Penile cancer is an uncommon malignancy that occurs most frequently in developing countries. Two pathways for penile carcinogenesis are currently recognized: one driven by human papillomavirus (HPV) infection and another HPV-independent route, associated with chronic inflammation. Progress on the clinical management of this disease has been slow, partly due to the lack of preclinical models for translational research. However, exciting recent developments are changing this landscape, with new in vitro and in vivo models becoming available. These include mouse models for HPV+ and HPV- penile cancer and multiple cell lines representing HPV- lesions. The present review addresses these new advances, summarizing available models, comparing their characteristics and potential uses and discussing areas that require further improvement. Recent breakthroughs achieved using these models are also discussed, particularly those developments pertaining to HPV-driven cancer. Two key aspects that still require improvement are the establishment of cell lines that can represent HPV+ penile carcinomas and the development of mouse models to study metastatic disease. Overall, the growing array of in vitro and in vivo models for penile cancer provides new and useful tools for researchers in the field and is expected to accelerate pre-clinical research on this disease.
Cancers. 2021 Jan 26*** epublish ***
Beatriz Medeiros-Fonseca, Antonio Cubilla, Haissa Brito, Tânia Martins, Rui Medeiros, Paula Oliveira, Rui M Gil da Costa
Centre for the Research and Technology of Agro-Environmental and Biological Sciences (CITAB), University of Trás-os-Montes and Alto Douro, UTAD, 5001-801 Vila Real, Portugal., Instituto de Patología e Investigación and Universidad Nacional de Asunción, Asunción, Paraguay., Maranhão Tumour and DNA Biobank (BTMA), Post-graduate Programme in Adult Health (PPGSAD), Federal University of Maranhão (UFMA), São Luís 65080-805, Brazil., Molecular Oncology and Viral Pathology Group, CI-IPOP, IPO-Porto, 4200-072 Porto, Portugal.