Quantitative methylation-specific PCR for the detection of aberrant DNA methylation in liquid-based Pap tests

Kahn, Steven L.; Ronnett, Brigitte M.; Gravitt, Patti E.; Gustafson, Karen S.

doi:10.1002/cncr.23258

Cited by 56 publications

(46 citation statements)

References 27 publications

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“…In previous studies DAPK promoter hypermethylation was observed in 2% of normal, 17-55% of HGSILs samples and 45-100% of cancer cases (21,(34)(35)(36)(39)(40)(41)(42)(45)(46)(47)(48). In the present study DAPK promoter hypermethylation was detected in 66.7% of premalignant lesions, percentage which is higher than in previous reports (34)(35)(36) and it was able to distinguish early from late stages of cervical oncogenesis progression. DAPK promoter methylation status seemed to be the best cervical oncogenesis quantitative and qualitative marker, as it was the only marker that was negative in normal tissues.…”

Section: Discussionmentioning

confidence: 84%

“…Loss of DAPK expression has been shown to occur in a number of malignancies including cervical cancer by enhancing the metastatic potential of cancer cells (40)(41)(42)(43)(44). In previous studies DAPK promoter hypermethylation was observed in 2% of normal, 17-55% of HGSILs samples and 45-100% of cancer cases (21,(34)(35)(36)(39)(40)(41)(42)(45)(46)(47)(48). In the present study DAPK promoter hypermethylation was detected in 66.7% of premalignant lesions, percentage which is higher than in previous reports (34)(35)(36) and it was able to distinguish early from late stages of cervical oncogenesis progression.…”

Section: Discussionmentioning

confidence: 98%

“…In the present study, we investigated the methylation profiles in the promoter region of hTERT, MGMT and DAPK genes in normal, premalignant and cervical cancer specimens, as the existing data on the methylation status of these genes is limited and results are conflicting (22,(32)(33)(34)(35)(36). hTERT gene plays a critical role in cell division and serves as a mitotic clock for cell proliferation (17).…”

Section: Discussionmentioning

confidence: 99%

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Correlation of promoter hypermethylation in hTERT, DAPK and MGMT genes with cervical oncogenesis progression

Iliopoulos

Oikonomou²,

Messinis³

et al. 2009

Oncol Rep

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Abstract. DNA hypermethylation occurs during the multistep process of cervical carcinogenesis. We investigated whether the methylation status in the promoter region of a potential oncogene, the human telomerase reverse transcriptase (hTERT), and the tumor suppressor genes deathassociated protein kinase (DAPK) and O 6 -methylguanine DNA methyltransferase (MGMT), were able to distinguish the early from late stages of cervical oncogenesis. The methylation status in the promoter of these genes was analyzed using real-time MethyLight analysis in 115 cervical specimens, including normal, premalignant [atypical squamous epithelial cells (ASCUS), low-grade squamous intraepithelial lesions (LGSIL), high-grade squamous intraepithelial lesions (HGSIL)] and cancer specimens. Clinicopathological parameters (cytology, histology, grade, stage) were compared to the levels of pro-moter hypermethylation. We found that hTERT, MGMT and DAPK hypermethylation levels were increased during cervical oncogenesis progression. hTERT promoter hypermethylation was able to distinguish normal from cancer (p=0.008), normal from premalignant (p=0.036), as well as premalignant from cervical cancer cases (p=0.003). A significant association was also observed between all three genes and the grade of cervical cancer, with hTERT showing a better association (p<0.0001). Our data suggest that the combination of hTERT, MGMT, DAPK promoter hypermethylation could have a potential function as molecular biomarker of cervical oncogenesis progression.

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Section: Discussionmentioning

confidence: 84%

Section: Discussionmentioning

confidence: 98%

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Correlation of promoter hypermethylation in hTERT, DAPK and MGMT genes with cervical oncogenesis progression

Iliopoulos

Oikonomou²,

Messinis³

et al. 2009

Oncol Rep

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“…In this study, the hypermethylation of DAPK promoter was detectable in liquid-based Pap test sample by MSP method. The advantage of using Pap test samples is one kind of noninvasive samples, contains exfoliating cells from the transformation zone of the cervix; thus, the presence of DNA in exfoliating cells has offered an opportunity to find out the predictive and diagnosis biomarkers for CC [27][28][29]. In addition, MSP method is the simple, rapid and inexpensive method that determine the methylation status of CpG islands.…”

Section: Discussionmentioning

confidence: 99%

Identification of Frequent Promoter Methylation of Death-Associated Protein Kinase in Liquid-Based Papanicolaous Test Samples in Vietnamese Population

Truong

Lao

2017

Asian J Pharm Clin Res

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Objective: The infection of high-risk human papillomavirus (HPV) genotypes, particularly HPV-16 and HPV-18, is known to cause cervical cancer (CC); however, aberrant DNA methylation of death-associated protein kinase (DAPK), a member of tumor suppressor gene family, are required for cervical tumorigenesis. The aim of our study was to evaluate the hypermethylation frequency of CpG belonged to DAPK promoter, in Vietnamese patients, as well as to study about the association between hypermethylation, and high-risk HPV infection leading to CC.Methods: Methylation-specific-polymerase chain reaction (MSP) was performed to analyze methylation status from 109 liquid-based papanicolaous test samples, collected from local hospital and were identified whether HPV/or non-HPV, high-risk/low-risk HPV infection, then was confirmed by sequencing. Results:In the case of high-risk HPV infection, the frequency of DAPK gene hypermethylation was 66.67% (24 of 36 cases). Meanwhile, low hypermethylation status was found in low-risk and non-HPV infection, counting for 12.0% (3 of 25 cases), 2.1% (1 of 48 cases), respectively. Significant association of DAPK hypermethylation with high-risk, low-risk, and non-HPV infection was observed (p<0.0001). The DAPK hypermethylation increased the possibility to CC in the case of high-risk HPV infected with high incidence: Odds ratio=34.5 (95% confidence interval [CI]=10.15-117.23, p<0.01), relative risk=12.2 (95% CI=4.56-32.42, p<0.01). Conclusion:Based on those data, it suggested that MSP carried out on noninvasive samples will lead to potential method to screening, diagnosis and early diagnosis of cervical carcinoma in Vietnamese population.

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“…In contrast, stromal SPARC inhibits angiogenesis and limits tumor growth in ovarian cancer and glioblastoma (Said and Motamed, 2005;Chlenski et al, 2006Chlenski et al, , 2007Said et al, 2007a, b). Although stromal SPARC was correlated with poor prognosis in pancreatic and small cell lung cancer (Podhajcer et al, 2008), tumor cell SPARC expression was lost due to promoter hypermethylation in pancreatic (Sato et al, 2003), non-small cell lung (Suzuki et al, 2005;Pan et al, 2008), colon (Tai et al, 2005;Yang et al, 2007;Cheetham et al, 2008), cervical (Sova et al, 2006;Kahn et al, 2008), endometrial (Rodriguez-Jimenez et al, 2007) and ovarian cancers (Socha et al, 2009). Stromal SPARC may promote immune/inflammatory cell recruitment in the juxtatumoral stroma (Sangaletti et al, 2003), but may also exert an antiinflammatory role (Said et al, 2007b;Pan et al, 2008).…”

Section: Introductionmentioning

confidence: 99%

The role of SPARC in the TRAMP model of prostate carcinogenesis and progression

et al. 2009

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SPARC (Secreted Protein Acidic and Rich in Cysteine), is a matricellular glycoprotein that is produced by tumor and/or neighboring stroma. In human prostate cancer, SPARC immunoreactivity is highest in metastatic lesions but distinct contributions of tumoral and stromal SPARC to tumorigenesis and progression are unclear. To determine the role of SPARC in primary prostate tumorigenesis, we crossed SPARC-null (SP À/À ) with TRAMP (Transgenic Adenocarcinoma of Mouse Prostate) mice.mice exhibited accelerated cancer development and progression. Compared to their fewer proliferating cells, and decreased cyclins A and D1 with increased p21Cip and p27 Kip . Similar effects on proliferation and cell-cycle regulators were observed in human prostate cancer cell lines, transiently transfected with pSPARC. TRAMP þ /SP À/À tumors exhibited decreased stromal collagen, enhanced matrix metalloproteinase activity and increased vascular endothelial growth factor, proinflammatory cytokines. To determine the contribution of stromal SPARC, we evaluated subcutaneous tumor growth of TRAMP cell lines in syngeneic SP þ / þ and SP À/À mice. Enhanced growth, decreased stromal collagen and increased proteolysis were noted in SP À/À mice. Our findings demonstrate that both tumor and stromal SPARC are limiting for primary prostate tumorigenesis and progression, through effects on the cell cycle and the creation of a less favorable tumor microenvironment.

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Quantitative methylation-specific PCR for the detection of aberrant DNA methylation in liquid-based Pap tests

Cited by 56 publications

References 27 publications

Correlation of promoter hypermethylation in hTERT, DAPK and MGMT genes with cervical oncogenesis progression

Correlation of promoter hypermethylation in hTERT, DAPK and MGMT genes with cervical oncogenesis progression

Identification of Frequent Promoter Methylation of Death-Associated Protein Kinase in Liquid-Based Papanicolaous Test Samples in Vietnamese Population

The role of SPARC in the TRAMP model of prostate carcinogenesis and progression

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