Characteristics of women with dysplasia or carcinoma in situ of the cervix uteri

Harris, Ruth W.; Brinton, Louise A.; Cowdell, R. H.; Dc, Skegg; Smith, P. G.; Vessey, Martin; Doll, Richard

doi:10.1038/bjc.1980.246

Cited by 234 publications

(23 citation statements)

References 18 publications

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“…The relationship between cigarette smoking and apparent HPV infection has also been studied [Harris et al, 1980;Trevathan et al, 19831. The evidence for a positive relationship is not conclusive, but we, a t any rate, selected our samples from nonsmokers.…”

Section: Discussionmentioning

confidence: 99%

Detection of human papillomavirus deoxyribonucleic acid by filter in situ hybridization during pregnancy

Czeglédy

Gergely

Endrödi

1989

Journal of Medical Virology

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Samples taken from 101 healthy pregnant women (49 over and 52 under the 20-week gestational period) and 108 healthy nonpregnant women were tested for human papillomavirus (HPV) types. Using 6, 11, 16, and 18 HPV DNA probes, 3-5 x 10(5) exfoliated cells scraped from the cervix were tested by filter in situ hybridization (FISH). Thirty-five of the pregnant women (34.6%) had evidence of the presence of HPV DNA: with 11.8% (12/101) HPV 6; 7.9% (8/101) HPV 11; 8.9% (9/101) HPV 16; and 5.9% (6/101) HPV 18 positivity. HPV DNA was detected in 20.4% (22/108) of the non-pregnant women. Compared with the healthy, nonpregnant group, the higher level of asymptomatic cervical HPV infection was mainly due to the accumulation of HPV 16 and 18 nucleic acids during the gestational period: with detection of HPV 16 in 8/49 cases (16.3%) and of HPV 18 DNA sequences in 4/49 (7.6%) cases. Screening 6-8 weeks after delivery indicated a decline of HPV positivity. Of the 4/12 HPV type 16 positive mothers, only one retained the presence of HPV 16 DNA, whereas neither of the 2/12 type 18 positive women reacted after birth with the type 18 radioactive probe.

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Section: Discussionmentioning

confidence: 99%

Detection of human papillomavirus deoxyribonucleic acid by filter in situ hybridization during pregnancy

Czeglédy

Gergely

Endrödi

1989

Journal of Medical Virology

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“…Of note is that there was no control population who neither took the pill nor had the IUCD, making comparison with the background incidence of dysplasia or invasive cancer difficult. Harris et al (1980) (22) reported an increased risk of intraepithelial neoplasia with increasing duration of use for pill users. Ebeling et al (1987) (23) found that the risk of cervical cancer decreased after adjusting for sexual behavior and interval since last Pap smear but remained statistically significant or at borderline significance for long-term users of the pill (7þ years) and early onset users (< 24 years) with relative risks of 1.8 and 3.0, respectively.…”

Section: Prospective Studiesmentioning

confidence: 99%

The role of steroid contraceptive hormones in the pathogenesis of invasive cervical cancer: A review

Moodley

Moodley²,

Chetty

et al. 2003

International Journal of Gynecological Cancer

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Invasive cervical cancer remains a leading cause of morbidity and mortality, especially among women in the developing world where screening is either deficient or absent. Of all agents linked to the causation of this disease, high-risk human papillomavirus (HPV) appears to be the strongest factor. However, not all women with HPV develop cervical cancer. Steroid contraception has been postulated to be one mechanism whereby HPV exerts its tumorigenic effect on cervical tissue. Steroids are thought to bind to specific DNA sequences within transcriptional regulatory regions on the HPV DNA to either increase or suppress transcription of various genes. Although some earlier studies were reassuring as no increased incidence of cervical cancer was observed, subsequent research has shown a causative association, especially among long-term users. The role of steroids was further enhanced by the discovery of hormone receptors in cervical tissue. Some earlier studies of oral contraceptive steroids found no increased risk, even after controlling for other risk factors, including smoking and number of partners. However, prospective studies have shown a greater progression of dysplasia to carcinoma-in-situ with more than 6 years of oral steroid contraceptive use. Similar findings were also evident from other work, including the Royal College of General Practitioners Oral Contraception Study. The WHO Collaborative Study of Neoplasia and Steroid Contraceptives showed a relative risk of 1.2 for invasive cancer in users of the long-acting progestational contraceptive, depo-medroxyprogesterone acetate. However, in users of more than 5 years duration, an estimate of 2.4 was reported. The upstream regulatory region (URR) of the HPV type 16 viral genome, mediates transcriptional control of the HPV genome and is thought to contain enhancer elements that are activated by steroid hormones. It has been shown that steroid hormones bind to specific glucorticoid-response elements within HPV-DNA. Experimental evidence has revealed that high–risk type HPV 16 are able to stimulate the development of vaginal and cervical squamous cell carcinomas in transgenic mice exposed to slow-release pellets of 17 β-estradiol in the presence of human keratin-14 promoter. Squamous cell carcinomas developed in a multi-stage pathway only in transgenic mice and not in nontransgenic mice. The E6 oncoprotein of HPV 16 has been shown to bind to the p53 tumor suppressor gene and stimulate its degradation by a ubiquitin-dependent protease system. Steroid hormones are thought to increase the expression of the E6 and E7 HPV 16 oncogenes, which in turn bind to and degrade the p53 gene product, leading to apoptotic failure and carcinogenesis. However, the molecular basis of this remains to be proven.

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“…related to smoking, socioeconomic status and diet have also been proposed as causes of pre-malignant cervical disease (Brisson et al, 1988;Brock et al, 1989a, b;Cuzick et al, 1990;Guijon et al, 1985;Harris et al, 1980;Jones et a/., 1990;La Vecchia et al, 1986;Schneider and Shah, 1989;Trevathan et al, 1983).…”

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confidence: 99%

Human papillomavirus and cervical intraepithelial neoplasia grade II‐III: A population‐based case‐control study

Olsen¹,

Gjøen²,

Sauer³

et al. 1995

Intl Journal of Cancer

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The association between certain human papillomaviruses (HPV) and cervical intraepithelial neoplasia (CIN) is well documented, but there is uncertainty about the strength of association and the role of co-factors is unclear. This population-based case-control study in Norwegian women 20-44 years of age included 103 cases with histologically confirmed CIN II-III and 234 age-matched and randomly selected controls. Cytological specimens from the cervix were analyzed using the polymerase chain reaction (PCR). In all, 91% of the cases and 15% of the controls were HPV DNA positive, giving a crude odds ratio (OR) of 67.2 (95% confidence interval: 28.6-157.5). The association between HPV 16 and CIN II-III was even stronger (crude OR = 123.9; 46.7 - 328.5). In logistic regression analysis, additional to HPV, only a high number of sexual partners and a low educational level contributed independently to the risk. The adjusted OR for the association between HPV and CIN II-III was 72.8 (95% CI: 27.6-191.9). The association between HPV and CIN remains very strong even after adjustment for proposed confounding factors. The results therefore support the role of HPV as a causative agent in the development of CIN.

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Characteristics of women with dysplasia or carcinoma in situ of the cervix uteri

Cited by 234 publications

References 18 publications

Detection of human papillomavirus deoxyribonucleic acid by filter in situ hybridization during pregnancy

Detection of human papillomavirus deoxyribonucleic acid by filter in situ hybridization during pregnancy

The role of steroid contraceptive hormones in the pathogenesis of invasive cervical cancer: A review

Human papillomavirus and cervical intraepithelial neoplasia grade II‐III: A population‐based case‐control study

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