Lung adenocarcinoma and human papillomavirus infection

Our plain-English summary of Lung adenocarcinoma and human papillomavirus infection, by Y.C. Chen, J.H. Chen, K. Richard, et al (Cancer, 2004).

The study

• Authors: Y.C. Chen, J.H. Chen, K. Richard, P.Y. Chen, D.C. Christiani
• Journal: Cancer
• Published: 2004;101(6):1428-36
• Type of article: Review
• Cited by: 58 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Abstract

Over the past three decades, the incidence of lung adenocarcinoma has increased worldwide. Most individuals with lung adenocarcinoma (especially women) are nonsmokers. Reported risk factors for the development of lung adenocarcinoma include cigarette smoking; exposure to cooking fumes, air pollution, second-hand smoke, asbestos, and radon; nutritional status; genetic susceptibility; immunologic dysfunction; tuberculosis infection; and asthma. Human papillomavirus (HPV) infection is a known risk factor for the development of squamous cell carcinoma (SCC), but it has not been thoroughly assessed as a potential risk factor for the development of pulmonary adenocarcinoma. More than 50% of people are infected with HPV during their lifetimes, either via intrauterine or postnatal infection. Recent studies involving Taiwanese patients have demonstrated a possible association between HPV infection and the risk of developing pulmonary adenocarcinoma. HPV transmission pathways have not yet been conclusively identified. The observation of certain types of HPV in association with cervical and oral SCC raises the possibility of sexual transmission of HPV from the cervix to the oral cavity, with subsequent transmission to the larynx and then to the lung. HPV infection and metaplasia in lung tissue may increase an individual's susceptibility to the tumorigenesis of pulmonary adenocarcinoma. Further epidemiologic and pathologic investigations will be necessary to establish a causal relation.

Copyright 2004 American Cancer Society.

In plain English

This article was a review, not a new study. The authors searched Medline, PubMed and Embase for research published up to 2004 on human papillomavirus (HPV) infection and lung adenocarcinoma. Asbestos appeared briefly: occupational asbestos exposure was listed as a previously reported risk factor, and the authors stated that women's exposure to asbestos, radon and air pollution was low compared with tobacco smoke. The review presented no asbestos data of its own. In the reviewed studies, HPV was found in the lungs of 9% to 42% of Asian and 0% to 36% of Western lung adenocarcinoma patients. One Taiwanese study reported an odds ratio of 10.12 (95% confidence interval 3.88 to 26.38) for HPV-16/18 infection in nonsmoking women with lung cancer over 60, compared with female smokers of that age. For a Taiwanese blood study, the review's table listed HPV-16 in 50 of 90 lung cancer patients (56%) and HPV-18 in 29 of 90 (32%), but its text described the 56% as adenocarcinoma patients positive for both types. The authors concluded that HPV infection may increase lung adenocarcinoma risk.

We wrote this plain-English summary from the full article with the help of AI, and a second AI model checked each sentence against the article. It is not the authors' wording; the abstract and the article are their own account.

What the study did and found

• Design: Review of published literature (no new data collected)
• Who was studied: Published articles found through Medline and PubMed (1966 to 2004) and Embase (1991 to 2004). The reviewed studies covered lung cancer patients in Taiwan, China, Japan, the U.S., France, Finland and Poland.
• Exposure: HPV infection, mainly types 16 and 18, along with others such as types 6, 11, 31, 33 and 35. Asbestos was not the review's subject. Occupational exposure to asbestos and radon was listed as a previously reported risk factor for lung adenocarcinoma. The authors also stated that women's exposure to asbestos, radon and air pollution is low compared with their exposure to tobacco smoke. No asbestos data were presented.
• Main results:
  • Among Asians with lung adenocarcinoma in the reviewed studies, the percentage with HPV infection in the lung ranged from 9% to 42%.
  • Among individuals with lung adenocarcinoma in Western studies, the prevalence of HPV infection in the lung ranged from 0% to 36%.
  • In one Taiwanese study (Cheng et al., 2001), nonsmoking women with lung cancer older than 60 had a higher risk of HPV-16/18 infection than female smokers of the same age: odds ratio 10.12 (95% confidence interval 3.88 to 26.38).
  • For the Taiwanese blood study (Chiou et al., 2003), the review's Table 3 lists HPV-16 in 50 of 90 lung cancer patients (56%) and HPV-18 in 29 of 90 (32%). The review's text instead says 56% of patients with lung adenocarcinoma were positive for HPV-16 and HPV-18, which does not match the table.
  • In that same Taiwanese blood study, as described in the review, lung cancer risk was increased by a factor of 6.5 (95% CI 3.7 to 11.3) for HPV-16, by 9.2 (95% CI 4.2 to 20.2) for HPV-18, and by 76 (95% CI 9.8 to 582.1) for both types together.
  • In one U.S. study (Yousem et al.), none of 28 adenocarcinomas or small cell carcinomas were positive for HPV. The only Western serum study found 2 of 51 adenocarcinoma patients (4%) positive for HPV type 16.
  • In a Japanese cohort, HPV DNA was found in 18 of 23 adenosquamous carcinomas (78%).
• The authors' conclusion: The authors concluded that findings in Taiwanese women suggest a possible link between HPV and lung adenocarcinoma in female nonsmokers. They said HPV infection may increase the risk of lung adenocarcinoma, that the mechanism is unclear, and that further studies are necessary.
• Limitations the authors state:
  • Few studies have assessed this risk, and those that have involved relatively small cohorts.
  • Low viral loads and differences in tumor sampling and HPV detection methods may explain the wide variation in reported HPV detection rates.
  • Few U.S. studies exist, and they did not report patient ethnicity. Some Western studies lacked data on patient gender.
  • HPV transmission pathways have not been identified.

Topics

The National Library of Medicine indexes this study under subjects our site covers: Lung cancer.

Medical terms in this study, explained in our Lexicon: Lung Adenocarcinoma, Squamous Cell Carcinoma, Adenocarcinoma, Tumorigenesis.

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