Human Papillomavirus Type-16 Homologous Dna in Normal Human Ectocervix

Cox, M. F.; Meanwell, CliveA.; Nj, Maitland; Blackledge, George; Scully, Crispian; Jordan, J.H.

doi:10.1016/s0140-6736(86)91965-3

Cited by 72 publications

(29 citation statements)

References 4 publications

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“…In some papers which do, the subjects come from a limited number of clinics or hospitals, but it is still not clear whether any further selection has taken place (Cox et al, 1986;Lorincz et al, 1986;Macnab et al, 1986;Meanwell et al, 1987;Schneider et al, 1987;Scholl et al, 1985;Wagner et al, 1984;Wickenden et al, 1985). Information on the source of cases is important in the choice of the control group.…”

Section: Hpv Prevalence Surveysmentioning

confidence: 99%

“…Some doubt has recently been cast on the role of the virus in cervix cancer by reports of high prevalence of HPV 16 and 18 in normal cervical tissue (Cox et al, 1986;Macnab et al, 1986;Meanwell et al, 1987;Reeves et al, 1987;, and the possibility that the apparent association with cervical neoplasia disappears after age-adjustment (Meanwell et al, 1987). In the light of the continuing debate about the importance of HPV infection in the aetiology of cervical cancer (Editorial, 1987a,b;Mufioz & Bosch, 1987) and confronted by practical problems in the design of our own epidemiological study, we decided to critically evaluate the available epidemiological evidence, which consists of prevalence surveys of HPV in various population groups, and some cohort studies of women with cervical HPV infection or low-grade dysplasia.…”

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confidence: 99%

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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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Section: Hpv Prevalence Surveysmentioning

confidence: 99%

mentioning

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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“…However, both HPV-16 and HPV-18 can be detected in women with undetectable or minimal cervical abnormality (3,4), and it is unclear what factors trigger HPV-16 or HPV-18 to initiate cellular transformation to a malignant phenotype.…”

Section: Introductionmentioning

confidence: 99%

The HPV-activating cellular transcription factor Brn-3a is overexpressed in CIN3 cervical lesions.

Ndisdang¹,

Morris²,

Chapman³

et al. 1998

J. Clin. Invest.

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The cervical cellular transcription factors Brn-3a and Brn-3b have antagonistic effects on transcription of the human papilloma virus types 16 and 18 E6 and E7 oncogenes, with Brn-3a activating expression and Brn-3b repressing it. We therefore measured expression of Brn-3a and Brn-3b mRNAs in biopsies from 16 women with no detectable cervical abnormality, and in 14 women with cervical intraepithelial neoplasia grade 3 (CIN3) lesions. Although the mean level of Brn-3b expression was similar in both groups, the mean level of Brn-3a expression was over 300-fold higher in the CIN3 samples when compared with normals. Elevated expression of Brn-3a was also detected in 16 histologically normal regions of the cervix adjacent to the CIN3 lesions, indicating that elevation of Brn-3a levels is not confined to the lesion in women with CIN3, and is thus not a consequence of the oncogenic process.

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“…These viruses produce oncogenic proteins E6 and E7 which are capable of transforming cells to a malignant phenotype and it is now generally accepted that the production of these proteins by HPV-16 or HPV-18 results in cervical cancer. However, infection with both HPV-16 and HPV-18 can be detected in women with no cervical abnormality (Burghardt, 1984;Cox et al, 1986). Moreover, most infections with HPV-16 or HPV-18 in young women are of short duration with median clearance times of approximately 1 year with long term persistence of the virus being associated with signi®cant risk of progression to cancerous lesions such as cervical intraepithelial neoplasia type 3 (CIN3) (Nobbenhuis et al, 1999).…”

mentioning

confidence: 99%

The Brn-3a transcription factor plays a key role in regulating the growth of cervical cancer cells in vivo

Ndisang¹,

Budhram-Mahadeo²,

Pedley

et al. 2001

Oncogene

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The cellular Brn-3a transcription factor is known to activate transcription of the genes encoding the human papilloma virus E6 and E7 proteins and is over-expressed in women with cervical neoplasia. We show that cervical cell lines with reduced Brn-3a expression show a greatly reduced ability to form tumours in nude mice compared to control cells and also show reduced expression of the HPV E6 and cellular Bcl-2 oncogenes. These e ects are also observed in cervical cells over-expressing the related Brn-3b factor, which is known to antagonize activation of HPV gene expression by Brn-3a. These results demonstrate, for the ®rst time, that inhibition of Brn3a expression or enhanced Brn-3b expression can inhibit cervical cell-derived tumour growth in vivo as well as in vitro. Hence they establish Brn-3a as a key factor in cervical tumorigenesis and as a potential therapeutic target in human cervical neoplasia. Oncogene (2001) 20, 4899 ± 4903.

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Human Papillomavirus Type-16 Homologous Dna in Normal Human Ectocervix

Cited by 72 publications

References 4 publications

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

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

The HPV-activating cellular transcription factor Brn-3a is overexpressed in CIN3 cervical lesions.

The Brn-3a transcription factor plays a key role in regulating the growth of cervical cancer cells in vivo

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