Objectives: Female lung cancer patients with no smoking habit and non-mucinous adenocarcinoma have a higher rate of epidermal growth factor receptor (EGFR) gene mutations, which is related to tyrosine kinase inhibitors (TKIs) sensitivity. Unfortunately the cause of EGFR gene mutations is still elusive. In this study, we search for the association between Merkel cell polyomavirus (MCPyV) infection and EGFR gene mutations.
Materials and methods: We studied 189 non-small cell lung cancer (NSCLC) samples for the presence of MCPyV large T (LT) DNA, LT antigen and EGFR hotspot mutations. Clinicopathological parameters of this cohort were also analyzed.
Results: Thirty out of 163 adenocarcinoma and 2 out of 18 squamous cell carcinoma were found to have MCPyV LT DNA by PCR. Immunostaining also showed LT protein expression in most of the DNA positive samples. EGFR mutations were more frequently detected in female (P=0.009) and non-smoking patients (P=0.0001). Furthermore, a significant association between MCPyV infection and EGFR mutations was found (P=0.001).
Conclusion: Our study shows that MCPyV LT DNA is present in a subgroup of NSCLC, which is significantly correlated with EGFR mutations. To the best of our knowledge, this is the first study to find an association between MCPyV infection and EGFR hotspot mutations. These results support the possibility that MCPyV has a partial role in the carcinogenesis of NSCLC in a subgroup of patients.
Keywords: Epidermal growth factor receptor; Lung cancer; Merkel cell polyomavirus; Mutagen; Mutation; Pathogenesis.
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