Methylation of p16 in primary gynecologic malignancy

Wong, Yick Fu; Chung, Tony K.H.; Cheung, Tak Hong; Nobori, Tsutomu; Yu, Alice L.; Yu, John; Batova, Ayse; Lai, Ka-Bik; Chang, A.M.Z.

doi:10.1016/s0304-3835(98)00327-9

Cited by 77 publications

(53 citation statements)

References 9 publications

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“…A minimal degree of methylation can be registered as "positive methylation" depending on the original DNA concentration, primer sets and the number of cycles used for PCR [32,33]. Indeed in different populationsof patients the p16 INK4a methylation was determined in 25-57% of invasive cervical squamous cell carcinomas (I-IV FIGO stages) by MSP [22][23][24][25][26][27]. Our results of MSP analysis of the same p16 INK4a region with the same set of primers in invasive SCC (I-III FIGO stages) are in close agreement with these findings.…”

Section: Discussionmentioning

confidence: 99%

“…1) [30]. Exactly this region of the p16 INK4a CpG island was reported to be methylated in many types of tumors including cervical squamous cell carcinomas [3,[22][23][24][25][26][27]30]. The presence of methylated alleles was revealed in 6 out of 26 (23%) squamous cell carcinomas .…”

Section: Analysis Of the 5' Cpg Island Methylation By Msp And Bisulfimentioning

confidence: 99%

“…Along with the detection of p16 ink4a expression in the majority of the HR-HPV-positive cervical tumors, hypermethylation of p16 INK4a promoter has been demonstrated in 25-57% of cervical carcinomas by methylationspecific PCR, MSP [22][23][24][25][26][27]. Hypermathylation of p16 INK4a promoter is a well known mechanism of suppression of the gene transcription [4,5].…”

Section: Introductionmentioning

confidence: 99%

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Up-regulation of expression and lack of 5' CpG island hypermethylation of p16 INK4ain HPV-positive cervical carcinomas

Ivanova

Golovina²,

Завалишина

et al. 2007

BMC Cancer

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Background: High risk type human papilloma viruses (HR-HPV) induce carcinomas of the uterine cervix by expressing viral oncogenes E6 and E7. Oncogene E7 of HR-HPV disrupts the pRb/E2F interaction, which negatively regulates the S phase entry. Expression of tumor suppressor p16 ink4a drastically increases in majority of HR-HPV associated carcinomas due to removal of pRb repression. The p16 ink4a overexpression is an indicator of an aberrant expression of viral oncogenes and may serve as a marker for early diagnostic of cervical cancer. On the other hand, in 25-57% of cervical carcinomas hypermethylation of the p16 INK4a promoter has been demonstrated using a methylation-specific PCR, MSP. To evaluate a potential usage of the p16 INK4a 5' CpG island hypermethylation as an indicator of tumor cell along with p16 ink4a overexpression, we analyzed the methylation status of p16 INK4a in cervical carcinomas

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Section: Discussionmentioning

confidence: 99%

Section: Analysis Of the 5' Cpg Island Methylation By Msp And Bisulfimentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Up-regulation of expression and lack of 5' CpG island hypermethylation of p16 INK4ain HPV-positive cervical carcinomas

Ivanova

Golovina²,

Завалишина

et al. 2007

BMC Cancer

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“…Its function is involved in the inhibition of cell cycle progression by encoding an inhibitor of cyclin-dependent kinase (CDK) 4 and CDK6 (28). Wong et al (29) and Dong et al (26) detected 31.6% (31/98) and 30% (16/53) of methylated p16 in squamous cervical carcinoma, respectively. The results of the present study identified that the methylation frequency of p16 was relatively low in precancerous stages, and that the methylation frequency was increased in CIN II and CIN III.…”

Section: Discussionmentioning

confidence: 99%

Promoter methylation status of the tumor suppressor genes p16 and cadherin 1 in cervical intraepithelial neoplasia

Lee

et al. 2017

Oncology Letters

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Abstract. Cervical cancer is the second most common female cancer worldwide. DNA methylation is one of a number of epigenetic regulation mechanisms leading to gene silencing in neoplastic cells. Aberrant methylation results in the silencing of tumor suppressor gene expression, and has been detected in a high percentage of human cancers. In the present study, the methylation status of three tumor suppressor genes, retinoic acid receptor β (RARβ), p16 and cadherin 1 (CDH1), and the inflammatory-associated cyclooxygenase-2 (COX-2) gene, was examined at distinct stages of cervical intraepithelial neoplasia (CIN). The results of the present study revealed that the COX-2 gene was unmethylated between CIN I and carcinoma specimens. The RARβ gene exhibited a minimal change in methylation frequency, whereas the CDH1 methylation level was increased <2-fold between CIN I and carcinoma. Notably, the methylation frequency of p16 was 13.2% in normal specimens; 18.2% in CIN I; 35.7% in CIN II; 31.6% in CIN III; and 15.4% in carcinoma. By contrast, the methylation frequency of p16 increased between CIN I and carcinoma in the absence of high-risk group papillomaviruses. The results of bisulfite sequencing indicated that the 10 CpG sites were all methylated in p16 gene methylation-positive individuals. The results of the present study demonstrate that the methylation frequency of p16 and CDH1 was progressively increased during the development of malignant stages in CIN, and may be an additional tool for current cytomorphology-based screening of cervical cell specimens.

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“…p16 is more frequently methylated in advanced tumors (Wong et al, 1999) thus suggesting that its reactivation could have therapeutic value. In a study performed on 62 cases of squamous cell carcinomas, Cheung et al showed that promoter methylation of PTEN was found in 58% of patients with persistent disease while those who died of the disease had a significantly higher percentage of PTEN methylation.…”

Section: Markers Of Chromosomal Stabilitymentioning

confidence: 99%