Lifetime cigarette smoke and second-hand smoke and cervical intraepithelial neoplasm—A community-based case–control study☆

Tsai, Hsiu Ting; Tsai, Yi-Hsuan; Yang, Sheau-Fang; Wu, Kaung-Hsiung; Chuang, Hung‐Yi; Wu, Trong Neng; Ho, Chi Kung; Lin, Cheng Chieh; Kuo, Ying Se; Wu, Ming Tsang

doi:10.1016/j.ygyno.2006.11.012

Cited by 56 publications

(68 citation statements)

References 27 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…A community-based case-control study was conducted in Kaohsiung City, and 529 patients (mean age, 46.2±13.2) were enrolled in the present study between January 2008 and September 2010. The procedure of patient enrollment was as previously described (15). Cervical scrapings were obtained from female patients who attended the Department of Obstetrics and Gynecology, Kaohsiung Medical University Hospital (Kaohsiung, Taiwan) or from the community health clinics of Great Kaohsiung City (southern part of Taiwan).…”

Section: Methodsmentioning

confidence: 99%

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

Lee

et al. 2017

Oncology Letters

View full text Add to dashboard Cite

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.

show abstract

Section: Methodsmentioning

confidence: 99%

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

Lee

et al. 2017

Oncology Letters

View full text Add to dashboard Cite

show abstract

“…A later study (Coker et al, 2002) looked at risk of low grade and high grade cervical squamous intraepithelial lesions (LSIL and HSIL, respectively) in HPV positive never-smokers and reported a significant association with exposure to secondhand tobacco smoke. In a community-based case-control study, Tsai et al (2007) observed a markedly increased risk for both CIN1 and CIN2 in both HPV-positive and HPV-negative women exposed to second-hand tobacco smoke. Only Coker et al (2002) and Tsai et al (2007) controlled for HPV status in women.…”

Section: (B) Cervical Intraepithelial Lesions and Neoplasiamentioning

confidence: 98%

“…In a community-based case-control study, Tsai et al (2007) observed a markedly increased risk for both CIN1 and CIN2 in both HPV-positive and HPV-negative women exposed to second-hand tobacco smoke. Only Coker et al (2002) and Tsai et al (2007) controlled for HPV status in women. Sobti et al (2006) reported that cervical cancer risk is increased in individuals exposed to second-hand tobacco smoke with GSTM1 (null), GSTT1 (null) and GSTP1 (Ile 105 Val) genotypes, with odd ratios ranging from 6.4 to 10.2.…”

Section: (B) Cervical Intraepithelial Lesions and Neoplasiamentioning

confidence: 98%

“…A total of 10 new studies have been identified: one cohort study (Table 2.11 available at http://monographs.iarc.fr/ENG/Monographs/ vol100E/100E-02-Table2.11.pdf) and nine casecontrol studies (Buckley et al, 1981;Brown et al, 1982;Hellberg et al, 1986;Hirose et al, 1996;Coker et al, 2002;Wu et al, 2003;Tay & Tay, 2004;Sobti et al, 2006;Tsai et al, 2007;Table 2.12 available at http://monographs.iarc.fr/ ENG/Monographs/vol100E/100E-02-Table2.12. pdf).…”

Section: Cancer Of the Cervixmentioning

confidence: 99%

See 1 more Smart Citation

Secondhand Tobacco Smoke

2011

Encyclopedia of Cancer

View full text Add to dashboard Cite

“…In addition, it is now generally accepted that smoking is a common environmental causative agent associated with cervical cancer (Hellberg et al, 1988;McCann et al, 1992;Prokopczyk et al, 1997;Tsai et al, 2007), and interestingly, some studies have now shown a powerful synergy between HPV-16 and cervical cancer in situ for smokers (Anthony et al, 2006). Despite this, little is known about the mechanism by which smoking and its related substances influence cervical carcinogenesis.…”

Section: Introductionmentioning

confidence: 99%

The cellular transcription factor Brn-3a and the smoking-related substance nicotine interact to regulate the activity of the HPV URR in the cervix

et al. 2010

View full text Add to dashboard Cite

The cellular transcription factor Brn-3a differentially regulates different human papilloma virus (HPV)-16 variants that are associated with different risks of progression to cervical carcinoma in infected humans. The upstream regulatory regions (URRs) of high-and intermediate-risk HPV-16 variants are activated by the cellular transcription factor Brn-3a, whereas the URR of a low-risk HPV-16 variant is not. In this study, we show in transfection assays that Brn-3a and the smoking-related substance nicotine produce stronger responsiveness of the URR of the low-and high-risk variants than with either factor alone, but not the intermediate-risk variant. We determined that this synergistic activity of Brn-3a/ nicotine is due to two nucleotide differences in the URR, crucial for oncogenic E6/E7 transactivation. Mutant constructs in which the nucleotide residues were substituted alter Brn-3a/nicotine responsiveness. Importantly, women smokers with high levels of Brn-3a infected with low-or high-risk HPV-16 variants have augmented E6 levels, and were more frequently diagnosed with higher grades of cervical intraepithelial neoplasia (CIN) and cancer, as compared with non-smokers who were infected with similar variants and expressed similar levels of Brn3a. Therefore, this study defines the specific interplay between the cellular transactivator Brn-3a, the environmental smoking-related substance nicotine and specific HPV variants in cervical carcinogenesis, and thus helps to explain why some women are susceptible to rapid CIN progression and cancer and others are not.

show abstract

Lifetime cigarette smoke and second-hand smoke and cervical intraepithelial neoplasm—A community-based case–control study☆

Cited by 56 publications

References 27 publications

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

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

Secondhand Tobacco Smoke

The cellular transcription factor Brn-3a and the smoking-related substance nicotine interact to regulate the activity of the HPV URR in the cervix

Contact Info

Product

Resources

About