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The effects of deregulated DNA damage signalling on cancer chemotherapy response and resistance
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The effects of deregulated DNA damage signalling on cancer chemotherapy response and resistance
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Journal Article
The effects of deregulated DNA damage signalling on cancer chemotherapy response and resistance
2012
Overview
Key Points
DNA repair defects are targets for chemotherapy drugs.
DNA damage response (DDR) genes are also targets for resistance mechanisms that are acquired during chemotherapy treatment.
To enhance chemotherapy response, the DDR may be targeted by reactivation of p53, by inhibition of cell cycle checkpoints or by inhibition of DNA repair processes.
Therapy resistance of homologous recombination (HR)-deficient tumours may be caused by genetic reversion of the HR defect, by residual HR activity, by rewiring of DNA repair pathways or by tumour heterogeneity.
Robust biomarkers are required to maximize the effectiveness of therapy targeting HR deficiency.
The best possible treatments might involve combinations of chemotherapy drugs and/or targeted therapeutics to eradicate tumours before resistant tumour cell clones arise.
DNA damage response signalling pathways are often altered in tumours, which can affect their response to chemotherapy and targeted therapies. This Review discusses the mechanisms by which altered DNA damage responses elicit such therapy resistance.
Tumours with specific DNA repair defects can be completely dependent on back-up DNA repair pathways for their survival. This dependence can be exploited therapeutically to induce synthetic lethality in tumour cells. For instance, homologous recombination (HR)-deficient tumours can be effectively targeted by DNA double-strand break-inducing agents. However, not all HR-defective tumours respond equally well to this type of therapy. Tumour cells may acquire resistance by invoking biochemical mechanisms that reduce drug action or by acquiring additional alterations in DNA damage response pathways. A thorough understanding of these processes is important for predicting treatment response and for the development of novel treatment strategies that prevent the emergence of therapy-resistant tumours.
Publisher
Nature Publishing Group UK,Nature Publishing Group
