Prevalence of human papillomavirus type 16 DNA sequences in cervical intraepithelial neoplasia and invasive carcinoma of the cervix

McCance, Dennis J.; Campion, Michael J.; Clarkson, P. K.; Chesters, P. M.; Jenkins, David; Singer, Albert

doi:10.1111/j.1471-0528.1985.tb03019.x

Cited by 193 publications

(58 citation statements)

References 11 publications

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“…Similar prevalence was shown for HPV type 16 and 18 in dysplastic lesions by other authors (van Den Brule et al, 1991;Cornelissen et al, 1992;Cuzick et al, 1994;Holowaty et al, 1999;Voglino et al, 2000). Observation of a higher frequency of HR-HPV types in women with severe dysplastic lesions and CIS than in mild dysplsia is also in agreement with earlier reports (McCance et al, 1985;Cornelissen et al, 1992;Cuzick et al, 1994;Delvenne et al 1994). Gradual increase in the frequency of high risk HPV types 16 and 18 from mild to moderate to severe dysplastic lesions to invasive cervical cancer suggests that the frequency of high risk HR-HPV infection changes as a function of severity of cervical lesions.…”

Section: Discussionsupporting

confidence: 92%

Telomerase activity as an adjunct to high-risk human papillomavirus types 16 and 18 and cytology screening in cervical cancer

et al. 2006

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Telomerase is a ribonucleoprotein comprising an RNA template, the telomerase-associated protein and its catalytic subunit, human telomerase reverse transcriptase (hTERT). Telomerase activation is a critical step in cellular immortalisation and development of cancer. Enhanced telomerase activity has been demonstrated in cervical cancer. In the present study telomerase activity and hTERT mRNA expression were evaluated and correlated with the presence of human papillomavirus (HPV) infection and cytological changes in the cervical lesions. Telomerase activity was assayed by telomeric repeat amplification protocol, hTERT mRNA expression by reverse transcriptase polymerase chain reaction and presence of high risk HPV (HR-HPV) infection by polymerase chain reaction. Out of 154 cervical samples of different cytology, 90 (58.44%) were positive for HR-HPV types 16/18, while among 55 normal cervical scrapes, 10 (18.18%) were HPV DNA positive. All 59 invasive cancer samples showed a very high telomerase activity. Among dysplasia, seven (63.6%) mild dysplasia, 18 (100%) of moderate, 20 (100%) of severe dysplasia and 6 (100%) carcinoma in situ (CIS) samples were positive with mild to moderate to high to very high telomerase activity respectively. Seven (12.7%) samples of apparently normal cervical scrapes were weakly positive for telomerase activity. We observed a good correlation (Po0.001) between telomerase activity and HR-HPV 16/18 positivity with a sensitivity of 88.1% for HPV and 100% for telomerase activity. It is suggested that telomerase activity may be used as an adjunct to cytology and HPV DNA testing in triaging women with cervical lesions.

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Section: Discussionsupporting

confidence: 92%

Telomerase activity as an adjunct to high-risk human papillomavirus types 16 and 18 and cytology screening in cervical cancer

et al. 2006

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“…However, in studies of CIN, the definition of a case is generally based on cytological and histological criteria, and it can be difficult to distinguish, on morphological grounds only, CIN from the subclinical HPV infection sometimes referred to as 'flat and atypical condylomas' (Koss, 1987). A number of studies have reported high rates of reclassification from CINI to HPV infection using recently developed cytological criteria, which may also reflect a high prevalence of mixed CIN/HPV lesions (Meisels et al, 1982(Meisels et al, , 1983 (Crum et al, 1986;Schneider et al, 1987;Wagner et al, 1984 (Meanwell et al, 1987), and only two others even mention the mean age of cases and controls (McCance et al, 1985;Toon et al, 1986).…”

Section: Definition Of Cases and Controlsmentioning

confidence: 99%

“…The table gives the number of subjects tested in each cervical lesion group (invasive carcinoma, cervical intraepithelial neoplasia, referred to as CIN, or normal), and the percentage positive for various types of HPV in each group. In five of these studies, HPV prevalence rates are given separately for the three degrees of CIN (Lorincz et al, 1986;McCance et al, 1985;Schneider et al, 1985;Schneider et al, 1987;Wagner et al, 1984). The initial impression is that within each study women with cervical neoplasia have HPV DNA of types 16 and 18 detectable in their cervical cells more frequently than women with normal cervices, that the prevalence rates increase with the severity of the lesion, and that there is a considerable variation in prevalence within each lesion group, although most of the studies are based on small numbers and different hybridisation techniques have been used.…”

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confidence: 99%

Does human papillomavirus cause cervical cancer? The state of the epidemiological evidence

Muñóz

Bosch²,

Kaldor³

1988

Br J Cancer

188

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Summary The human papillomavirus has emerged over the past decade as the leading candidate to be the sexually transmitted aetiological factor in cervical cancer. Although it appears that papillomavirus types 16 and 18 are associated with a higher risk of advanced cervical neoplasia, most of the evidence comes from studies which do not satisfy basic epidemiological requirements, and are therefore difficult to interpret. The most significant problems are the small sample size, potentially biased selection of study subjects, the difficulties in cytologically distinguishing precancerous lesions from papilloma infection of the cervix, the unknown specificity and sensitivity of the various hybridisation methods for determining papillomavirus infection status, and the statistical analyses and presentation of results. On the basis of the existing studies, one is forced to conclude that, while experimental data suggest an oncogenic potential for HPV, the epidemiological evidence implicating it as a cause of cervical neoplasia is still rather limited.

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“…These observations all point to the existence of a venereally transmitted causative agent (Beral, 1974) and there is now much evidence to indicate that certain types of the human papilloma virus (HPV) have a central role in this process. HPV DNA has been found in invasive cancers (Durst et al, 1983;zur Hausen, 1984;McCance et al, 1985;Grubb, 1986), pre-invasive lesions (Walker et al, 1984;Campion et al, 1985;De Villiers et al, 1987) and has been found to be related to progression of disease (Campion et al, 1986). Promiscuity in men has also been linked to increased risk in their sexual partners (Buckley et al, 1981;Zunzunegui et al, 1986) and recent studies have shown that males harbour human papilloma virus in penile lesions Villa & Lopes, 1986) and that sexual partners share increased risk of genital cancer (Kessler, 1976;Smith et al, 1980;Barrasso et al, 1987).…”

mentioning

confidence: 99%

A case-control study of cervix cancer in Singapore

Cuzick

Stavola²,

McCance³

et al. 1989

Br J Cancer

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Summary Cervix cancer is about twice as common in Asia as in the Western world and its incidence varies among different Asian ethnic groups. A study based in Singapore, the population of which comprises Chinese, Indians and Malaysians, offers the opportunity to evaluate whether the same risk factors are important in this part of the world as in the West.A total of 135 cases and an equal number of controls were interviewed and details concerning reproductive and sexual history, smoking, hygiene, socio-economic status and education were collected. Seventy-three cases had invasive cancer while 62 had micro-invasive disease or CIN III. The most important risk factors were parity and number of sexual partners. Smoking was rare in cases and controls and did not appear to be an important determinant of risk. Of the socio-economic factors, education appeared most predictive and lowered the risk. Age at first intercourse was strongly correlated with education (positively) and parity (negatively), but not with number of sexual partners. Biopsies were available for HPV DNA analysis in 38 cases and 37% were positive, mostly for HPV type 16. All these factors gave similar risks in invasive and preinvasive disease.A fairly consistent picture of risk factors for cervical cancer is now emerging from studies in Western Countries (Cramer, 1982). The most important of these are factors related to sexual behaviour and elevated risks have been associated with multiple sexual partners and having been divorced

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Prevalence of human papillomavirus type 16 DNA sequences in cervical intraepithelial neoplasia and invasive carcinoma of the cervix

Cited by 193 publications

References 11 publications

Telomerase activity as an adjunct to high-risk human papillomavirus types 16 and 18 and cytology screening in cervical cancer

Telomerase activity as an adjunct to high-risk human papillomavirus types 16 and 18 and cytology screening in cervical cancer

Does human papillomavirus cause cervical cancer? The state of the epidemiological evidence

A case-control study of cervix cancer in Singapore

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