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Tina Dalianis



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    P2.10 - Prevention and Tobacco Control (ID 176)

    • Event: WCLC 2019
    • Type: Poster Viewing in the Exhibit Hall
    • Track: Prevention and Tobacco Control
    • Presentations: 1
    • Moderators:
    • Coordinates: 9/09/2019, 10:15 - 18:15, Exhibit Hall
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      P2.10-01 - Analysis of Human Papilloma Viruses (HPV) and Human Polyoma Viruses (HPyV) in Lung Cancer from Swedish Never-Smokers (ID 2845)

      10:15 - 18:15  |  Author(s): Tina Dalianis

      • Abstract
      • Slides

      Background

      A possible role for oncogenic infections in the etiology of lung cancer has been investigated in a large number of studies, with contradictory results. High-risk mucosal human papillomaviruses (HPV), recognized as being associated with cervical cancer and oropharyngeal cancer, has been suggested as a causative factor also in lung cancer [1,2], whereas other studies found no, or at most very limited, involvement of HPV in lung cancer [3,4].

      To investigate human papillomaviruses (HPV) and human polyomaviruses (HPyV) as possible causative factors behind lung cancer in never-smokers, we analyzed the presence of these viruses in a subset of tumors within a larger Swedish cohort of never-smoking lung cancer patients [Swedish Molecular Initiative against Lung cancer, SMIL; Salomonsson et al. Abstract WCLC 2019].

      Method

      Eighty-seven surgically resected lung cancer samples from never-smokers, diagnosed 2005-2014 in Stockholm, Sweden, were analyzed by Luminex assays for the presence of 27 HPV types (including all HPV types currently regarded as high-risk types) and for 10 HPyV species (BKPyV, JCPyV, KIPyV, WUPyV, TSPyV, MWPyV, HPyV6, 7, 9, and 10).

      Result

      All samples were positive for the β-globin gene, confirming the presence, amplification and detection of cellular DNA. All samples were negative for the HPV types included in the assay. The only viral DNA detected in the tumors were low amounts of Merkel cell polyomavirus (MCPyV) DNA, of unknown significance, in 15 samples.

      Conclusion

      Our study shows no evidence for neither HPV nor HPyV in the etiology of lung cancer in Swedish never-smokers.

      References

      1. Syrjanen, K. Detection of human papillomavirus in lung cancer: Systematic review and meta-analysis. Anticancer Res 2012, 32, 3235-3250.

      2. Ragin, C.; Obikoya-Malomo, M.; Kim, S.; Chen, Z.; Flores-Obando, R.; Gibbs, D.; Koriyama, C.; Aguayo, F.; Koshiol, J.; Caporaso, N.E., et al. Hpv-associated lung cancers: An international pooled analysis. Carcinogenesis 2014, 35, 1267-1275.

      3. Koshiol, J.; Rotunno, M.; Gillison, M.L.; Van Doorn, L.J.; Chaturvedi, A.K.; Tarantini, L.; Song, H.; Quint, W.G.; Struijk, L.; Goldstein, A.M., et al. Assessment of human papillomavirus in lung tumor tissue. J Natl Cancer Inst 2011, 103, 501-507.

      4. Tang K.W.; Alaei-Mahabadi B.; Samuelsson T.; Lindh M.; Larsson E. The landscape of viral expression and host gene fusion and adaptation in human cancer. Nat Commun 2013, 4, 2513.

      5. Swedish Molecular Initiative against Lung cancer, SMIL; Salomonsson A. et al. Lung cancer in never-smokers: A nationwide population based mapping of targetable alterations. 20th World Conference on Lung Cancer (Barcelona, 7-10 Sept, 2019)

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