DNA Damage Response from Molecular Mechanisms to Cancer Therapy

Dear Colleagues,

The DNA damage response (DDR) could be defined as a double face of tumour: both the cause and treatment. Some DDR proteins are involved in the cancer-prone syndrome as in the ataxia telangiectasia (ATM) or Nijmegen Breakage syndrome (Nibrin), correlating them as tumour-developing factors. Conversely, the DNA repair defects are used as the “Achille’s heel” of cancer, favouring treatment with DNA damage agents through radiation therapy or cisplatin generating various kinds of DNA lesions (single or double strand breaks), although the side effects exerted on healthy tissue limits the use of this cancer therapy. In this scenario, the identification of novel therapeutic strategies based on the personal genetic makeup could be essential for improving the cancer treatments. To this aim, the dissection of novel proteins involved in the DDR plays an important role in cancer therapy. The discovery of highly selective actions of PARP inhibitors for BRCA1-/- breast cancer cells opened a “synthetic lethal era”. BRCA1 is one of the first players in the homologous recombination (HR), the error-free DNA repair mechanism based on the use of sister chromatids for genetic information stability. Moreover, the appearance of various resistance mechanisms to PARP inhibitors, such as functional BRCA1 and BRCA2 reactivation, the loss of 53BP1, or replication fork stability, suggest the necessary discovery of new players in order to bypass the tumour-resistance phenomena through the identification of alternative therapeutic targets.

This Special Issue will highlight novel discoveries in the context of the DNA damage response, from molecular mechanisms to clinical aspects, as potential novel strategies for cancer therapy. 

Dr. Luigi Alfano
Prof. Dr. Antonio Giordano
Guest Editors

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