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Some hrHPV genotypes incur higher risk of precancer than others.1

Addressing the need for enhanced risk stratification

As the inclusion of HPV triage testing in cervical screening results in the identification of more women at high risk, a new limitation is emerging — the lack of enhanced risk stratification that can identify those women who require more aggressive management.1

Current practice can involve repeating cytology and pooled hrHPV DNA testing in 6 or 12 months for women with borderline or low-grade dyskaryosis cytology and a positive hrHPV DNA result, following colposcopy without treatment of CIN1. This approach, while an improvement on cytology alone in the early detection of precancer or cervical cancer, remains limited by:

  • Lack of HPV 16/18 genotype-specific results, which allows for risk stratification
  • Delays in clinical intervention for those at highest risk.
  • Uncertainty and anxiety on the part of both clinician and patient when the patient has repeat borderline or low-grade dyskaryosis cytology and a positive hrHPV DNA result.

HPV 16/18 genotyping identifies women at the greatest risk of ≥CIN3.

Rate of ≥CIN3 by hrHPV status

10-year cumulative incidence rate of CIN3 by hrHPV status2

10-year Cumulative Incidence Rate of CIN3 by hrHPV Status

Women with HPV 16 and 18 are at greatest risk of developing high-grade cervical lesions2

In a seminal study of 20,810 women in the Kaiser Permanente healthcare system, of the population of women with normal cytology, those who were HPV 16 positive and those who were HPV 18 positive were shown to be at the highest risk of developing ≥CIN3.

Discover a woman’s risk for ≥CIN2.

These case studies are intended to provide educational information and the materials and opinions referenced may not be supported by Roche in their entirety. While we do our best to fact check all information presented, you should not rely on this information as complete, or always up-to date. Nothing in the case studies is intended to constitute medical advice and the case studies should not be relied on for this or any other purpose.

  • Acronyms:


1. cobas® 4800 HPV Test US package insert. April 2011.

2. Khan MJ, Castle PE, Lorincz AT, et al. The elevated 10-year risk of cervical precancer and cancer in women with human papillomavirus (HPV) type 16 or 18 and the possible utility of type-specific HPV testing in clinical practice. J Natl Cancer Inst. 2005;97(14):1072-1079.

3. The American Congress of Obstetricians and Gynecologists. ACOG Practice Bulletin. Clinical Management Guidelines for Obstetrician-Gynecologists: Screening for Cervical Cancer. November, 2012.

4. Legood R, Smith M, Lew JB, et al. Cost effectiveness of human papillomavirus test of cure after treatment for cervical intraepithelial neoplasia in England: economic analysis from NHS Sentinel Sites Study. BMJ 2012;345:e7086 doi: 10.1136/bmj.e7086. published 31 October 2011.

5. Bosch FX, de Sanjosé S. Human papillomavirus and cervical cancer — burden and assessment of causality. J Natl Cancer Inst Monogr. 2003;31:3-13.

6. Bulk S, Berkhof J, Bulkmans NW, et al. Preferential risk of HPV16 for squamous cell carcinoma and of HPV18 for adenocarcinoma of the cervix compared to women with normal cytology in The Netherlands. Br J Cancer. 2006;94(1):171-175.

7. Ault KA, Joura EA, Kjær SK, et al. Adenocarcinoma in situ and associated human papillomavirus type distribution observed in two clinical trials of a quadrivalent human papillomavirus vaccine. Int J Cancer. 2011;128(6):1344-1353.

8. de Sanjosé S, Quint WG, Alemany L, et al. Human papillomavirus genotype attribution in invasive cervical cancer: a retrospective cross-sectional worldwide study. Lancet Oncol. 2010;11(11):1048-1056.

9. Kjær SK, Frederiksen K, Munk C, Ifner T. Long-term absolute risk of cervical intraepithelial neoplasia grade 3 or worse following human papillomavirus infection: role of persistence. J Natl Cancer Inst. 2010;102(19):1478-1488.-