Effect of smoking cessation on cervical lesion size

Szarewski, Anne; Sasieni, Peter; Edwards, Robert P.; Cuzick, Jack; Jarvis, Martin J.; Steele, S. J.; Guillebaud, John

doi:10.1016/s0140-6736(96)91417-8

Cited by 117 publications

(55 citation statements)

References 17 publications

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“…The fact that the significant excess risk for CIN 2-3 associated with smoking was not reduced by adjustment for HPV indicates that smoking does indeed have a causal association with CIN 2-3. This is also supported by reports indicating that smoking cessation facilitates regression of CIN (Szarewski et al, 1996). Whether smoking is an entirely independent risk factor or works as a risk modifier of HPV exposure could not be disclosed in the present study.…”

Section: Discussionsupporting

confidence: 83%

Smoking, diet, pregnancy and oral contraceptive use as risk factors for cervical intra-epithelial neoplasia in relation to human papillomavirus infection

et al. 2000

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Smoking, nutrition, parity and oral contraceptive use have been reported as major environmental risk factors for cervical cancer. After the discovery of the very strong link between human papillomavirus (HPV) infection and cervical cancer, it is unclear whether the association of these environmental factors with cervical cancer reflect secondary associations attributable to confounding by HPV, if they are independent risk factors or whether they may act as cofactors to HPV infection in cervical carcinogenesis. To investigate this issue, we performed a population-based case–control study in the Västerbotten county of Northern Sweden of 137 women with high-grade cervical intra-epithelial neoplasia (CIN 2–3) and 253 healthy age-matched women. The women answered a 94-item questionnaire on diet, smoking, oral contraceptive use and sexual history and donated specimens for diagnosis of present HPV infection (nested polymerase chain reaction on cervical brush samples) and for past or present HPV infections (HPV seropositivity). The previously described protective effects of dietary micronutrients were not detected. Pregnancy appeared to be a risk factor in the multivariate analysis ( P < 0.0001). Prolonged oral contraceptive use and sexual history were associated with CIN 2–3 in univariate analysis, but these associations lost significance after taking HPV into account. Smoking was associated with CIN 2–3 (odds ratio (OR) 2.6, 95% confidence interval (CI) 1.7–4.0), the effect was dose-dependent ( P = 0.002) and the smoking-associated risk was not affected by adjusting for HPV, neither when adjusting for HPV DNA (OR 2.5, CI 1.3–4.9) nor when adjusting for HPV seropositivity (OR 3.0, CI 1.9–4.7). In conclusion, after taking HPV into account, smoking appeared to be the most significant environmental risk factor for cervical neoplasia. © 2000 Cancer Research Campaign

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Section: Discussionsupporting

confidence: 83%

Smoking, diet, pregnancy and oral contraceptive use as risk factors for cervical intra-epithelial neoplasia in relation to human papillomavirus infection

et al. 2000

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“…However, infection with HR HPV does not invariably lead to the development of high grade cervical lesions and there is a clear requirement for other cofactors, presumably to advance the oncogenic process initiated by HR HPV (zur Hausen, 1999). The effects of co-factors are difficult to measure objectively because of the dominant effects of HR HPV infection but tobacco smoking has consistently been associated with cervical cancer (Szarewski et al, 1996) and has been found recently to induce genomic instability in head and neck cancers (Schantz et al, 2000). Other potential co-factors include oral contraceptive use and other sexually transmitted diseases.…”

mentioning

confidence: 99%

Abnormal FHIT expression profiles in cervical intraepithelial neoplastic (CIN) lesions

Terry

Londesborough

et al. 2002

Br J Cancer

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Abnormal fragile histidine triad transcripts were found in 20 -30% of CIN2/3 lesions and 11% of normal cervical biopsies by RT -PCR. Bi-allelic loss of the fragile histidine triad gene and the loss of fragile histidine triad protein expression detectable by immunochemical staining with a polyclonal fragile histidine triad specific antibody was rare. The genomic changes showed no association with the presence of human papillomavirus types which carry high risk for cervical cancer (high risk human papillomavirus) as assessed by a type-specific multiplex PCR. The presence of abnormal fragile histidine triad transcripts in a subset of CIN2/3 lesions with no high risk human papillomavirus suggests that this could be an independent risk factor associated with an alternative carcinogenic pathway. Cervical cancer is the second most common malignancy in women worldwide. It is generally accepted that the development of cervical cancer from precancers (CIN2/3) involves multistep molecular changes and is therefore a preventable disease if precancers are detected and treated early.The major risk factor for CIN2/3 and cancer is infection with high risk human papillomavirus (HR HPV) types which include HPV16, HPV18, HPV31, HPV33, HPV35, HPV45, HPV51, HPV52, HPV56, HPV58, HPV59 and HPV68. One or more of these virus types have been reported to be present in 90 -95% of CIN2/3 lesions and in nearly all cancers (Lorincz et al, 1992;Bosch et al, 1995; Walboomers et al, 1996). However, infection with HR HPV does not invariably lead to the development of high grade cervical lesions and there is a clear requirement for other cofactors, presumably to advance the oncogenic process initiated by HR HPV (zur Hausen, 1999). The effects of co-factors are difficult to measure objectively because of the dominant effects of HR HPV infection but tobacco smoking has consistently been associated with cervical cancer (Szarewski et al, 1996) and has been found recently to induce genomic instability in head and neck cancers (Schantz et al, 2000). Other potential co-factors include oral contraceptive use and other sexually transmitted diseases.Genomic instability has been found in cervical neoplasia and commonly involves the short arm of chromosome 3. Results reported so far are based on small numbers of samples and show no clear correlation between genomic changes and lesion grades (Butler et al, 2000;Yoshino et al, 2000). Allelic loss and microsatellite instability were found to occur in lesions with or without malignant potential in similar proportion Chu et al, 1998;Yoshino et al, 1998;Butler et al, 2000;Lin et al, 2000). Inconsistent results were also obtained in the analysis of abnormal transcripts encoded by the fragile histidine triad (FHIT) gene at chromosome 3p14.2. These are also indicative of genomic instability (Sozzi et al, 1996) but the incidence reported varies from 30 to 80% in cervical cancer and 0 to 40% in normal tissue (Greenspan et al, 1997;Chu et al, 1998;Muller et al, 1998;Su et al, 1998;Yoshino et al, 1998;Nakagawa et al, 1999;...

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“…Individuals were selected into the study on the basis of the exposure (whether or not they had had HPV screening), not the outcome, and as such a case control design would not have been appropriate. Therefore, potential confounders such as age, smoking status, parity and contraceptive use were recorded (smoking and parity increase the risk of CIN progression 18,19 ). These data were divided into categories for ease of analysis: age into 30 years or less, 31-40, 41-50 and 51 years or more; contraceptive into none, oestrogen and progesterone excess (postmenopausal, use of Depoprovera, Implanon and the Mirena Coil); parity as none, one and more than two.…”

Section: Materials and Methods;mentioning

confidence: 99%

The impact of HPV cervical screening on negative large loop excision of the transformation zone (LLETZ): A comparative cohort study

Manley

Wills

Morris

et al. 2016

Gynecologic Oncology

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Link to publication record in Explore Bristol Research PDF-document This is the author accepted manuscript (AAM). The final published version (version of record) is available online via Elsevier at http://www.sciencedirect.com/science/article/pii/S0090825816300889. Please refer to any applicable terms of use of the publisher. University of Bristol -Explore Bristol Research General rightsThis document is made available in accordance with publisher policies. Please cite only the published version using the reference above. Full terms of use are available: http://www.bristol.ac.uk/pure/about/ebr-terms Abstract:Objective: To determine the incidence and predictors of negative large loop excision of the transformation zone (LLETZ) following the introduction of Human papillomavirus (HPV) cervical screening.Method: A retrospective cohort study. Two independent cohorts, who attended for a LLETZ procedure, before and after the introduction of HPV cervical screening were compared. For each cohort, 401 individuals were randomly selected from a colposcopy database. Clinical and colposcopic variables were extracted. The incidence of negative LLETZ was estimated in each cohort. Regression analysis was used to adjust for potential confounders and explore predictors of negative LLETZ.Results: Eighty women (19.9%) from the pre-HPV testing cohort and 54 women (13.4%) from the post-HPV cohort were negative for cervical intraepithelial neoplasia (RR 0.75, CI: 0.55 to 0.93). In the post-HPV testing cohort, independent predictors of negative LLETZ were low grade cytology (RR 3.60, CI: 2.18-5.97) and a type 3 transformation zone (TZ) (RR 2.88, CI: 1.76-4.72). Women with both low grade cytology and a TZ type 3 were 8.6 times more likely to have a negative LLETZ (absolute risk 40%, 95% CI: 27-54%). Conclusions:Despite a 25% reduction in negative LLETZ following the introduction of HPV cervical screening, the incidence is still high. These results highlight the importance of continuing to improve the specificity of cervical intraepithelial neoplasia screening; this should include the use of biomarkers that detect HPV transforming infections and techniques that sample an entirely endocervical transformation zone.

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Effect of smoking cessation on cervical lesion size

Cited by 117 publications

References 17 publications

Smoking, diet, pregnancy and oral contraceptive use as risk factors for cervical intra-epithelial neoplasia in relation to human papillomavirus infection

Smoking, diet, pregnancy and oral contraceptive use as risk factors for cervical intra-epithelial neoplasia in relation to human papillomavirus infection

Abnormal FHIT expression profiles in cervical intraepithelial neoplastic (CIN) lesions

The impact of HPV cervical screening on negative large loop excision of the transformation zone (LLETZ): A comparative cohort study

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