Cutaneous papillomaviruses and non-melanoma skin cancer: causal agents or innocent bystanders?
- 1Viral Transformation Mechanisms, Deutsches Krebsforschungszentrum (DKFZ), Germany
- 2Molecular and Cellular Therapy Group, Leloir Institute Foundation (FIL), Argentina
There is still controversy in the scientific field about whether certain types of cutaneous human papillomaviruses (HPVs) are causally involved in the development of non-melanoma skin cancer (NMSC). Deciphering the etiological role of cutaneous HPVs requires - besides tissue culture systems - appropriate preclinical models to match the obtained results with clinical data from affected patients. Clear scientific evidence about the etiology and underlying mechanisms involved in NMSC development is fundamental to provide reasonable arguments for public health institutions to classify at least certain cutaneous HPVs as group 1 carcinogens. This in turn would have implications on fundraising institutions and health care decision makers to force – similarly as for anogenital cancer – the implementation of a broad vaccination program against “high-risk” cutaneous HPVs to prevent NMSC as the most frequent cancer worldwide. Precise knowledge of the multi-step progression from normal cells to cancer is a prerequisite to understand the functional and clinical impact of cofactors that affect the individual outcome and the personalized treatment of a disease. This overview summarizes not only recent arguments that favor the acceptance of a viral etiology in NMSC development but also reflects aspects of causality in medicine, the use of empirically meaningful model systems and strategies for prevention.
Keywords: cutaneous papillomaviruses, hit-and-run mechanism, Mastomys coucha, causality, Skin Cancer, NMSC, Animal Models, Vaccination, UV exposure, Translational research
Received: 22 Jan 2018;
Accepted: 16 Apr 2018.
Edited by:Herbert J. Pfister, Universität zu Köln, Germany
Reviewed by:Nicholas A. Wallace, Kansas State University, United States
Thomas R. Broker, University of Alabama at Birmingham, United States
Copyright: © 2018 Hasche, Vinzón and Rösl. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence: Prof. Frank Rösl, Deutsches Krebsforschungszentrum (DKFZ), Viral Transformation Mechanisms, Im Neuenheimer Feld 242, Heidelberg, 69120, Germany, email@example.com