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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.

This study found that selectively inactivating ribonucleotide excision repair in mouse epidermis leads to DNA damage, keratinocyte intraepithelial neoplasia, and squamous cell carcinoma, indicating a potential tumor-promoting mechanism related to compromised genome maintenance.

This study found that selective inactivation of ribonucleotide excision repair in mouse epidermis led to spontaneous DNA damage, skin inflammation, and the development of squamous cell carcinoma, suggesting potential implications for cancer development in humans.

This study found that transient mtDNA double strand breaks in mice accelerated aging in certain tissues through increased reactive oxygen species, independent of p21/p53 pathway mediation.

This article discusses the factors influencing anticancer therapeutic regimens and reviews mechanisms of action and side effects of major chemotherapeutic agents without reporting new research findings.