HPV infections and lung cancer

Our plain-English summary of HPV infections and lung cancer, by K.J. Syrjänen (Journal of Clinical Pathology, 2002).

The study

• Author: K.J. Syrjänen
• Journal: Journal of Clinical Pathology
• Published: 2002;55(12):885-91
• Type of article: Review
• Cited by: 111 articles, as counted by NIH iCite
• Read it: PubMed · Publisher · Free full text

Abstract

Because of the major clinical impact of bronchial cancer worldwide, the possibility that human papillomavirus (HPV) contributes to its pathogenesis as a co-carcinogen is an intriguing one. Bronchial squamous cell carcinoma develops through well defined precursor lesions, often at the sites of squamous metaplasia. Benign squamous cell papillomas are rare but HPV DNA has been found in almost half of those studied, implicating a causal association. In invasive bronchial cancer, morphological changes seen in HPV lesions elsewhere are often seen. HPV DNA has been detected in 21.7% of the 2,468 bronchial carcinomas analysed to date and the same high risk types implicated in other squamous cell cancers have been identified. Clearly, more effort should be focused on assessing the role of HPV in bronchial carcinogenesis, by analysing the synergistic effects of carcinogenic agents (cigarette smoke, radiation, asbestos, etc) and HPV in different experimental settings.

In plain English

This article was a review by a single author of published research on whether human papillomavirus (HPV) may play a part in bronchial (lung) tumours. It reported no new patients. Instead, the author pooled earlier studies that tested tumour tissue for HPV DNA. In 61 benign bronchial squamous cell papillomas, HPV DNA was found in 29, mostly the low-risk types HPV-6 and HPV-11. Across 2468 bronchial carcinomas studied up to May 2002, HPV DNA was reported in 536 (21.7%). Detection rates in individual studies ranged from 0% to 100%, and the rate in lung adenocarcinomas was much lower. The review did not study asbestos directly. It described other researchers' laboratory experiments in which an HPV-immortalised human bronchial cell line (BEP2D) underwent stepwise malignant transformation after exposure to asbestos fibres or radiation. The author concluded that HPV might act as a co-carcinogen in bronchial cancer and that the hypothesis still awaits final confirmation. The author called for more research, including studies of combined effects of HPV with cigarette smoke, radiation and asbestos.

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: Narrative literature review of published studies on HPV and primary bronchial tumours (benign papillomas and carcinomas), including a pooled tally of HPV DNA detection results
• Who was studied: Published studies from several countries, up to May 2002. They covered 61 benign bronchial squamous cell papillomas and 2468 bronchial carcinomas tested for HPV DNA.
• Exposure: HPV infection, detected by hybridisation methods or PCR, including high-risk types 16, 18, 31, 33 and 35 and low-risk types 6 and 11. Asbestos appears only as a suspected co-factor and in other researchers' cell-line experiments using an HPV-immortalised bronchial cell line (BEP2D).
• Main results:
  • Benign bronchial squamous cell papillomas: HPV DNA was found in 29 of 61 lesions analysed, predominantly HPV-6 and HPV-11.
  • Bronchial carcinomas in 24 studies published until January 1998: 201 of 1061 (18.9%) contained HPV DNA. HPV-16 accounted for 49.8% of positive cases and HPV-18 for 21.8%.
  • Additional mostly Japanese or Chinese studies from 1985 to 1997: 32 of 156 extra carcinoma cases (20.5%) were HPV DNA positive.
  • Studies from 1998 to 2002: 303 of 1251 newly analysed carcinomas (24.2%) contained HPV DNA.
  • All bronchial carcinomas combined: HPV DNA was reported in 536 of 2468 (21.7%).
  • In lung adenocarcinomas the HPV detection rate was much lower, and many studies found no HPV DNA in these tumours.
  • Other researchers' experiments with the BEP2D cell line suggested that activation of the insulin receptor pathway and inactivation of DCC and Ku70 may cooperate in asbestos-induced malignant transformation of these cells.
• The authors' conclusion: The author concluded that HPV might contribute to bronchial cancer as a co-carcinogen. In the author's view, the roughly 20% HPV prevalence leaves room for other agents, and more clinical, epidemiological and laboratory research is needed, including on the combined effects of cigarette smoke, radiation, asbestos and HPV.
• Limitations the authors state:
  • Only a small number of bronchial papilloma cases have been reported, so there are no well documented data on their biological behaviour.
  • HPV detection rates varied widely between studies, from 0% to 100%.
  • The hypothesis that HPV plays a role in bronchial carcinogenesis is still awaiting final confirmation.
  • Some studies reported at least partly the same patients; these were counted only once.

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 Cancer, Squamous Cell Carcinoma, Squamous Cell, Carcinoma, Carcinogenesis, Synergistic Effect, Carcinogenic.

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• Association of SV40 with human tumours — B. Jasani, A. Cristaudo, et al. (2001)
• New molecular and epidemiological issues in mesothelioma: role of SV40 — M. Carbone, S. Fisher, et al. (1999)
• Simian virus 40 is present in most United States human mesotheliomas, but it is rarely present in non-Hodgkin's lymphoma — P. Rizzo, M. Carbone, et al. (1999)

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