutated gene in human cancer; this gene is mutated in up to 50% of human tumors. It has a critical role in the cell cycle, apoptosis and cell senescence, and it participates in many crucial physiological and pathological processes. Polymorphisms of p53 have been suggested to be associated with genetically determined susceptibility in various types of cancer. Another process involved with the Aberrant methylation of the promoter is an alternative epigenetic change in genetic mechanisms, leading to tumor suppressor gene inactivation. In the present study, we examined the TP53 Arg72Pro and Pro47Ser polymorphisms using PCR-RFLP and the pattern of methylation of the p53 gene by methylation-specific PCR in 90 extra-axial brain tumor samples. Patients who had the allele Pro of the TP53 Arg72Pro polymorphism had an increased risk of tumor development (odds ratio, OR = 3.23; confidence interval at 95%, 95%CI = 1.71-6.08; P = 0.003), as did the allele Ser of TP53 Pro47Ser polymorphism (OR = 1.28; 95%CI = 0.03-2.10; P = 0.01).Comparison of overall survival of patients did not show significant differences. In the analysis of DNA methylation, we observed that 37.5% of meningiomas, 30% of schwannomas and 52.6% of metastases were hypermethylated, suggesting that methylation is important for tumor progression. We suggest that TP53 Pro47Ser and Arg72Pro polymorphisms and DNA hypermethylation are involved in susceptibility for developing extra-axial brain tumors.

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Section: Discussionmentioning

confidence: 99%

Polymorphisms and DNA methylation of gene TP53 associated with extra-axial brain tumors

Almeida

Custódio²,

Pinto³

et al. 2009

Genet. Mol. Res.

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“…Loss of CDH1 expression during tumor progression has led to the hypothesis that it is a tumor suppressor gene [37]. Unlike the CDH1 gene, the p16 gene is hypermethylated, mainly in the intestinal type of GC [11,38]. This epigenetic marker was associated recently with tumor location and H. pylori infection in GC [39].…”

Section: Potential Of Methylated Dna In Cancer Diagnosticsmentioning

confidence: 99%

DNA methylation and microRNA biomarkers for noninvasive detection of gastric and colorectal cancer

Toiyama

Okugawa

Goel

2014

Biochemical and Biophysical Research Communications

134

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Cancer initiation and progression is controlled by both genetic and epigenetic events. Epigenetics refers to the study of mechanisms that alter gene expression without permanently altering the DNA sequence. Epigenetic alterations are reversible and heritable, and include changes in histone modifications, DNA methylation, and non-coding RNA-mediated gene silencing. Disruption of epigenetic processes can lead to altered gene function and malignant cellular transformation. Aberrant epigenetic modifications occur at the earliest stages of neoplastic transformation and are now believed to be essential players in cancer initiation and progression. Recent advances in epigenetics have not only offered a deeper understanding of the underlying mechanism(s) of carcinogenesis, but have also allowed identification of clinically relevant putative biomarkers for the early detection, disease monitoring, prognosis and risk assessment of cancer patients. At this moment, DNA methylation and non-coding RNA including with microRNAs (miRNAs) and long non-coding RNAs (lncRNAs) represent the largest body of available literature on epigenetic biomarkers with the highest potential for cancer diagnosis. Following identification of cell-free nucleic acids in systematic circulation, increasing evidence has demonstrated the potential of cell-free epigenetic biomarkers in the blood or other body fluids for cancer detection. In this article, we summarize the current state of knowledge on epigenetic biomarkers — primarily DNA methylation and non-coding RNAs — as potential substrates for cancer detection in gastric and colorectal cancer, the two most frequent cancers within the gastrointestinal tract. We also discuss the obstacles that have limited the routine use of epigenetic biomarkers in the clinical settings and provide our perspective on approaches that might help overcome these hurdles, so that these biomarkers can be readily developed for clinical management of cancer patients.

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“…However, the loss of CDKN2A function due mainly to promoter hypermethylation is common in human cancers, including colorectal cancer,19 hepatocellular carcinoma,20 gastric carcinoma,21 and breast cancer 22. The diagnostic accuracy of methylated CDKN2A in discriminating cancer cells from normal tissues has also been investigated.…”

Section: Introductionmentioning

confidence: 99%

The association between methylated <em>CDKN2A</em> and cervical carcinogenesis, and its diagnostic value in cervical cancer: a meta-analysis

Zhou

Zhou³

et al. 2016

TCRM

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BackgroundCervical cancer is the second deadliest gynecologic malignancy, characterized by apparently precancerous lesions and cervical intraepithelial neoplasia (CIN), and having a long course from the development of CIN to cervical cancer. Cyclin-dependent kinase inhibitor 2A (CDKN2A) is a well-documented tumor suppressor gene and is commonly methylated in cervical cancer. However, the relationship between methylated CDKN2A and carcinogenesis in cervical cancer is inconsistent, and the diagnostic accuracy of methylated CDKN2A is underinvestigated. In this study, we attempted to quantify the association between CDKN2A methylation and the carcinogenesis of cervical cancer, and its diagnostic power.MethodsWe systematically reviewed four electronic databases and identified 26 studies involving 1,490 cervical cancers, 1,291 CINs, and 964 controls. A pooled odds ratio (OR) with corresponding 95% confidence intervals (95% CI) was calculated to evaluate the association between methylated CDKN2A and the carcinogenesis of cervical cancer. Specificity, sensitivity, the area under the receiver operating characteristic curve, and the diagnostic odds ratio were computed to assess the effect of methylated CDKN2A in the diagnosis of cervical cancer.ResultsOur results indicated an upward trend in the methylation frequency of CDKN2A in the carcinogenesis of cervical cancer (cancer vs control: OR =23.67, 95% CI =15.54–36.06; cancer vs CIN: OR =2.53, 95% CI =1.79–3.5; CIN vs control: OR =9.68, 95% CI =5.82–16.02). The specificity, sensitivity, area under the receiver operating characteristic curve, and diagnostic odds ratio were 0.99 (95% CI: 0.97–0.99), 0.36 (95% CI: 0.28–0.45), 0.93 (95% CI: 0.91–0.95), and 43 (95% CI: 19–98), respectively.ConclusionOur findings indicate that abnormal CDKN2A methylation may be strongly correlated with the pathogenesis of cervical cancer. Our results also demonstrate that CDKN2A methylation might serve as an early detector of cervical cancer. These findings require further confirmation.

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Methylation status of ANAPC1, CDKN2A and TP53 promoter genes in individuals with gastric cancer

Cited by 29 publications

References 26 publications

Polymorphisms and DNA methylation of gene TP53 associated with extra-axial brain tumors

Polymorphisms and DNA methylation of gene TP53 associated with extra-axial brain tumors

DNA methylation and microRNA biomarkers for noninvasive detection of gastric and colorectal cancer

The association between methylated <em>CDKN2A</em> and cervical carcinogenesis, and its diagnostic value in cervical cancer: a meta-analysis

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