Cervical cancer risk factors

Prevention

Preventable cases of cervical cancer, UK

HPV

Cervical cancer cases linked to human papillomavirus (HPV) infection, UK

Oral contraceptives

Cervical cancer cases linked to the use of oral contraceptives, UK

Smoking

Cervical cancer cases linked to exposure to tobacco smoke, UK

100% of cervical cancer cases each year in the UK are linked to major lifestyle and other risk factors.[1]

Cervical cancer is associated with a number of risk factors.[2,3]

Cervical Cancer Risk Factors

  Increases risk Decreases risk
'Sufficient' or 'convincing' evidence
  • Diethylstilbestrol (in utero exposure)[a]
  • Oestrogen-progestogen contraceptives
  • Human immunodeficiency virus (HIV) type 1
  • Human papillomavirus (HPV) types 16, 18, 31, 33, 35, 39, 45, 51, 52, 56, 58, 59
  • Tobacco smoking
 
'Limited' or 'Probable' evidence
  • HPV types 26, 53, 66, 67, 68, 70, 73, 82
 

International Agency for Research on Cancer (IARC) and World Cancer Research Fund/American Institute for Cancer Research (WCRF/AICR) classifications.

a IARC classifies evidence on in utero diethylstilbestrol exposure as sufficient for cervical adenocarcinoma; and as limited for cervical squamous cell carcinoma.

Last reviewed:

International Agency for Research on Cancer (IARC) classifies the role of this risk factor in cancer development.[1]

HPV infection

All cervical cancers in the UK are linked to HPV, because HPV is a necessary cause of cervical cancer;[2,3] however some HPV types are high-risk for cervical cancer, others are low-risk.

HPV infection is common, but progresses to cervical cancer in a minority of cases.[4] Around 12% of women without cervical abnormalities in the UK and Ireland are infected with high-risk HPV types, a meta-analysis has shown.[5] The highest prevalence is in younger women.[5] Around half of HPV infections clear within 6-12 months, though high-risk HPV types persist longer than low-risk types, a meta-analysis showed.[6]

Fewer than 10% of persistent HPV infections progress to carcinoma in situ,[6] which left untreated, can progress to cervical cancer.[4]

HPV16 and HPV18 account for 58% and 16% respectively of all cervical cancer cases in Europe, a pooled analysis showed.[7] These types are protected against by the UK HPV vaccination programme.

Cervical cancer risk is not associated with infection with low-risk HPV types, cohort studies have shown.[8,9] Cervical cancer risk is higher in women with genital warts (GW) versus those without, a cohort study showed;[10] though GW are usually caused by low-risk HPV types (6 and 11), co-infection with high-risk HPV types is likely.[10]

HPV exposure

Other factors may be associated with cervical cancer risk because they increase the risk of Human papillomavirus (HPV) exposure or persistent HPV infection (and/or may have direct effects, independent of HPV).[11]

Cervical cancer risk is almost three times higher in women who have had 6 or more sexual partners, compared with those who have had only one, a pooled analysis showed.[12] Cervical cancer risk is around doubled in women who first had sexual intercourse aged 14 or younger, compared with those who did so aged 25 or older, a pooled analysis showed.[12]

Cervical cancer risk is around halved in women whose only current male sexual partner is circumcised, compared with those whose partner is uncircumcised, a pooled analysis showed;[13] HPV prevalence is lower in circumcised versus uncircumcised men, a meta-analysis showed.[14]

References

  1. International Agency for Research on Cancer. List of Classifications by cancer sites with sufficient or limited evidence in humans, Volumes 1 to 117. Accessed January 2017.
  2. Parkin DM, Boyd L, Walker LC. The fraction of cancer attributable to lifestyle and environmental factors in the UK in 2010. Br J Cancer 2011;105(S2):S77-S81.
  3. Walboomers JM, Jacobs MV, Manos MM, et al. Human papillomavirus is a necessary cause of invasive cervical cancer worldwide. J Pathol 1999;189(1):12-9.
  4. Kulasingam SL, Havrilesky L, Ghebre R, Myers ER. Screening for Cervical Cancer: A Decision Analysis for the U.S. Preventive Services Task Force. Rockville (MD): Agency for Healthcare Research and Quality (US); 2011.
  5. Anderson L, O'Rorke M, Jamison J, Wilson R, Gavin A; HPV Working Group members Prevalence of human papillomavirus in women attending cervical screening in the UK and Ireland: new data from northern Ireland and a systematic review and meta-analysis. J Med Virol 2013;85(2):295-308.
  6. Rositch AF, Koshiol J, Hudgens MG. Patterns of persistent genital human papillomavirus infection among women worldwide: a literature review and meta-analysis. Int J Cancer 2013;133(6):1271-85.
  7. Smith JS, Lindsay L, Hoots, et al. Human papillomavirus type distribution in invasive cervical cancer and high-grade cervical lesions: a meta-analysis update. Int J Cancer 2007;121(3):621-32.
  8. Castle PE, Hunt WC, Langsfeld E, Wheeler CM; New Mexico HPV Pap Registry Steering Committee. Three-year risk of cervical precancer and cancer after the detection of low-risk human papillomavirus genotypes targeted by a commercial test. Obstet Gynecol 2014;123(1):49-56.
  9. Thomsen LT, Frederiksen K, Munk C, et al. High-risk and low-risk human papillomavirus and the absolute risk of cervical intraepithelial neoplasia or cancer. Obstet Gynecol 2014;123(1):57-64.
  10. Blomberg M, Friis S, Munk C, Bautz A, Kjaer SK. Genital warts and risk of cancer: a Danish study of nearly 50 000 patients with genital warts. J Infect Dis 2012;205(10):1544-53.
  11. Cogliano VJ, Baan R, Straif K, et al. Preventable exposures associated with human cancers. J Natl Cancer Inst 2011;103(24):1827-39.
  12. International Collaboration of Epidemiological Studies of Cervical Cancer. Cervical carcinoma and sexual behaviour: collaborative reanalysis of individual data on 15,461 women with cervical carcinoma and 29,164 women without cervical carcinoma from 21 epidemiological studies. Cancer Epidemiol Biomarkers Prev 2009;18(4):1060-9.
  13. Castellsagué X, Bosch FX, Muñoz N. Male circumcision, penile human papillomavirus infection, and cervical cancer in female partners. N Engl J Med 2002;346(15):1105-12.
  14. Albero G, Castellsagué X, Giuliano AR, Bosch FX. Male circumcision and genital human papillomavirus: a systematic review and meta-analysis. Sex Transm Dis 2012;39(2):104-13.
Last reviewed:

International Agency for Research on Cancer (IARC) classifies the role of this risk factor in cancer development.[1]

Cervical cancer risk is 6 times higher in women with HIV/AIDS, versus women in the general population, a meta-analysis showed.[2] Cervical cancer risk among women with HIV may be reduced by treatment with highly active antiretroviral therapy (HAART), perhaps because HAART improves immune function to support Human papillomavirus (HPV) clearance.[3-6]

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International Agency for Research on Cancer (IARC) classifies the role of this risk factor in cancer development.[1] An estimated 10% of cervical cancers in the UK are linked to use of OCs.[2]

Cervical cancer risk is up to doubled in current OC users who have used OCs for 5+ years, compared with never users, pooled- and meta-analyses have shown.[3-5] Cervical cancer risk may increase with longer duration of use,[3,4] but is no higher in women who last took OCs 10+ years ago, compared with never-users.[3]

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Having children

Cervical cancer risk is 15% higher in women who have had 1 full-term pregnancy compared with those who have had none, a pooled analysis showed; the risk increases with number of full-term pregnancies.[1] Cervical cancer risk among parous women is 64% higher in those with 7+ full-term pregnancies, versus those with 1 or 2, this pooled analysis showed.[1] The association with parity is limited to squamous cell carcinoma, with no association for adenocarcinoma, this pooled analysis showed.[1] The reasons for these associations are unknown.

Younger age at first giving birth

Cervical cancer risk among parous women is 77% higher in those under 17 years old at their first full-term pregnancy, compared with those aged 25 or older, a pooled analysis has shown; the risk decreases with older age at first full-term pregnancy.[1] The association with age at first full-term pregnancy is limited to squamous cell carcinoma, with no association for adenocarcinoma, this pooled analysis showed.[1]

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International Agency for Research on Cancer (IARC) classifies the role of this risk factor in cancer development.[1] An estimated 7% of cervical cancers in the UK are linked to tobacco smoking.[2]

Cervical squamous cell carcinoma (SCC) risk is 46% higher in current smokers versus never-smokers, a pooled analysis showed.[3] Cervical SCC (invasive or in situ) risk increases with number of cigarettes smoked per day, a pooled analysis showed.[3]

Cervical SCC risk is not associated with past smoking, only current smoking, a pooled analysis showed.[3] Carcinoma in situ risk is 83% higher in current smokers, and 32% higher in past smokers, versus never-smokers, a pooled analysis showed.[3] Cervical adenocarcinoma risk is not associated with smoking, a pooled analysis showed.[3] Cervical cancer risk may be higher in current smokers because they are more likely to have human papillomavirus (HPV) infection (more likely to contract HPV, less able to clear HPV, or both),[4] or because smoking causes cancerous progression in HPV-infected cells.[3]

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Cervical squamous cell carcinoma risk is 74-80% higher in women with a first-degree relative (mother, sister, daughter) with cervical squamous cell carcinoma, compared with the general population, a cohort study showed.[1] Cervical adenocarcinoma risk is 39-69% higher in women with a first-degree relative with cervical squamous cell carcinoma, compared with the general population, a cohort study showed.[1]

This probably reflects shared environmental risk factors including human papillomavirus (HPV) infection, as well as possible genetic factors.[1]

Last reviewed:

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