Invited Commentary

Abstract

A viral etiology of cancer is not a novel concept in the oncology field, inasmuch as some of the earliest scientific breakthroughs to an understanding of human cancers came from seminal laboratory work with tumors caused by viruses such as the Rous sarcoma virus. In a recent Lancet Oncology article, it was estimated that approximately 16%, or 2 million, of cancer cases worldwide can be attributable to an infectious cause [1de Martel C. Ferlay J. Franceschi S. et al.Global burden of cancers attributable to infections in 2008: a review and synthetic analysis.Lancet Oncol. 2012; 13: 607-615Abstract Full Text Full Text PDF PubMed Scopus (1736) Google Scholar], and just over 600,000 cases worldwide are associated specifically with human papillomavirus (HPV) infection [2Forman D. de Martel C. Lacey C.J. et al.Global burden of human papillomavirus and related diseases.Vaccine. 2012; 30: F12-F23Crossref PubMed Scopus (1103) Google Scholar]. The worldwide HPV prevalence averages 11%, but it can be as high as 20% to 30% in regions such as eastern Europe, eastern Africa, and the Caribbean. In the remainder of Europe, northern Africa, and Asia, the prevalence ranges between 7% and 10%. In North America, the prevalence of HPV is estimated at 5%. Although HPV prevalence is higher in less developed countries and lower in more developed ones, even the low prevalence rates seen in developed countries translates into real patients with real cancers. Much is now known about the oncogenic properties and mechanistic pathways of HPV infection in carcinogenesis. Although HPV 16 and HPV 18 are the subtypes most commonly associated with cervical carcinoma, the current article by Chen and colleagues [3Chen S.P. Hsu N.Y. Wu J.Y. et al.Association of p53 codon 72 genotypes and clinical outcome in human papillomavirus-infected lung cancer patients.Ann Thorac Surg. 2013; 95: 1196-1203Abstract Full Text Full Text PDF PubMed Scopus (12) Google Scholar] provides data to suggest that in lung cancer, more important than mere HPV infection are the combined effects of HPV oncogenic proteins E6 and E7 (although only E6 demonstrated strong associations in this study) and p53 polymorphisms, which result in increased p53 degradation and further loss of a key tumor suppressor in cells at risk. Another important point is that not all lung cancers are derived from inhaled carcinogens of smoking tobacco, and the mechanistic pathways discussed here constitute another possible pathway for lung cancer to develop in the nonsmoking patient. From an epidemiologic standpoint, many are cautiously optimistic that the recently developed HPV vaccine may be able to prevent many such cancers in the future. Association of p53 Codon 72 Genotypes and Clinical Outcome in Human Papillomavirus-Infected Lung Cancer PatientsThe Annals of Thoracic SurgeryVol. 95Issue 4PreviewWe recently reported that high-risk human papillomavirus (HPV) 16/18 E6 protein was associated with p53 protein degradation in lung cancer. The present study addressed the relationship between the different p53 genotypes and HPV oncoprotein expression with respect to p53 protein degradation and clinical outcome in primary lung cancer patients. Full-Text PDF