Exploiting DNA Damage Response (DDR) Inhibitors in Cancer Therapy

Dear Colleagues,

Deregulation of the DNA damage response (DDR) is very common in cancers. Genomic instability driven by a specific deficiency in DDR can make cancer cells more dependent on the remaining and still functional DDR pathways. The possibility of specifically targeting the remaining functional DDR pathways and/or exacerbating the existing defects has proven to be an effective therapeutic strategy to kill cancer cells and has introduced the concept of synthetic lethality to the field. The unraveling of the key players in DDR, their specific inactivation in different tumor types and the synthesis of specific chemical inhibitors of DDR represent a new, highly relevant, targeted approach in cancer therapy. Multiple novel DDR inhibitors have been developed over the past two decades, including the PARP, ATR, ATM, CHK1/2, and WEE1 inhibitors.

We invite all scientists working in the DDR field to participate in this Special Issue. Original research articles, reviews, or shorter perspective articles on all aspects related to DDR pathways are welcome, including topics such as new molecular and cellular functions of the key players of DDR and novel approaches with current, under clinical development, or newly emerging DDR inhibitors on different types of tumors. Articles on the functional characterization of new rational drug combinations with the involvement of DDR inhibitors are especially encouraged. Special attention will be paid to the causes and consequences of replication stress, and how to exploit inherent high oxidative stress and disrupt nucleotide metabolism to treat cancer. Relevant topics include single and combined DDR inhibitor treatments; identification of cancer-type-specific biomarkers in response to DDR inhibitors; discovery of new rational drug combinations; identification of resistance mechanisms to DDR-targeting therapies and possible strategies for overcoming such resistance mechanisms.

Dr. Laura Carrassa
Dr. Kumar Sanjiv
Guest Editors

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• DDR targets (PARP, ATR, ATM, CHK1, WEE1)
• DDR inhibitors
• Cancer-type-specific biomarkers in response to DDR inhibitors
• Rational drug combinations with DDR inhibitors and synthetic lethality
• Overcoming resistance mechanisms to DDR Targeting Therapies
• Replication stress
• Oxidative DNA damage
• Nucleotide metabolism