HPV8 Field Cancerization in a Transgenic Mouse Model Is Due to Lrig1+ Keratinocyte Stem Cell Expansion

    Simone Lanfredini, Carlotta Olivero, Cinzia Borgogna, Federica Calati, Kate Powell, Kelli-Jo Davies, Marco De Andrea, Sarah Harries, Hiu Kwan Carolyn Tang, Herbert Pfister, Marisa Gariglio, Girish K. Patel
    Studysummary This study found that in a transgenic mouse model, β-HPV infection led to increased skin thickness and proliferation of specific keratinocyte stem cells, which may contribute to squamous cell carcinoma development. Our plain-language summary of this paper — not a Tressless recommendation.
    The study used a transgenic mouse model to explore the role of Lrig1+ keratinocyte stem cells in HPV8-induced skin carcinogenesis. It found that the expansion of these stem cells in the hair follicle junctional zone led to thicker skin and hyperproliferative epidermis, predisposing the skin to squamous cell carcinoma. The research highlighted that β-HPV reactivation in these cells contributed to field cancerization, with multiple pre-cancerous lesions developing, particularly in sun-exposed areas. The study provided insights into the mechanisms of β-HPV-induced skin cancer, suggesting similar processes could occur in human conditions like epidermodysplasia verruciformis and actinic keratosis.
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