34 citations,
August 2018 in “Cancer research” Fixing DNA errors is crucial to prevent skin cancer.
The study demonstrates that selective inactivation of ribonucleotide excision repair (RER) in mouse epidermis leads to spontaneous DNA damage, epidermal hyperproliferation, loss of hair follicle stem cells, and hair follicle function. This results in the development of keratinocyte intraepithelial neoplasia and invasive squamous cell carcinoma with complete penetrance, despite a strong type I interferon response and skin inflammation. These findings suggest that impairments in RER-mediated genome maintenance could be a significant factor in promoting tumor development in human cancer.
The study demonstrates that selective inactivation of ribonucleotide excision repair (RER) in mouse epidermis leads to spontaneous DNA damage, epidermal hyperproliferation, loss of hair follicle stem cells, and hair follicle function. This condition results in the development of keratinocyte intraepithelial neoplasia and invasive squamous cell carcinoma with complete penetrance, despite a strong type I interferon response and skin inflammation. These findings suggest that impairments in RER-mediated genome maintenance could be a significant factor in promoting tumor development in human cancer.
42 citations,
December 2016 in “Cell Death & Differentiation” Damaging mitochondrial DNA in mice speeds up aging due to increased reactive oxygen species, not through the p53/p21 pathway.
3 citations,
February 1976 in “Pediatric Clinics of North America” The conclusion is that effective cancer treatment often requires a combination of therapies, but must be carefully managed due to serious side effects and the risk of immunosuppression.