Harnessing Cancer Vulnerability by Targeting the DNA Damage Response

Dear Colleagues,

In the precision medicine era, while agents that suppress oncogenic kinases have changed the standard of care for many cancers, no effective therapies are available for tumours, such as breast and ovarian cancer (OC), which are lacking in actionable driver cancer mutations. Luckily, the genome instability induced by the high frequency of DNA damage repair (DDR) defects has opened new avenues and treatment perspectives for such tumours. As a matter of fact, the enzymatic inhibition of the Poly(ADP-ribose) polymerases (PARPs) 1 and 2 has pioneered a synthetic lethality-based target therapy strategy for treatment of tumours characterised by DDR defects, for instance, breast and ovarian cancer carrying BRCA1 and BRCA2 mutations.

My main interest in launching this Special Issue is to focus the discussion on innovative data in order to support clinical strategies for extending the advantages of PARP inhibitors beyond BRCA mutant cancers and towards a wider number of patients, through the use of novel biomarkers of homologous recombination repair deficiency as well as of predictive biomarkers of sensitivity. I would like to attract research and/or review articles to explore the potential application of PARP inhibitors in early treatment schemes, including neoadjuvant, adjuvant, and chemo/radio-prevention approaches. In fact, it is my firm conviction that the challenge of combinatorial therapeutic strategies, including different DDR inhibitor, immune-checkpoint inhibitors, and/or non-DDR agents, able to induce chemical BRCAness, must be pursued and encouraged.

Dr. Angela Celetti
Guest Editor

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