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lüll Clinical relevance of the homologous recombination machinery in cancer therapy Miyagawa KCancer Sci 2008[Feb]; 99 (2): 187-94Cancer chemotherapy and radiotherapy kill cancer cells by inducing DNA damage, unless the lesions are repaired by intrinsic repair pathways. DNA double-strand breaks (DSB) are the most deleterious type of damage caused by cancer therapy. Homologous recombination (HR) is one of the major repair pathways for DSB and is thus a potential target of cancer therapy. Cells with a defect in HR have been shown to be sensitive to a variety of DNA-damaging agents, particularly interstrand crosslink (ICL)-inducing agents such as mitomycin C and cisplatin. These findings have recently been applied to clinical studies of cancer therapy. ERCC1, a structure-specific endonuclease involved in nucleotide excision repair (NER) and HR, confers resistance to cisplatin. Patients with ERCC1-negative non-small-cell lung cancer were shown to benefit from adjuvant cisplatin-based chemotherapy. Imatinib, an inhibitor of the c-Abl kinase, has been investigated as a sensitizer in DNA-damaging therapy, because c-Abl activates Rad51, which plays a key role in HR. Furthermore, proteins involved in HR have been shown to repair DNA damage induced by a variety of other chemotherapeutic agents, including camptothecin and gemcitabine. These findings highlight the importance of HR machinery in cancer therapy.|*Recombination, Genetic[MESH]|Antineoplastic Agents/therapeutic use[MESH]|DNA Breaks, Double-Stranded[MESH]|DNA Topoisomerases, Type II/metabolism[MESH]|Enzyme Inhibitors/pharmacology[MESH]|Humans[MESH]|Models, Biological[MESH]|Neoplasms/*genetics/*therapy[MESH]|Protein-Tyrosine Kinases/antagonists & inhibitors/metabolism[MESH]|Rad51 Recombinase/genetics/metabolism[MESH]|Topoisomerase II Inhibitors[MESH] |