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This study found that benign tumors with a high risk of malignant progression primarily arise from hair follicle cells when a mutant ras gene is expressed in a specific population of epidermal cells in mice.

This study found that metabolic adaptations in skin epithelial stem cells, specifically redox ratio recovery and glycolytic flux modulation, define competitive outcomes between wild-type and mutant cells in different oncogenic environments.

This study found that injury-induced proliferation of wild-type cells can suppress oncogenic growth in Ras-mosaic skin.

This study found that despite carrying an activating Hras mutation, hair follicle stem cells integrate into normal skin without causing tumors, unlike similar mutations in the epidermis, suggesting unique tumor-suppressing mechanisms in hair follicles.

This study found that H-Ras activation in aged mouse skin leads to increased dysplasia and progression to in situ squamous cell carcinoma, highlighting an age-linked connection between immune changes, senescence, and cancer risk.