DNA repair pathways as targets for cancer therapy

DNA repair pathways as targets for cancer therapy

2008 | Helleday, T; Petermann, Eva; Lundin, C; Hodgson, B; Sharma, RA
DNA repair pathways are critical targets for cancer therapy, as cancer cells often rely on specific repair mechanisms for survival. Inhibitors of DNA repair can enhance the effectiveness of chemotherapy and radiotherapy by increasing the toxicity of DNA-damaging agents. These inhibitors work by selectively increasing DNA damage in cancer cells, minimizing side effects in normal cells. DNA repair pathways, such as homologous recombination (HR) and base excision repair (BER), are frequently mutated in cancer, making them attractive targets. PARP inhibitors, for example, are effective in cancers with defects in HR, such as BRCA1 and BRCA2 mutations. Clinical trials are ongoing to test PARP inhibitors in combination with other therapies. Additionally, DNA repair inhibitors can be used to amplify replication stress, converting lesions into fatal ones. Targeting DNA repair pathways offers a promising approach for more selective and effective cancer treatments. However, challenges remain, including the potential for resistance and the need for reliable biomarkers to identify suitable patients. Overall, DNA repair inhibitors represent a significant advancement in cancer therapy, offering a targeted approach with potential for improved outcomes.DNA repair pathways are critical targets for cancer therapy, as cancer cells often rely on specific repair mechanisms for survival. Inhibitors of DNA repair can enhance the effectiveness of chemotherapy and radiotherapy by increasing the toxicity of DNA-damaging agents. These inhibitors work by selectively increasing DNA damage in cancer cells, minimizing side effects in normal cells. DNA repair pathways, such as homologous recombination (HR) and base excision repair (BER), are frequently mutated in cancer, making them attractive targets. PARP inhibitors, for example, are effective in cancers with defects in HR, such as BRCA1 and BRCA2 mutations. Clinical trials are ongoing to test PARP inhibitors in combination with other therapies. Additionally, DNA repair inhibitors can be used to amplify replication stress, converting lesions into fatal ones. Targeting DNA repair pathways offers a promising approach for more selective and effective cancer treatments. However, challenges remain, including the potential for resistance and the need for reliable biomarkers to identify suitable patients. Overall, DNA repair inhibitors represent a significant advancement in cancer therapy, offering a targeted approach with potential for improved outcomes.
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Understanding DNA repair pathways as targets for cancer therapy