Human Papillomavirus Infection and Lung Cancer

Abstract

Lung cancer continues to be the most common neoplasia and represents the leading cause of cancer-related death in the world. Nonetheless, contrary to expected projections, the decrease in incidence expected by decrease in tobacco exposure has been partially halted due to an increasing amount of lung cancer cases in nonsmokers, particularly in female patients. This led to the development of new hypotheses in terms of lung cancer etiology, including the involvement of oncogenic viruses such as the human papillomavirus (HPV). HPV role in the pathophysiology of lung cancer, including adenocarcinoma and squamous cell carcinoma, is currently under research. Exposure to HPV, and the resulting infection, can occur in several possible ways, including sexual transmission and airborne fomites. Main pathogenic occurrences include alterations in inhibition of p53 and retinoblastoma. This chapter presents the current evidence as to the role of HPV in the development of lung cancer, methods to establish HPV infection, and also explores the role of predisposing factors, as well as immunological and inflammatory factors in nonsmokers. Additionally, the role of other molecular factors, such as EGFR, interleukins 6 and 10, and others, is discussed. Finally, future perspectives in this new paradigm of lung cancer in nonsmokers are broadly reviewed.

Infection with human cytomegalovirus, Epstein-Barr virus, and high-risk types 16 and 18 of human papillomavirus in EGFR-mutated lung adenocarcinoma

“…The reason for more frequent HPV infection in LA with EGFR gene mutations could be the viral protein E6. This protein upstream regulates the inhibitors of apoptosis of the EGFR/ PI3K/AKT signaling pathway and may play a central role in NSCLC cancer tumorigenesis with EGFR gene mutations and HPV infection (40,41). Previous studies have confirmed HPV as part of the etiology of cervical and oropharyngeal cancer, but the association with lung cancer has not been fully established (12,25).…”

Uniting Latin America Through Research: How Regional Research Can Strengthen Local Policies, Networking, and Outcomes for Patients With Lung Cancer

“…The results would suggest that genetics plays an important role in the disparities observed, and this in turn could be further explored to better understand cancer development and even suggest novel therapeutic targets. 27 Other achievements by CLICaP include the characterization of lung cancer in young patients, 28 treatment outcomes in Hispanic patients and potential biomarkers for response, 29,30 mechanisms of resistance to treatment with first-generation tyrosine kinase inhibitors, 31 molecular epidemiology of ALK rearrangements, 32 EGFR exon 20 insertions, 33 EGFR amplifications, 34 KRAS mutations, 35 patterns of progression to treatment with tyrosine kinase inhibitors, 36 outcomes of immunotherapy in Hispanic individuals, 37 characteristics of small cell lung cancer, 38 mesothelioma, 39 thymomas, 40 squamous cell carcinoma, 41 and real-world data from Hispanic individuals treated with novel agents. 42 Furthermore, CLICaP started a mentoring program that seeks to offer effective networking and mentoring opportunities for talented oncologists and investigators from Latin America to promote leadership and address current limitations within the regional setting.…”

Correlation between HPV PCNA, p16, and p21 Expression in Lung Cancer Patients

“…However, other types of tumors have been associated with the activity of HPV [1,2]. One of these possible HPVrelated cancers is lung cancer; however, the presence and activity of the virus remain controversial [3][4][5].…”