From the Editor

Why do so many women aged 65 years and older die of cervical cancer?

Author and Disclosure Information

 

References

Health systems could use information technology to mitigate these problems. For example, health systems could deploy software to assemble every cervical screening result on each woman and pre‑sent those results to clinicians in a single integrated view in the electronic record. Additionally, once all lifetime screening results are consolidated in one view, artificial intelligence systems could be used to analyze the totality of results and identify women who would benefit by continued screening past age 65 and women who could safely discontinue screening.

Option 2: Adopt the Australian approach to cervical cancer screening. The current Australian approach to cervical cancer screening is built on 3 pillars: 1) school-based vaccination of all children against hrHPV, 2) screening all women from 25 to 74 years of age every 5 years using nucleic acid testing for hrHPV, and 3) providing a system for the testing of samples self-collected by women who are reluctant to visit a clinician for screening.13 Australia has one of the lowest cervical cancer death rates in the world.

Option 3: Continue screening most women past age 65. Women >65 years of age are known to be infected with hrHPV genotypes. hrHPV infection causes cervical cancer. Cervical cancer causes many deaths in women aged >65 years. There is no strong rationale for ignoring these three facts. hrHPV screening every 5 years as long as the woman is healthy and has a reasonable life expectancy is an option that could be evaluated in randomized studies.

Given the high rate of cervical cancer death in women >65 years of age, I plan to be very cautious about discontinuing cervical cancer screening until I can personally ensure that my patient has no evidence of hrHPV infection.

Vaccination to prevent cancer is superior to screening and treating cancer

In 2008, Harald zur Hausen, MD, received the Nobel Prize in Physiology or Medicine for discovering that human papilloma virus (HPV) caused cervical cancer. In a recent study, 74% of cervical cancers were associated with HPV 16 or 18 infections. A total of 89% of the cancers were associated with one of the high-risk HPV genotypes, including HPV 16/18/31/33/45/52/58.1

Recently, HPV has been shown to be a major cause of oropharyngeal cancer. The Centers for Disease Control and Prevention calculated that in CY2015 in the United States there were 18,917 cases of HPV-associated oropharyngeal squamous cell cancer and 11,788 cases of cervical cancer.2 Most cases of HPV-associated oropharyngeal cancer occur in men, and HPV vaccination of boys may help to prevent this cancer type. Oncogenic HPV produce two proteins (E6 and E7) that promote viral replication and squamous cell growth by inhibiting the function of p53 and retinoblastoma protein. The immortalized HeLa cell line, derived from Ms. Henrietta Lack's cervical cancer, contains integrated HPV18 nucleic acid sequences.3,4

The discovery that HPV causes cancer catalyzed the development of nucleic acid tests to identify high-risk oncogenic HPV and vaccines against high-risk oncogenic HPV genotypes that prevent cervical cancer. From a public health perspective, it is more effective to vaccinate the population against oncogenic HPV genotypes than to screen and treat cancer. In the United States, vaccination rates range from a high of 92% (District of Columbia) and 89% (Rhode Island) to a low of 47% (Wyoming) and 50% (Kentucky and Mississippi).5 To reduce HPV-associated cancer mortality, the gap in vaccination compliance must be closed.

References

  1. Kjaer SK, Munk C, Junge J, et al. Carcinogenic HPV prevalence and age-specific type distribution in 40,382 women with normal cervical cytology, ACSUC/LSIL, HSIL, or cervical cancer: what is the potential for prevention? Cancer Causes Control. 2014;25:179-189.
  2. Van Dyne EA, Henley SJ, Saraiya M, et al. Trends in human papillomavirus-associated cancers - United States, 1999-2015. MMWR Morb Mortal Wkly Rep. 2018;67:918-924.
  3. Rosl F, Westphal EM, zur Hausen H. Chromatin structure and transcriptional regulation of human papillomavirus type 18 DNA in HeLa cells. Mol Carcinog. 1989;2:72-80.
  4. Adey A, Burton JN, Kitzman, et al. The haplotype-resolved genome and epigenome of the aneuploid HeLa cancer cell line. Nature. 2013;500:207-211.
  5. Walker TY, Elam-Evans LD, Singleton JA, et al. National, regional, state, and selected local area vaccination coverage among adolescents aged 13-17 years - United States, 2016. MMWR Morb Mortal Wkly Rep. 2017;66:874-882.

Next Article: