Objective： To investigate the association of XRCC4 polymorphic variants at G-1394T （rs6869366） with colorectal cancer susceptibility. Methods： In this hospital-based case-control study, the association of XRCC4 po...Objective： To investigate the association of XRCC4 polymorphic variants at G-1394T （rs6869366） with colorectal cancer susceptibility. Methods： In this hospital-based case-control study, the association of XRCC4 polymorphism with colorectal cancer risk in Chinese population was investigated. In total, 171 patients with colorectal cancer and 171 healthy individuals matched for age and gender were selected. The genomic DNAs of the patients and controls were extracted from peripheral blood and the 300 bp target DNA was amplified with Polymerase Chain Reaction. The products were then digested with restriction endonuclease HinclI, followed by agarose electrophoresis to identify the genotype. Results： We found a significant difference in the frequency of the XRCC4 G-1394T genotype between the colorectal cancer and control groups in female （1/127 vs 8/122, P〈0.05）. Those with G/T at XRCC4 G-1394T showed a decreased risk of colorectal cancer susceptibility compared with those with T/T （OR 0.113, 95%CI 0.014-0.932）. However, in overall population or in male, there was no significant difference of the distribution between the colorectal cancer and control groups. Conclusion： Our findings with decreased risk of colorectal cancer susceptibility suggested that the G allele of XRCC4 G-1394T were associated in female.展开更多
目的探讨XRCC4(X-ray cross-complementing group 4)作为检测结直肠癌的新型肿瘤标志物的应用价值。方法收集术前行PETCT检查的结直肠癌患者的切除肿瘤组织21例,应用ELISA法检测肿瘤组织中XRCC4蛋白表达情况,并与术前PETCT的标准摄取值(...目的探讨XRCC4(X-ray cross-complementing group 4)作为检测结直肠癌的新型肿瘤标志物的应用价值。方法收集术前行PETCT检查的结直肠癌患者的切除肿瘤组织21例,应用ELISA法检测肿瘤组织中XRCC4蛋白表达情况,并与术前PETCT的标准摄取值(SUV)相比对,进行相关性分析。结果肿瘤组织内XRCC4蛋白高表达,且与PETCT中SUV值密切相关(P<0.01)。结论 XRCC4蛋白作为新一代肿瘤标志物可能参与肿瘤细胞的能量代谢;结合PETCT检查,XRCC4蛋白可为结直肠癌的诊断与治疗提供一种新的思路。展开更多
DNA double-strand breaks （DSBs） are introduced in cells by ionizing radiation and reactive oxygen species. In addition, they are commonly generated during V（D）J recombination, an essential aspect of the developing...DNA double-strand breaks （DSBs） are introduced in cells by ionizing radiation and reactive oxygen species. In addition, they are commonly generated during V（D）J recombination, an essential aspect of the developing immune system. Failure to effectively repair these DSBs can result in chromosome breakage, cell death, onset of cancer, and defects in the immune system of higher vertebrates. Fortunately, all mammalian cells possess two enzymatic pathways that mediate the repair of DSBs： homologous recombination and non-homologous end-joining （NHEJ）. The NHEJ process utilizes enzymes that capture both ends of the broken DNA molecule, bring them together in a synaptic DNA-protein complex, and finally repair the DNA break. In this review, all the known enzymes that play a role in the NHEJ process are discussed and a working model for the co-operation of these enzymes during DSB repair is presented.展开更多
Nonhomologous DNA end joining （NHEJ） is the primary pathway for repair of double-strand DNA breaks in human cells and in multicellular eukaryotes. The causes of double-strand breaks often fragment the DNA at the sit...Nonhomologous DNA end joining （NHEJ） is the primary pathway for repair of double-strand DNA breaks in human cells and in multicellular eukaryotes. The causes of double-strand breaks often fragment the DNA at the site of damage, resulting in the loss of information there. NHEJ does not restore the lost information and may resect additional nucleotides during the repair process. The ability to repair a wide range of overhang and damage configurations reflects the flexibility of the nuclease, polymerases, and ligase of NHEJ. The flexibility of the individual components also explains the large number of ways in which NHEJ can repair any given pair of DNA ends. The loss of information locally at sites of NHEJ repair may contribute to cancer and aging, but the action by NHEJ ensures that entire segments of chromosomes are not lost.展开更多
文摘Objective： To investigate the association of XRCC4 polymorphic variants at G-1394T （rs6869366） with colorectal cancer susceptibility. Methods： In this hospital-based case-control study, the association of XRCC4 polymorphism with colorectal cancer risk in Chinese population was investigated. In total, 171 patients with colorectal cancer and 171 healthy individuals matched for age and gender were selected. The genomic DNAs of the patients and controls were extracted from peripheral blood and the 300 bp target DNA was amplified with Polymerase Chain Reaction. The products were then digested with restriction endonuclease HinclI, followed by agarose electrophoresis to identify the genotype. Results： We found a significant difference in the frequency of the XRCC4 G-1394T genotype between the colorectal cancer and control groups in female （1/127 vs 8/122, P〈0.05）. Those with G/T at XRCC4 G-1394T showed a decreased risk of colorectal cancer susceptibility compared with those with T/T （OR 0.113, 95%CI 0.014-0.932）. However, in overall population or in male, there was no significant difference of the distribution between the colorectal cancer and control groups. Conclusion： Our findings with decreased risk of colorectal cancer susceptibility suggested that the G allele of XRCC4 G-1394T were associated in female.
文摘目的探讨XRCC4(X-ray cross-complementing group 4)作为检测结直肠癌的新型肿瘤标志物的应用价值。方法收集术前行PETCT检查的结直肠癌患者的切除肿瘤组织21例,应用ELISA法检测肿瘤组织中XRCC4蛋白表达情况,并与术前PETCT的标准摄取值(SUV)相比对,进行相关性分析。结果肿瘤组织内XRCC4蛋白高表达,且与PETCT中SUV值密切相关(P<0.01)。结论 XRCC4蛋白作为新一代肿瘤标志物可能参与肿瘤细胞的能量代谢;结合PETCT检查,XRCC4蛋白可为结直肠癌的诊断与治疗提供一种新的思路。
文摘DNA double-strand breaks （DSBs） are introduced in cells by ionizing radiation and reactive oxygen species. In addition, they are commonly generated during V（D）J recombination, an essential aspect of the developing immune system. Failure to effectively repair these DSBs can result in chromosome breakage, cell death, onset of cancer, and defects in the immune system of higher vertebrates. Fortunately, all mammalian cells possess two enzymatic pathways that mediate the repair of DSBs： homologous recombination and non-homologous end-joining （NHEJ）. The NHEJ process utilizes enzymes that capture both ends of the broken DNA molecule, bring them together in a synaptic DNA-protein complex, and finally repair the DNA break. In this review, all the known enzymes that play a role in the NHEJ process are discussed and a working model for the co-operation of these enzymes during DSB repair is presented.
文摘Nonhomologous DNA end joining （NHEJ） is the primary pathway for repair of double-strand DNA breaks in human cells and in multicellular eukaryotes. The causes of double-strand breaks often fragment the DNA at the site of damage, resulting in the loss of information there. NHEJ does not restore the lost information and may resect additional nucleotides during the repair process. The ability to repair a wide range of overhang and damage configurations reflects the flexibility of the nuclease, polymerases, and ligase of NHEJ. The flexibility of the individual components also explains the large number of ways in which NHEJ can repair any given pair of DNA ends. The loss of information locally at sites of NHEJ repair may contribute to cancer and aging, but the action by NHEJ ensures that entire segments of chromosomes are not lost.
