EGFR mutations and human papillomavirus in lung cancer

Lung Cancer. 2012 Nov;78(2):144-7. doi: 10.1016/j.lungcan.2012.08.011. Epub 2012 Sep 10.

Abstract

Our previous study reported a frequent detection of human papillomavirus (HPV) genome in primary lung adenocarcinomas of the recurrent patients who were responsive to epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitor, suggesting that HPV presence in lung cancer may be related to a genetic background related to EGFR mutations. The present study examined the association between the HPV presence and mutations in exons 19 and 21 of EGFR gene in Japanese lung cancer patients. Thirteen (31%) out of 42 cases had EGFR mutations. Although these mutations were tended to be observed in females, non-smokers, or adenocarcinomas, there was no statistically significant associations. HPV DNA was found in 7/42 (17%) lung tumors. The frequency of HPV presence did not differ in histological types. The presence of HPV DNA was significantly related to EGFR mutations (P=0.021), especially in adenocarcinomas of the lung (P=0.014). HPV-positive lung tumors accounted for 38% and 7% of those with and without EGFR mutations, respectively. Our results suggest that EGFR mutations are associated with HPV presence in Japanese patients with lung cancer.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adenocarcinoma / genetics*
  • Adenocarcinoma / virology
  • Aged
  • Carcinoma, Squamous Cell / genetics*
  • Carcinoma, Squamous Cell / virology
  • ErbB Receptors / genetics*
  • Female
  • Human papillomavirus 16 / genetics
  • Human papillomavirus 16 / physiology*
  • Humans
  • Lung Neoplasms / genetics*
  • Lung Neoplasms / virology
  • Male
  • Mutation
  • Papillomavirus Infections / genetics*
  • Papillomavirus Infections / virology
  • Viral Load

Substances

  • ErbB Receptors