Ribonucleotide Excision Repair Is Essential to Prevent Squamous Cell Carcinoma of the Skin

    August 2018 in “ Cancer research ”
    Björn Hiller, Anja Hoppe, Christa Haase, Christina Hiller, Nadja Schubert, Werner Müller, Martin A.M. Reijns, Andrew P. Jackson, Thomas A. Kunkel, Joerg Wenzel, Rayk Behrendt, Axel Roers
    Studysummary In this study, researchers found that selectively disabling ribonucleotide excision repair in mouse epidermis caused DNA damage, skin inflammation, and led to skin cancer, suggesting a potential role for this repair mechanism in tumorigenesis. Our plain-language summary of this paper — not a Tressless recommendation.
    The study demonstrated that selective inactivation of ribonucleotide excision repair (RER) in the epidermis of mice, due to loss of RNase H2, leads to spontaneous DNA damage, skin inflammation, and a type I interferon response. This genetic alteration resulted in epidermal hyperproliferation, loss of hair follicle stem cells, impaired hair follicle function, and the development of keratinocyte intraepithelial neoplasia and invasive squamous cell carcinoma with complete penetrance. The findings indicate that RER is crucial for preventing DNA damage that can lead to skin cancer, suggesting that compromised RER may be a significant factor in promoting tumor development in human cancers.
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