The Role of Human Papilloma Virus in Lung Cancer: A Review of the Evidence

Papillomaviruses are small nonenveloped DNA viruses that infect squamous epithelial cells. These viruses have been found in many organisms. Human papillomaviruses (HPVs) give rise to a large spectrum of epithelial lesions, mainly benign hyperplasia (eg, warts and papillomas) with low malignant potential. There is a subgroup of HPV, the “high-risk” HPV, which is associated with precancerous and cancerous lesions. A small fraction of people infected with high-risk HPV will develop cancers that usually arise many years after the initial infection (Psyrri and Dimaio, Nat Clin Pract Oncol. 2008;5:24–31). Nonsmall cell lung cancer is a heterogeneous disease. The most common histologic subtypes include squamous cell carcinoma, adenocarcinoma, and large cell carcinoma. Despite different histologies, nonsmall cell lung cancers are often classified together because of similarities in approach and management of the disease. In this article, we reviewed the current literature on lung cancer and HPV. On the basis of this data, we suggested a possible mechanism of carcinogenesis induced by HPV.

[1]  C. Meijer,et al.  HPV-mediated transformation of the anogenital tract. , 2005, Journal of clinical virology : the official publication of the Pan American Society for Clinical Virology.

[2]  K. Syrjänen,et al.  HPV infections and lung cancer , 2002, Journal of clinical pathology.

[3]  N. S. Murthy,et al.  Infection of human papillomavirus type 18 and p53 codon 72 polymorphism in lung cancer patients from India. , 2005, Chest.

[4]  C. Clavel,et al.  Detection of human papillomavirus DNA in bronchopulmonary carcinomas by Hybrid Capture II , 2000, Cancer.

[5]  C. Yoon,et al.  alpha(6) Integrin is the main receptor of human papillomavirus type 16 VLP. , 2001, Biochemical and biophysical research communications.

[6]  M. Ciotti,et al.  Human papillomavirus infections in lung cancer. Detection of E6 and E7 transcripts and review of the literature. , 2007, Anticancer research.

[7]  K. Münger,et al.  Targeted degradation of the retinoblastoma protein by human papillomavirus E7‐E6 fusion proteins. , 1992, The EMBO journal.

[8]  Ya‐Wen Cheng,et al.  The presence of human papillomavirus type 16/18 DNA in blood circulation may act as a risk marker of lung cancer in Taiwan , 2003, Cancer.

[9]  S. Akiba,et al.  Human papillomavirus in lung carcinomas among three Latin American countries. , 2006, Oncology reports.

[10]  T. Kiyono,et al.  Both Rb/p16INK4a inactivation and telomerase activity are required to immortalize human epithelial cells , 1998, Nature.

[11]  T. Kiyono,et al.  Basic mechanisms of high‐risk human papillomavirus‐induced carcinogenesis: Roles of E6 and E7 proteins , 2007, Cancer science.

[12]  D. Lowy,et al.  In vitro biological activities of the E6 and E7 genes vary among human papillomaviruses of different oncogenic potential , 1991, Journal of virology.

[13]  M. Scheffner,et al.  Localization of the E6-AP regions that direct human papillomavirus E6 binding, association with p53, and ubiquitination of associated proteins , 1993, Molecular and cellular biology.

[14]  M. Pillai,et al.  Human papillomavirus and disease mechanisms: relevance to oral and cervical cancers. , 2005, Oral diseases.

[15]  K. Luh,et al.  Epidemiologic characteristics and multiple risk factors of lung cancer in Taiwan. , 1990, Anticancer research.

[16]  A. Levine,et al.  Association of human papillomavirus types 16 and 18 E6 proteins with p53. , 1990, Science.

[17]  K. Syrjänen,et al.  Detection and expression of human papillomavirus oncogenes in non-small cell lung cancer. , 2006, Oncology reports.

[18]  M. Mahmoodi,et al.  Relationship between lung cancer and human papillomavirus in north of Iran, Mazandaran province. , 2007, Cancer letters.

[19]  K. Syrjänen Condylomatous changes in neoplastic bronchial epithelium. Report of a case. , 1979, Respiration; international review of thoracic diseases.

[20]  M. Vidal,et al.  Human papillomavirus 16 E6 oncoprotein binds to interferon regulatory factor-3 and inhibits its transcriptional activity. , 1998, Genes & development.

[21]  D. DiMaio,et al.  Human papillomavirus in cervical and head-and-neck cancer , 2008, Nature Clinical Practice Oncology.

[22]  G. Sheu,et al.  The association of human papillomavirus 16/18 infection with lung cancer among nonsmoking Taiwanese women. , 2001, Cancer research.

[23]  C. Clavel,et al.  Prevalence of human papillomaviruses in lung carcinomas: a study of 218 cases , 2005, Modern Pathology.

[24]  J. Manoukian,et al.  Lung involvement in juvenile onset recurrent respiratory papillomatosis: a systematic review of the literature. , 2008, International journal of pediatric otorhinolaryngology.

[25]  Ya‐Wen Cheng,et al.  Human papillomavirus 16/18 E6 oncoprotein is expressed in lung cancer and related with p53 inactivation. , 2007, Cancer research.

[26]  H. Kang,et al.  EGFR mutations and human papillomavirus in squamous cell carcinoma of tongue and tonsil. , 2007, European journal of cancer.

[27]  M. Ergun,et al.  Detection and Typing of Human Papillomavirus in Non-Small Cell Lung Cancer , 2004, Respiration.

[28]  H. Dosaka-akita,et al.  Human papillomavirus type 18 DNA and E6-E7 mRNA are detected in squamous cell carcinoma and adenocarcinoma of the lung. , 1995, British Journal of Cancer.

[29]  Ya‐Wen Cheng,et al.  Different human papillomavirus 16/18 infection in Chinese non-small cell lung cancer patients living in Wuhan, China. , 2006, Japanese journal of clinical oncology.