DNA Damage Repair in Cancers

Dear Colleagues,

Despite its stability, DNA continuously faces damage from endogenous and exogenous sources, prompting the evolution of the DNA damage response (DDR) in cells. Mutations in DDR genes predispose to the development of cancer, emphasising the importance of the DDR's critical role in preventing tumorigenesis by maintaining genome stability. Genome instability resulting from DDR oncogene activation or tumour suppressor loss is a hallmark of cancer, facilitating tumourigenesis and recurrence. This inherent genome instability of rapidly proliferating tumours has offered therapeutic opportunities. Although treatments such as radiotherapy and DNA-damaging chemotherapeutics exploit this vulnerability, they lack selectivity, damage healthy tissues, and cause unwanted side effects.

Over the past two decades, leveraging the concept of synthetic lethality, where cancer cells depend on alternative pathways, has proven to be powerful in identifying targeted therapeutic approaches. One such approach that has made its way into clinical practice involves PARP inhibitors, which exploit synthetic lethality in tumours lacking DNA repair factors BRCA1 or BRCA2. In addition to PARP inhibitors, several new DDR targets, with small-molecule inhibitors undergoing clinical trials, have also been identified, marking a promising frontier in cancer treatment.

Therefore, in this Special Issue we extend an invitation for original basic research utilising pre-clinical in vitro and/or in vivo approaches, as well as reviews, with an emphasis on the identification and characterisation of novel DDR genes, molecular targets for anticancer treatments, especially those previously considered undruggable, and novel methodologies within this domain.

Dr. Ilirjana Bajrami
Guest Editor

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• DDR genes
• cancer
• synthetic lethality
• undruggable targets
• DNA repair
• DNA replication
• immunotherapy