New Potential Therapeutic Approaches by Targeting Rad51- Dependent Homologous Recombination

Abstract

Cellular DNA is constantly exposed to the effects of endogenous or environmental agents such as free radicals, radiation and chemicals. In higher organisms, these nucleic alterations are estimated at several thousands of lesions per cell [1] which can correspond to the loss of bases and also to the breaking of one or both strands of the DNA double helix. Among these DNA breaks, the double-strand break (DSB) is the most harmful because it is the most diffi‐ cult to repair. A human cell can accumulate up to 50 DSBs per cell cycle [2]. Unrepaired DSBs can have serious consequences such as permanent cell cycle arrest or cell death by apoptosis. Imperfect repair can also lead to major syndromes such as genetic disorders, pre‐ mature aging or malignant cell generation.