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genetic susceptibility factor
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  遗传易感性
     Genetic susceptibility factor accounts for about 1/4~1/5 proportion in the formation of gastric cancer familial aggregation.
     胃癌呈现家庭聚集性的原因中 ,遗传易感性作用约占 1/5~ 1/4。
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     Our results indicate that the ECRGl 290Gln variant allele might be a genetic susceptibility factor for developing ESCC, especially in the smoking population.
     此结果提示,ECRG1基因中的Gln等位基因为食管癌的危险遗传易感性因素,并与环境存在交互作用。 原因可能是Arg290Gln多态改变引起的Arg-to-Gln的改变导致了ECRGl的丝氨酸蛋白水解酶保守结构域在空间构象上的异常,从而引起ECRGl蛋白功能的异常。
短句来源
     Conclusion: Genetic susceptibility factor accounts for about 1 /4 proportion in the formation of gastric cancer familial aggregation in Yang Zhong. It suggests that research on the interaction between genetic susceptibility and environmental factor is one of the most important steps in the primary
     结论:扬中市胃癌呈明显家族聚集性的原因中,遗传易感性因素作用约占 1/4,指出阐明遗传易感基因与环境因素交互作用的研究对胃癌病因预防至关重要。
短句来源
  遗传易感因子
     Conclusion IL-6 gene-634C/G polymorphism may be a genetic susceptibility factor for the progression of diabetic nephropathy.
     结论 IL 6基因 6 34C/G多态性可能是糖尿病肾病进展的一个遗传易感因子
短句来源
     i.e., The result is helpful for further research on the genetic susceptibility factor of lung cancer.
     本研究为进一步寻找云南人群肺癌遗传易感因子奠定了基础
短句来源
  遗传易感因素
     Conclusions GSTP1 gene polymorphism may be a genetic susceptibility factor involved in the development of reflux esophagitis.
     结论 GSTP1基因 (10 4密码子A→G)多态可能是涉及反流性食管炎发生的遗传易感因素
短句来源
     Conclusion These findings suggest that STK15 Phe/Ile polymorphism may be a genetic susceptibility factor for colorectal cancer among Chinese.
     结论STK15Phe31Ile多态可能是大肠癌的遗传易感因素
短句来源
     [Conclusions] These results imply that GSTM1 gene delete may be a genetic susceptibility factor involved in the development of the HNs.
     【结论】 GSTM1基因缺失可能是涉及恶性血液病发生的遗传易感因素
短句来源
     Conclusion These findings suggest that 677CT polymorphism in MTHFR may be a genetic susceptibility factor for breast cancer among Chinese women.
     结论 MTHFR基因 6 77CT突变是女性乳腺癌的遗传易感因素
短句来源
     Conclusion These findings demonstrated that the genetic variation of MTHFR C677T should be a genetic susceptibility factor for colorectal cancer in a Chinese population.
     结论亚甲基四氢叶酸还原酶基因C677T基因多态性可能是我国大肠癌的遗传易感因素
短句来源
  “genetic susceptibility factor”译为未确定词的双语例句
     Conclusion Although there is no evidence to show the correlation between CYP2C19/CYP2D6(C100T) genetic polymorphisms and etiology of schizophrenia, the homozygote of CYP2C192 is possible a genetic susceptibility factor in Chinese subjects with schizophrenia.
     结论中国精神分裂症患者与健康人群在细胞色素氧化酶CYP2C19/CYP2D6遗传多态性上差异无统计学意义,CYP2C19*2的突变型纯合子可能是中国精神分裂症患者的一个易感因素。
短句来源
     Conclusion There was no IL-6/-597G/A polymorphism,but there was-572C/G polymorphism in Chinese Hans population. The latter may be a possible genetic susceptibility factor for ACS in Chinese Hans population.
     结论中国汉族人群中可能不存在IL-6基因-597G/A多态性,存在-572C/G多态性,后者可能是中国汉族人群ACS发病的易感基因之一。
短句来源
     Conclusion:IL-6/-572C/G polymorphism may be a possible genetic susceptibility factor for CHD in Chinese Hans population, but it does not affect serum IL-6 level.
     结论:IL-6基因-572C/G多态性可能是中国汉族人群CHD发病的遗传危险因素之一,但该多态性对血清IL-6水平无影响。
短句来源
     Conclusion IL-6/-597G/A polymorphism was not associated with susceptibility to CHD,but IL-6-572C/G polymorphism may be a possible genetic susceptibility factor for CHD in Chinese Hans population.
     结论IL-6基因-597G/A多态性可能与中国汉族人群CHD发病易感性无关,而-572C/G多态性可能是该人群CHD发病的易感基因之一,其可能通过对组织IL-6水平的影响及与血脂的协同作用参与CHD的发生。
短句来源
     Conclusion:The gene polymorphisms of CYP1B1 in exon 3 codon 432 may be a genetic susceptibility factor for ovarian cancer. The mutation of CYP1B1 gene increases the risk of ovarian cancer,and has positive correlation with ER expression.
     结论:CYP1B1基因密码子432突变等位基因与卵巢癌的发生有一定关系,突变基因型增加了卵巢癌的发病风险,且与ER的表达相关。
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  genetic susceptibility factor
MEFV mutations may act as a genetic susceptibility factor for vasculitides in FMF patients.
      
The DD genotype and D allele of ACE may be a genetic susceptibility factor contributing to scar formation in VUR.
      
There is some evidence of a genetic susceptibility factor that may predispose certain individuals to the development of nickel sensitivity.
      
To our knowledge, these data provide the first evidence that polymorphic variations in STK15 is a genetic susceptibility factor in breast cancer.
      
A putative genetic susceptibility factor has been proposed a potential mediator of this increased event risk.
      


Abstract Cancer formation is a multistage process involving tumor initiation, promotion, conversion, progression, and establishment. Genetic susceptibility factors, as well as occupational, environmental, and lifestyle/recrearlonal exposure to a host of factors including known and yet-to-be-characterized carcinogens contribute to cancer risks in humans.The association of a suspected carcinogenic exposure and cancer/disease risk can be and has been traditionally studied in populations using classic...

Abstract Cancer formation is a multistage process involving tumor initiation, promotion, conversion, progression, and establishment. Genetic susceptibility factors, as well as occupational, environmental, and lifestyle/recrearlonal exposure to a host of factors including known and yet-to-be-characterized carcinogens contribute to cancer risks in humans.The association of a suspected carcinogenic exposure and cancer/disease risk can be and has been traditionally studied in populations using classic epidemiologic methodologies in which factors affecting the frequency of appearance of a particular cancer/disease are typically evaluated by calculating and comparing the mean relatedness of a group with that cancer/disease with the mean of a group of age-and sex-matched controls. Even though inferences made from such approaches regarding a particular type of cancer/disease allow associations to be identified, causality remains not determinable. Moreover, classic epidemiologic techniques have limited applicability insofar as the assessment of risks in individuals is concerned.Molecular epidemiology is an emerging field that attempts to circumvent some of the aforementioned difficulties associated with classical epidemiologic approaches by emphasizing the use of molecular genetics and biochemical tools to evaluate an individual's cancer risks.It aims to prevent disease by using biological markers to identify risks well before clinical onset to allow effective intervention. By integrating our understanding of gene structure, function ,and abnormalities, with the development of in vitro and in vivo laboratory models, and the establishment of a battery of biological markers relevant to the measurement of molecular and genetic damages as well as to the diagnosis and prognosis of neoplastic diseases, molecular epidemiology can potentially help us to achieve the goal of advancing knowledge about health and disease among groups of people in ways that are appropriate for inference to larger populations.This report will attempt to illustrate these principles by presenting key methods in a conceptual framework to show how particular research techniques have provided insights into the problems of prostate cell transformation and carcinogenesis.

PRINCIPLESANDAPPLICATIONSOFMOLECULAREPIDEMIOLOGYANDSTUDIESOFHUMANPROSTATICCARCINOMATze-chenHsieh;ChunyungNgandJosephM.Wu(Dept...

Objectives To study the association between genetic polymorphisms of cytochrome P4502E1 (CYP2E1) and/or glutathione S transferase P1 (GSTP1) and susceptibility to esophageal cancer. Methods Genotyping of CYP2E1 and GSTP1 was performed using PCR based RFLP analysis on DNA isolated from surgically removed esophageal tissues or scraped esophageal epithelium from cancer cases ( n =45), severe epithelial hyperplasia cases ( n =45), and normal controls ( n =45). Results The variant genotypes (c1/c2...

Objectives To study the association between genetic polymorphisms of cytochrome P4502E1 (CYP2E1) and/or glutathione S transferase P1 (GSTP1) and susceptibility to esophageal cancer. Methods Genotyping of CYP2E1 and GSTP1 was performed using PCR based RFLP analysis on DNA isolated from surgically removed esophageal tissues or scraped esophageal epithelium from cancer cases ( n =45), severe epithelial hyperplasia cases ( n =45), and normal controls ( n =45). Results The variant genotypes (c1/c2 and c2/c2) detected by RsaI digestion was found in 17% of epithelial hyperplasia cases, 20.0% of esophageal cancer cases and 55.6% of controls, with the differences being statistically significant( P <0.001). Subjects carrying wild type genotype of CYP2E1 had more than 5 fold risk for developing severe epithelial hyperplasia (odds ratio, OR=5.78; 95% confidence interval, CI=2.2~15.2) and esophageal cancer (OR=5.00; 95% CI=2.0~12.8). No association with the risk of severe epithelial hyperplasia and esophageal cancer was observed for the DraI polymorphism of CYP2E1 or for the Awl26I polymorphism of GSTP1. Conclusion CYP2E1 is a genetic susceptibility factor involved in the early events for esophageal carcinogenesis.

目的研究与致癌物亚硝胺代谢激活有关的细胞色素P4502E1基因(CYP2E1),和与致癌物代谢解毒有关的谷胱甘肽转硫酶P1基因(GSTP1)多型性与食管癌易患性的关系。方法采用病例-对照分子流行病学方法。以PCR-RFLP方法分析食管癌、食管上皮重度增生病例,和与其年龄性别配对的正常对照者(各45例)CYP2E1和GSTP1的基因型。结果GSTP1基因型在病例和对照者中的分布无显著差别,但RsaI识别的CYP2E1基因型,在食管癌、食管上皮重度增生病例及其正常对照者中的分布差别显著。CYP2E1突变型基因频率在正常对照组中为55.6%,显著高于食管上皮重度增生病例(17.8%)和食管癌病例(20.0%;χ2=20.8,P<0.001);携带野生型CYP2E1的个体,发生食管上皮重度增生和食管癌的危险性,比携带变异型CYP2E1的个体各高5倍。结论CYP2E1基因是涉及食管癌变早期过程的遗传易患性因素。

AIM To study the association between genetic polymorphisms of cytochrome P 4502E1 ( CYP 2E1) and/?or glutathione S-transfarase M1 ( GS TM1) and susceptibility to gastric cancer, and to investigate the interaction of genetic and environmental factors in etiology of gastric cancer. METHODS A 1∶1 matched case-control study was conducted in Changle, Fujian Province, a high gastric cancer mortality area. A total of 101 pairs of cases and controls were matched on sex, age and nationality. Genotypes of the...

AIM To study the association between genetic polymorphisms of cytochrome P 4502E1 ( CYP 2E1) and/?or glutathione S-transfarase M1 ( GS TM1) and susceptibility to gastric cancer, and to investigate the interaction of genetic and environmental factors in etiology of gastric cancer. METHODS A 1∶1 matched case-control study was conducted in Changle, Fujian Province, a high gastric cancer mortality area. A total of 101 pairs of cases and controls were matched on sex, age and nationality. Genotypes of the CYP 2E1 and GST M1 genes were determined by the polymerase chain reaction. The methods of analysis was conditional logistic regression analysis. RESULTS Gastric cases were more likely to carry genotypes C1/?C2 and C2/?C2 than controls, 〔odds ratio (OR)=3 10,95% confidence interval (CI)=0 97-9 91〕. GSTM1 null genotype was a genetic susceptibility factor (OR=3 27,95%CI=1 14-9 39). Fish sauce intake(OR=14 74,95%CI=2 96-73 43),less consumption of fresh vegetables (OR=11 34,95%CI=1 98-64 78),and bad eating habits (OR=2 55,95%CI=1 14-5 73)were the risk factors of gastric cancer. CONCLUSION Genetic polymorphisms in enzymes involved in carcinogen metabolism and environmental risk factors may play an important role in the development of gastric cancer.

目的 研究与致癌物亚硝胺代谢激活有关的细胞色素P4502 E1 ( CYP2 E1) 和与致癌物代谢解毒有关的谷胱甘肽转硫酶( GSTM1) 基因多态与胃癌易患性,探讨环境基因在胃癌发病危险中的作用.方法 应用分子流行病学方法,在胃癌高发区福建省长乐市配比调查101 对原发性胃癌病例和按性别、年龄、民族配对的健康对照,PCR- RFLP 方法检测 CYP2E1 和 GSTM1 基因型,条件Logistic 回归模型进行资料分析.结果 胃癌病例平均年龄58-9 岁±11-0 岁,对照平均年龄58-6 岁±11-1 岁,两组年龄性别均衡可比. 胃癌病例CYP2E1的C1/ C2 或C2/ C2 基因频率高于对照,但差异无显著性意义〔比值比( OR) = 3-10 ,95 % 可信限( CI) = 0-97 - 9-91 〕.GSTM1 基因缺失与胃癌易患性有关( OR = 3-27 ,95 % CI=1-14 ~9-39) . 胃癌高发区居民长期食用鱼露( OR = 14-74 ,95 % CI= 2-96 ~73-43) 、少吃新鲜蔬菜( OR= 11-34 ,95 % CI=1-98 ~64-78) 和不良...

目的 研究与致癌物亚硝胺代谢激活有关的细胞色素P4502 E1 ( CYP2 E1) 和与致癌物代谢解毒有关的谷胱甘肽转硫酶( GSTM1) 基因多态与胃癌易患性,探讨环境基因在胃癌发病危险中的作用.方法 应用分子流行病学方法,在胃癌高发区福建省长乐市配比调查101 对原发性胃癌病例和按性别、年龄、民族配对的健康对照,PCR- RFLP 方法检测 CYP2E1 和 GSTM1 基因型,条件Logistic 回归模型进行资料分析.结果 胃癌病例平均年龄58-9 岁±11-0 岁,对照平均年龄58-6 岁±11-1 岁,两组年龄性别均衡可比. 胃癌病例CYP2E1的C1/ C2 或C2/ C2 基因频率高于对照,但差异无显著性意义〔比值比( OR) = 3-10 ,95 % 可信限( CI) = 0-97 - 9-91 〕.GSTM1 基因缺失与胃癌易患性有关( OR = 3-27 ,95 % CI=1-14 ~9-39) . 胃癌高发区居民长期食用鱼露( OR = 14-74 ,95 % CI= 2-96 ~73-43) 、少吃新鲜蔬菜( OR= 11-34 ,95 % CI=1-98 ~64-78) 和不良饮食习惯( OR = 2-55 ,95 % CI= 1-14 ~5-?

 
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