作者: Ranee Mehra , Ilya G. Serebriiskii
DOI: 10.1007/978-1-4614-8815-6_13
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摘要: DNA-damaging agents such as cisplatin and radiotherapy have provided a cornerstone of treatment for squamous cell cancers the head neck (SCCHN). Cells possess multiple mechanisms repairing different classes DNA damage, including base excision repair (BER), nucleotide (NER), mismatch (MMR), resolution intrastrand cross-linking by Fanconi anemia (FA) proteins, nonhomologous end joining (NHEJ), homologous recombination (HR). Preclinical limited degree clinical research has focused on evaluating whether changes in expression, mutation, or polymorphic variants many enzymes involved these pathways are resistance SCCHN. This chapter will first summarize proteins functioning complementary DNA-damage response pathways, then focus current data regarding their prognostic value clinic, noting limitations retrospective evaluations, discussing implications future research.