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Review
. 2002 Apr;55(4):244-65.
doi: 10.1136/jcp.55.4.244.

The causal relation between human papillomavirus and cervical cancer

F X Bosch  1 , A Lorincz, N Muñoz, C J L M Meijer, K V Shah
Affiliations
Review

The causal relation between human papillomavirus and cervical cancer

F X Bosch et al. J Clin Pathol. 2002 Apr.

Abstract

The causal role of human papillomavirus infections in cervical cancer has been documented beyond reasonable doubt. The association is present in virtually all cervical cancer cases worldwide. It is the right time for medical societies and public health regulators to consider this evidence and to define its preventive and clinical implications. A comprehensive review of key studies and results is presented.

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Figures

Figure 1
Figure 1
Evolution of epidemiological research on human papillomavirus (HPV) and cervical cancer in the past two decades. FISH, filter in situ hybridisation; GP-PCR, general primer PCR; HC I–II, hybrid capture first and second generation; PCR, polymerase chain reaction; SH, Southern blot hybridisation; TS-PCR, type specific PCR.
Figure 2
Figure 2
Scientific publications on human papillomavirus (HPV) identified by Medline and the number of research abstracts presented at the annual Papillomavirus International Conferences.
Figure 3
Figure 3
Prevalence of human papillomavirus (HPV) DNA in cases and controls in the IARC multicentre case–control study.
Figure 4
Figure 4
Selected examples of the strength of the associations (RR/ OR) between risk factors and human cancer; estimates of the attributable fraction (AF%) and of the protective fraction (PF%). Refs: the Philippines, Costa Rica, Bangkok, Taiwan, Greece, Italy, UK, Korea, and Taiwan.
Figure 5
Figure 5
Odds ratios (OR) and 95% confidence intervals for associations found in case–control studies using PCR methods between human papillomavirus 16 (HPV-16) (or its nearest surrogate) and invasive cervical cancers. *The OR estimate is ∞ owing to the absence of HPV positive controls. Adapted from IARC monograph 64, 1995.
Figure 6
Figure 6
Odds ratios (OR) and 95% confidence intervals for associations found in case–control studies using non-PCR methods between human papillomavirus 16 (HPV-16) (or its nearest surrogate) and invasive cervical cancers. *The OR estimate is ∞ owing to the absence of HPV positive controls. Adapted from IARC monograph 64, 1995.
Figure 7
Figure 7
Odds ratios (OR) and 95% confidence intervals for associations found in case–control studies after the year 2000. HPV, human papillomavirus.
Figure 8
Figure 8
Cumulative prevalence of human papillomavirus (HPV) types in cervical cancer. Taken from the IARC multicentre case–control study; preliminary data.
Figure 9
Figure 9
Age specific prevalence (%) of high rish (HR) human papillomavirus (HPV) DNA in 3700 women entering a screening programme and age specific incidence rate (x105) (ASIR) of cervical cancer in the Netherlands. Adapted from Jacobs et al and Parkin et al.
Figure 10
Figure 10
Mechanisms of human papillomavirus (HPV) carcinogenesis. HSIL, high grade squamous intraepithelial lesion; LSIL, low grade squamous intraepithelial lesion; RB, retinoblastoma gene.
See this image and copyright information in PMC

Comment in

  • Cervical cancer.
    van Diest PJ, Holzel H. van Diest PJ, et al. J Clin Pathol. 2002 Apr;55(4):241-2. doi: 10.1136/jcp.55.4.241. J Clin Pathol. 2002. PMID: 11919206 Free PMC article. No abstract available.

References

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    1. Bosch FX, Muñoz N, de Sanjosé S, et al. Risk factors for cervical cancer in Colombia and Spain. Int J Cancer 1992;52:750–58. - PubMed
    1. Schiffman MH, Bauer HM, Hoover RN, et al. Epidemiologic evidence showing that human papillomavirus infection causes most cervical intraepithelial neoplasia. J Natl Cancer Inst 1993;85:958–64. - PubMed
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