结直肠癌患病的糖尿病相关因素研究

目的了解糖尿病与结直肠癌患病的关系，明确糖尿病相关因素对结直肠癌发病的影响，为做好结直肠癌的一级预防提供思路。方法采用病例对照的方法分析同时期住院的结直肠癌（n=364）与非肿瘤患者（n=733）与糖尿病相关因素的关系及差异。对比分析两组患者的糖尿病患病情况、糖尿病家族史、结直肠癌家族史、并发病情况、吸烟、饮酒等生活行为以及血脂、血糖水平等方面的差异。结果肿瘤组糖尿病患者患结直肠癌的危险度是非糖尿病患者的1．72倍，有糖尿病家族史者患结直肠癌的危险度也明显增加，OR值为1．64；有结直肠癌家族史的糖尿病患者患结直肠癌的风险度（OR=3．23）高于无结直肠癌家族史的糖尿病患者（OR=1．57）；但通过进一步分层分析表明无论患者有无结直肠癌家族史，肿瘤组糖尿病患者所占比例均高于对照组。肿瘤组平均空腹血糖水平为5．61mmol／L，与对照组比较有显著性差异；其发生结直肠癌的危险度是血糖水平正常者的2．22倍。肿瘤组平均甘油三酯水平和胆固醇水平均低于非肿瘸组，但未见统计学差异。多因素回归分析显示：年龄、性别、糖尿病家族史、冠心病、高血压、吸烟、饮酒及血脂未进人方程，对结直肠癌未见显著影响；糖尿病及结直肠癌家族史对结直肠癌患病具有显著影响。结论糖尿病与结直肠癌患病存在一定的相关性，糖尿病增加了患结直肠癌的风险性，其是结直肠癌患病的独立危险因素。加强糖尿病的防治将对预防结直肠癌患病和改善预后有重要的作用。     

糖尿病患者合并结直肠癌的危险性分析

目的了鳃糖尿病是否为结直肠癌发病的重要危险因素。方法采用病例对照研究方法对758例（23～87岁）结直肠癌患者糖尿病合并状况及相关危险因素进行调查。结果糖尿病患者患结直肠癌的危险显著高于非糖尿病患者，且与糖尿病类型无关，相对危险度（0R值）为3．58；有糖尿病家族史和结直肠癌家族史者结直肠癌发生危险明显高于无家族史者，其OR值分别为2．53和3．30；糖尿病病程在10～20年组并发结直肠癌的危险性最高；与非糖尿病合并结直肠癌者相比，糖尿病合并结直肠癌患者发生淋巴结或其他组织器官转移的几率更高，其OR值为2．37。结论糖尿病可能是结直肠癌发生的危险因素之一，糖尿病家族史和结直肠癌家族史与糖尿病在结直肠癌的发生中有协同作用。合并糖尿病的结直肠癌患者易发生淋巴结或其他组织器官转移。     

结直肠癌患者术后吻合口瘘发生的危险因素分析

目的分析结直肠癌患者术后吻合口瘘发生的危险因素。方法对该院2006-01～2018-06行结直肠癌根治术治疗的459例患者临床资料进行回顾性分析,采用单因素和多因素Logisitc回归分析探讨术后吻合口瘘发生的危险因素。结果吻合口瘘发生率为9.80%(45/459)。多因素Logistic回归分析结果显示年龄(OR=2.815)、术前合并糖尿病(OR=4.872)、术前合并低蛋白血症(OR=3.258)、肿瘤距肛门缘距离(OR=4.153)是结直肠癌术后吻合口瘘发生的危险因素。结论年龄、术前合并糖尿病、术前合并低蛋白血症、肿瘤距肛门缘距离是结直肠癌术后吻合口瘘发生的危险因素,围术期应充分考虑这些因素的影响,并采取适当的预防措施。     

血脂异常患者结直肠早期癌发病的危险因素分析

探讨血脂异常患者结直肠早期癌发病的危险因素,以及他汀类药物在其中可能发挥的作用。回顾性分析2018年2月—2021年2月北京友谊医院消化科行内镜治疗合并血脂异常的结直肠肿物患者资料。根据结肠镜及病理结果将266例患者分为结直肠腺瘤组（n=174）和结直肠早期癌组（n=92）。分析两组患者临床资料的差异,采用Logistic回归分析血脂异常患者结直肠早期癌发病的危险因素。结果发现,与结直肠腺瘤组相比,结直肠早期癌组患者的男性比例（64.1%比25.9%）、吸烟比例（41.3%比14.4%）和饮酒比例（37.0% 比17.2%）更高,同时低密度脂蛋白胆固醇［（3.06±0.81） mmol/L比（2.60±0.74） mmol/L］和总胆固醇值更高［（5.27±1.22） mmol/L 比（4.61±1.06） mmol/L］,而他汀用药占比更低（27.2% 比52.9%）,差异均有统计学意义（P均<0.05）。多因素Logistic回归分析显示,男性（OR=3.641, 95%CI：1.694~7.826）、吸烟（OR=2.920, 95%CI：1.159~7.356）以及较高的低密度脂蛋白胆固醇（OR=2.203,95%CI：1.481~3.277）、较高的总胆固醇水平（OR=1.744,95%CI：1.329~2.289）是血脂异常患者结直肠早期癌发生的危险因素,而他汀用药史（OR=0.469,95%CI：0.236~0.932）对避免血脂异常患者结直肠早期癌的发生具有保护作用。应对血脂异常患者进行戒烟宣教,监测低密度脂蛋白胆固醇、总胆固醇水平,必要时使用他汀类药物促进血脂达标,同时积极进行结直肠癌的早期筛查。     

武汉市不同年龄公务员牙周炎危险因素的相关性研究

目的 调查武汉市不同年龄公务员牙周状况,并对其危险因素进行单因素和多因素分析. 方法 2007年1月至2008年3月采用随机整群抽样的方法 调查年龄30～79岁体检者493例的口腔状况,符合纳入标准458例,其中30～59岁(中青年组)288例,60～79岁(老年组)170例.其中牙周炎患者280例为病例组,无牙周炎178例为对照组.采用SQSERVER2000软件建立数据库,分别对年龄、性别、民族、学历、糖尿病、吸烟、饮酒、精神压力和口腔卫生习惯与牙周炎相关性进行单因素和多因素分析. 结果 458例检出280例牙周炎患者,患病率为61.1%.单因素分析结果 显示,年龄、学历,糖尿病、吸烟和口腔卫生习惯是患牙周炎的危险因素(OR值分别为0.44、2.27、3.44、1.75、9.82,P<0.05或P<0.01).多因素分析结果 显示,糖尿病和低学历(OR值分别为2.66、1.95,均为P<0.05)为牙周炎的危险因素.以年龄分层进行多因素分析时,中青年人糖尿病与牙周炎患病率无相关性.老年组糖尿病(OR=6.91,95%CI:1.27～37.42)是牙周炎的危险因素. 结论 牙周炎患病的危险因素较多,老年人糖尿病是牙周炎的患病的主要危险因素.     

中国人群老年性痴呆发病危险因素的荟萃分析

目的 探讨中国人群老年性痴呆(AD)发生的主要危险因素,为预防决策提供依据.方法 收集1980年1月至2008年11月国内外公开发表的关于AD发病危险因素独立病例对照研究,并用RevMan软件对这些文献进行荟萃综合定量,采用卡方值和p值分析各研究结果间的统计学异质性.结果 纳入本次荟萃分析的文献共有11篇,累计病例1 420例,对照2 901例.AD发生的危险因素合并相对危险度(OR)值及95%可信区间(95%CI)分别为:痴呆家族史[OR=2.62,95% CI(1.69～4.07)];丧偶[OR=1.53,95%CI(1.21～1.93)];饮酒[OR=0.87,95%CI(0.68～1.12)];吸烟[OR=0.80,95%CI(0.67～0.95)].结论 痴呆家族史和丧偶是目前影响中国人群AD发生的危险因素.     

绝经期前女性冠心病的临床特点及危险因素分析

目的探讨绝经期前女性冠状动脉粥样硬化性心脏病(CHD)的临床特点及相关危险因素。方法入选绝经期前女性CHD患者450例,并抽取同期通过冠状动脉造影确诊无CHD的400例女性患者作为对照。比较两组患者高血压、糖尿病、家族史、吸烟等危险因素及临床情况的差异。随访1年。结果 CHD组患者的高血压、糖尿病、吸烟和高血压家族史、糖尿病家族史、早期CHD家族史的比例均高于对照组(均为P<0.05)。两组患者的血脂水平(包括总胆固醇、三酰甘油、低密度脂蛋白胆固醇、高密度脂蛋白胆固醇)和体质指数,差异均无统计学意义(均为P>0.05)。Logistic回归分析显示,早期CHD家族史(OR:4.669,95%CI:1.982～22.577,P=0.018)和高血压病史(OR:3.665,95%CI:1.153～11.586,P=0.028)是绝经期前女性患CHD的独立危险因素。结论绝经期前的女性CHD患者常同时合并多种危险因素,高血压和早期CHD家族史是绝经期前女性患CHD的独立危险因素。需提高对绝经期前女性CHD高危人群的警惕性。     

结直肠癌相关脑梗死临床特点与发病机制的探讨

目的探讨结直肠癌相关脑梗死临床特点和发病机制。方法选择2005年1月～2018年8月在广西医科大学第一附属医院住院的结直肠癌相关脑梗死患者34例(相关脑梗死组),选择同时期住院治疗的单纯脑梗死患者34例(单纯脑梗死组)和单纯结直肠癌患者34例(对照组)。收集3组患者临床资料,并进行对比分析。结果与单纯脑梗死组比较,相关脑梗死组多支血管供血区(双侧前循环,双侧前循环+后循环)、皮质/皮质下、无脑卒中危险因素、隐源性脑梗死、预后不良、死亡比例和血浆D-二聚体水平明显升高,单支血管供血区(单发脑梗死)、预后良好比例明显降低,差异有统计学意义(P0.05,P0.01)。与对照组比较,相关脑梗死组癌症远处转移、血浆D-二聚体、癌胚抗原和CA125水平明显升高,差异有统计学意义(P0.05,P0.01)。多因素logistic回归分析显示,血浆D-二聚体和CA125是结直肠癌相关脑梗死患者的独立危险因素(OR=9.261,95%CI:1.000～1.002,P=0.002;OR=5.689,95%CI:1.003～1.032,P=0.002)。结论结直肠癌相关脑梗死以缺乏常见脑卒中危险因素、脑内出现累及多动脉供血区的多发性脑梗死、血浆D-二聚体、CA125和癌胚抗原水平显著升高及预后不良为临床特点,其发病机制可能与高凝状态导致血管内微小血栓形成有关。     

驻长沙军队老年干部脑卒中患病率和危险因素调查分析

目的:了解驻长沙军队男性老年干部脑卒中患病率及其危险因素。方法:采用整群抽样问卷调查方法,对2012年1～6月在湖南省长沙市解放军163医院体检或住院的军队男性老年(60岁以上)干部4217例进行调查并检测血糖、血脂、C反应蛋白(CRP)等相关指标,分析脑卒中的发生情况;采用非条件Logistic回归法进行相关危险因素分析。结果:驻长沙军队老年干部脑卒中患病率为20.3%,脑卒中的相关危险因素为吸烟(OR=2.859)、糖尿病家族史(OR=2.163)、高CRP水平(OR=1.834)、肥胖(OR=1.506)、高龄(OR=1.120),P均<0.01。结论:驻长沙军队男性老年干部脑卒中患病率较高,其危险因素是吸烟、有糖尿病家族史、高C反应蛋白水平、肥胖和高龄。     

日本血吸虫病对胃癌和结直肠癌发生的影响

目的探讨日本血吸虫病对胃癌及结直肠癌发生发展的影响。方法收集2014年1月-2018年12月皖南医学院弋矶山医院收治的合并血吸虫病及不合并血吸虫病的胃癌和结直肠癌患者临床资料,分成血吸虫病胃癌组和非血吸虫病胃癌组、血吸虫病结直肠癌组和非血吸虫病结直肠癌组。采用单因素分析和多因素logistic回归分析对胃癌和结直肠癌发病危险因素进行分析,探索血吸虫病对胃癌和结直肠癌发生发展的影响。对32例血吸虫病合并结直肠癌患者以及68例非血吸虫病结直肠癌患者进行电话随访,获取患者生存情况,计算并比较两组患者生存率。结果血吸虫病胃癌组患者113例、非血吸虫病胃癌组患者3741例,两组患者性别构成比、年龄、幽门螺杆菌感染率差异均有统计学意义(P均<0.05)。logistic回归分析表明,年龄、幽门螺杆菌感染和合并血吸虫病是胃癌发病的独立危险因素(P均<0.05)。血吸虫病结直肠癌组患者184例、非血吸虫病结直肠癌组患者2205例,两组年龄、性别构成比、有饮酒史者比例、粪便隐血阳性者比例差异均有统计学意义(P均<0.05);两组结直肠癌表型均以溃疡型居多,但非血吸虫病结直肠癌组浸润型和隆起型患者比例明显高于血吸虫病结直肠癌组(P=0.003)。logistic回归分析结果显示,年龄(P=0.003)、性别(P=0.002)、表型(P=0.005)以及合并血吸虫病(P=0.029)是结直肠癌的独立危险因素。经随访,血吸虫病结直肠癌患者5年生存率(68.90%)高于非血吸虫病结直肠癌患者(46.40%),其死亡患者平均年龄[(66.33±3.08)岁]亦高于后者[(56.29±1.94)岁],差异均有统计学意义(P均<0.05)。结论血吸虫病可能改变结直肠癌发病机制,导致血吸虫病和非血吸虫病结直肠癌患者在流行病学、临床特征以及5年生存率方面存在差异。血吸虫病流行区年龄>60岁的男性,且伴有不明原因贫血者,应定期进行消化道内镜检查和其他检查,以排除消化道肿瘤的可能性。     

Risk factors for sporadic colorectal cancer in southern Chinese

AIM： To investigate the role of smoking, alcohol drinking, family history of cancer, and body mass index （BMI） in sporadic colorectal cancer in southern Chinese. METHODS： A hospital-based case-control study was conducted from July 2002 to December 2008. There were 706 cases and 723 controls with their sex and age （within 5 years） matched. An unconditional logistic regression model was used to analyze the association between smoking, alcohol drinking, family history of cancer, BMI and sporadic colorectal cancer. RESULTS： No positive association was observed between smoking status and sporadic colorectal cancer risk. Compared with the non alcohol drinkers, the current and former alcohol drinkers had an increased risk of developing sporadic colorectal cancer （CRC） （adjusted OR = 8.61 and 95% CI = 6.15-12.05, adjusted OR = 2.30, 95% CI = 1.27-4.17）. Moreover, the increased risk of developing sporadic CRC wassignificant in those with a positive family history of cancer （adjusted OR = 1.62, 95% CI = 1.12-3.34） and in those with their BMI ≥ 24.0 kg/m^2 （adjusted OR = 1.39, 95% CI = 1.10-1.75）. Stratification analysis showed that the risk of developing both colon and rectal cancers was increased in current alcohol drinkers （adjusted OR = 7.60 and 95% CI = 5.13-11.25; adjusted OR = 7.52 and 95% CI = 5.13-11.01） and in those with their BMI ≥ 24.0 kg/m^2 （adjusted OR = 1.38 and 95% CI = 1.04-1.83; adjusted OR = 1.35 and 95% CI = 1.02-1.79）. The risk of developing colon cancer, but not rectal cancer, was found in former alcohol drinkers and in those with a positive family history of cancer （adjusted OR = 2.51 and 95% CI = 1.24-5.07; adjusted OR = 1.82 and 95% CI = 1.17-2.82）. CONCLUSION： Alcohol drinking, high BMI （≥ 24.0 kg/m^2） and positive family history of cancer are the independent risk factors for colorectal cancer in southern Chinese.     

Predictors of proximal neoplasia in patients without distal adenomatous pathology

BACKGROUND: Previous colorectal cancer screening studies have observed that some patients may have advanced proximal neoplasia without distal findings. Since these studies have included only gender, age, and family history as risk factors, they are limited in their ability to identify predictors of isolated proximal neoplasia. METHODS: Data were collected from the charts of 1,988 patients who presented for colonoscopy. Information gathered included endoscopic findings, histology, known risk factors for colorectal neoplasia, and smoking pattern. Our main outcome was the presence of proximal adenomatous neoplasia in patients who had no distal adenomas. We defined significant neoplasia as adenocarcinoma, high-grade dysplasia, villous polyps, adenomas 1 cm or greater or more than two adenomas of any size. RESULTS: Fifty-five patients had isolated significant proximal neoplasia that would have been missed on a flexible sigmoidoscopy. While patients older than 60 yr had a greater risk for this neoplasia (odds ratio = 3.01: 95% CI = 1.66-4.23; p < 0.001), those who took a daily aspirin had a reduced risk (OR = 0.60; 95% CI = 0.30-0.88; p < 0.05). A family history of colorectal cancer increased the patient's risk of having any adenomas (OR = 2.01; 95% CI = 1.33-3.40; p < 0.01) or villous tissue (OR = 2.03; 95% CI = 1.27-3.51; p < 0.05) in the proximal colon without distal findings. Smoking was associated with an increased risk of large (> 1 cm) isolated proximal tubular polyps (OR = 2.71; 95% CI = 1.64-4.46; p < 0.01) as well as isolated significant proximal neoplasia (OR = 2.30; 95% CI = 1.59-3.31; p < 0.01). CONCLUSIONS: Age greater than 60 yr, a history of at least 10 pack-years of smoking, and a family history of colorectal cancer increased the risk of finding significant proximal polyps in patients without distal pathology.     

Risk of colorectal adenomas in patients with a family history of colorectal cancer: some implications for screening programmes.

BACKGROUND AND AIMS: Most colorectal cancers (CRC) arise in colorectal adenomas. A case-control study was conducted to see whether a family history of CRC is associated with a higher prevalence of colorectal adenomas. SUBJECTS: Subjects were drawn from all patients who underwent colonoscopy at the Royal Brisbane Hospital between 1980-1982 and 1985, and included 141 cases with colorectal adenomas diagnosed at colonoscopy and 882 controls who were free of polyps at colonoscopy. METHODS: The prevalence of family history of CRC was compared between patients with adenomas and negative colonoscopy controls. RESULTS: Overall, patients with one first degree relative with CRC were at no greater risk for adenomas at colonoscopy than patients with no family history (odds ratio (OR) = 0.8, 95% confidence intervals (CI) = 0.4, 1.5). Patients with two or more affected first degree relatives had a more than doubled risk for adenomas (OR = 2.3, 95% CI = 0.5, 8.2), and were also more likely to carry moderately or severely dysplastic adenomas (OR = 14.1, 95% CI = 2.0, 62.9). CONCLUSIONS: These findings are consistent with the hypothesis that some families, in addition to those with familial adenomatous polyposis, have an increased susceptibility to develop colorectal adenomas, and that adenomas in such families may have a greater tendency to undergo malignant transformation.     

APE1 polymorphisms are associated with colorectal cancer susceptibility in Chinese Hans

AIM: To study the association between four base excision repair gene polymorphisms and colorectal cancer risk in a Chinese population.METHODS: Two hundred forty-seven colorectal cancer (CRC) patients and three hundred cancer-free controls were enrolled in this study. Four polymorphisms (OGG1 Ser326Cys, APE1 Asp148Glu, -141T/G in the promoter region, and XRCC1 Arg399Gln) in components of the base excision repair pathway were determined in patient blood samples using polymerase chain reaction with confronting two-pair primers. The baseline information included age, gender, family history of cancer, and three behavioral factors [smoking status, alcohol consumption, and body mass index (BMI)]. χ² tests were used to assess the Hardy-Weinberg equilibrium, the distributions of baseline characteristics, and the four gene polymorphisms between the cases and controls. Multivariate logistic regression analyses were conducted to analyze the correlations between the four polymorphisms and CRC risk, adjusted by the baseline characteristics. Likelihood ratio tests were performed to analyze the gene-behavior interactions of smoking status, alcohol consumption, and BMI on polymorphisms and CRC susceptibility.RESULTS: The APE1 148 Glu/Glu genotype was significantly associated with an increased risk of colorectal cancer (OR = 2.411, 95%CI: 1.497-3.886, P < 0.001 relative to Asp/Asp genotype). There were no associations between OGG1, XRCC1, or APE1 promoter polymorphisms and CRC risk. A multivariate analysis including three behavioral factors showed that the APE1 148 Glu/Glu genotype was associated with an increased risk for CRC among both smokers and non-smokers, non-drinkers and individuals with a BMI ≥ 25 kg/m² (ORs = 2.356, 3.299, 2.654, and 2.581, respectively). The XRCC1 399 Arg/Gln genotype was associated with a decreased risk of CRC among smokers and drinkers (OR = 0.289, 95%CI: 0.152-0.548, P < 0.001, and OR = 0.327, 95%CI: 0.158-0.673, P < 0.05, respectively). The APE1 promoter polymorphism -141 T/G genotype was associated with a reduced risk of colorectal cancer among subjects with a BMI < 25 kg/m² (OR = 0.214, 95%CI: 0.069-0.660, P < 0.05 relative to T/T genotype). There were significant gene-behavior interactions between smoking status and XRCC1 Arg399Gln, as well as BMI and APE1 -141T/G polymorphism (all P < 0.05).CONCLUSION: APE1 Asp148Glu is associated with increased CRC risk and smoking alters the association between XRCC1 Arg399Gln and CRC risk in the Chinese Han population.     

Elevated risk of colorectal cancer associated with the AA genotype of the cyclin D1 A870G polymorphism in an Indian population

Purpose: To investigate whether the common cyclin D1 (CCND1) A870G polymorphism is a risk factor for colorectal cancer (CRC) in an Indian population. Methods: In this study, 301 newly diagnosed CRC patients and 291 healthy control subjects were genotyped by the PCR-RFLP method. Genotype frequencies were compared between cases and controls, and the association of genotypes with CRC was studied. Results: The CCND1 870 A allele was more frequently observed in CRC patients than controls (0.63 vs. 0.56, P=0.01), and after adjustment for age, sex, smoking habits, family history, family income and the consumption of meat, fish, vegetables and fruit, an increased risk was observed for the AA genotype compared to the GG+AG genotype (OR=1.56; 95% CI: 1.10–2.21). The increased risk were also found for colon (OR=1.96; 95% CI: 1.08–3.57) and rectal cancer (OR=1.51; 95% CI: 1.04–2.19). No correlation was observed between genotypes and age of diagnosis of CRC (49.9, 48.7 and 49.4 years for the GG, AG and AA genotypes, respectively; P=0.84). Multivariate analysis also revealed a stronger positive association with the AA genotype among patients with high meat intake (OR=2.67; 95% CI: 1.29–5.51), and particularly significant inverse associations with the GG+AG genotypes were also found for those with high vegetable consumption (OR=0.46; 95% CI: 0.27–0.79 of 2–3 servings/day, and OR=0.31; 95% CI: 0.18–0.53 for >3 servings/day) and fish intake (OR=0.48; 95% CI: 0.28–0.82). Conclusion: These data support the hypothesis that the CCND1 A870G polymorphism may increase the risk of CRC in our Indian population.     

Cyclooxygenase 2 polymorphism and colorectal cancer： -765G〉C variant modifies risk associated with smoking and body mass index

AIM： To explore whether cyclooxygenase 2 （COX-2） -765G〉C polymorphism is associated with susceptibility of colorectal cancer （CRC） and to evaluate the risk of colorectal cancer in relation to environmental exposures and polymorphism. METHODS： We conducted a case-control study of 137 patients with colorectal cancer and 199 cancerfree controls in northeast China. Multivariate logistic regression analysis was performed to calculate the adjusted odds ratio （OR） and 95% confidence interval （95% CI）. RESULTS： The -765G〉C polymorphism was not independently associated with CRC risk. However, risk associated with the polymorphism differed by smoking and body mass index （BMI）. Smoking and BMI associated risks were stronger among those with -765GG genotype, showing that smokers had a 2.682-fold greater risk of CRC than nonsmokers （51/43 vs 68/126, P = 0.006）. Compared to those with a normal body mass index （BMI 18.5-22.9）, those with overweight （BMI 23-24.9） had a 3.909-fold higher risk of CRC （OR = 3.909, 95% CI = 2.081-7.344; P 〈 0.001）, while those with obesity （BMI 〉 25） had a 2.031- fold higher risk of CRC （OR = 1.107, 95% CI = 1.107-3.726; P = 0.022）. is not associated with an increased risk of CRC, -765GG genotype appears to be related to an increased risk in the presence of smoking and higher BMI.     

Association between family history and mismatch repair in colorectal cancer

BACKGROUND AND AIMS: Germline mutations in mismatch repair (MMR) genes cause a greatly increased risk of cancer of the gastrointestinal and female reproductive tracts (hereditary non-polyposis colorectal cancer (HNPCC)). Loss of MMR expression is common in colorectal cancer (CRC) overall. Such loss is assumed to be acquired predominantly, although a population of CRC cases will include individuals with unrecognised MMR mutations. This study examines the association between MMR gene expression and family history of cancer among the CRC population. METHODS: Individuals with CRC were identified from two well characterised populations: (1) consecutive hospital patients (n = 644) and (2) a population based cases series (n = 249). CRC was examined for expression of hMLH1 and hMSH2 using immunohistochemistry, and expression was related to family history using logistic regression. RESULTS: hMLH1 and hMSH2 expression was assessed in 732 CRCs with 8% showing loss of expression. No association was seen overall for hMLH1 or hMSH2 expression and family history of CRC. Loss of hMSH2 was predicted by family history of extracolonic cancer (odds ratio (OR) 5.78 (95% confidence interval (CI) 0.95-35.18)) and family history suggestive of HNPCC (OR 27.84 (95% CI 4.37-177.56)). Loss of hMLH1 was not predicted by family history of extracolonic cancer or a family history suggestive of HNPCC but was for a family history of at least two affected relatives (OR 4.88 (95% CI 1.25-19.03)). CONCLUSIONS: Individuals with hMSH2 deficient CRC in the general population exhibit a family history and other characteristics suggestive of HNPCC, and may carry germline MMR mutations. Loss of hMLH1 is only associated with a strong family history of extracolonic cancer at older ages, suggesting a novel mechanism of susceptibility.     

Glutathione-S-transferase （GSTM1, GSTrl） and the risk of gastrointestinal cancer in a Korean population

AIM: To evaluate the association of glutathione S-transferase mu (GSTM1) and glutathione S-transferase theta (GSTT1) null genotypes with the risk of gastric cancer (GC) and colorectal cancer (CRC) in a South Korean population.METHODS: We conducted a population-based, large-scale case-control study including 2213 GCs, 1829 CRCs, and 1699 controls. Null and non-null genotypes of GSTM1 and GSTT1 were determined using real-time PCR.RESULTS: The null genotypes of GSTM1 and GSTT1 were not significantly associated with elevated risk of gastric (OR = 1.070, 95% CI = 0.935-1.224; OR = 1.101, 95% CI = 0.963-1.259, respectively) or colorectal cancer (OR = 1.065, 95% CI = 0.923-1.228; OR = 1.041, 95% CI = 0.903-1.200, respectively). The frequency of the combined null GST genotype was not different between the two cancer groups and controls. Moreover, smoking, drinking, and age did not modify the association between these genotypes and the risk of gastric or colorectal cancer.CONCLUSION: GSTM1 and GSTT1 null genotypes were not associated with increased risk of GC or CRC in Koreans.     

Glutathione-S-transferase (GSTM1, GSTT1) and the risk of gastrointestinal cancer in a Korean population

AIM: To evaluate the association of glutathione S-transferase mu (GSTM1) and glutathione S-transferase theta (GSTT1) null genotypes with the risk of gastric cancer (GC) and colorectal cancer (CRC) in a South Korean population.METHODS: We conducted a population-based, largescale case-control study including 2213 GCs, 1829CRCs, and 1699 controls. Null and non-null genotypes of GSTM1 and GSTT1 were determined using realtime PCR.RESULTS: The null genotypes of GSTM1 and GSTT1 were not significantly associated with elevated risk of gastric (OR = 1.070, 95% CI = 0.935-1.224; OR = 1.101, 95% CI = 0.963-1.259, respectively) or colorectal cancer (OR = 1.065, 95% CI = 0.923-1.228; OR = 1.041, 95% CI = 0.903-1.200, respectively). The frequency of the combined null GST genotype was not different between the two cancer groups and controls.Moreover, smoking, drinking, and age did not modify the association between these genotypes and the risk of gastric or colorectal cancer.CONCLUSION: GSTM1 and GSTT1 null genotypes were not associated with increased risk of GC or CRC in Koreans.     

Risk factors for pancreatic cancer in Orientals

In order to assess what the risk factors for patients with pancreatic cancer (PC) in Taiwan are, a retrospective study was undertaken among 282 consecutively enrolled inpatients with confirmed pancreatic cancer within the past 5 years. For comparison, 282 age- and sex-matched controls were consecutively enrolled. A history of smoking, consumption of alcohol, diabetes mellitus, cholecystectomy and gastric surgery were thoroughly reviewed. Smoking and diabetes mellitus were very common among patients with pancreatic cancer compared with controls (P< 0.01). A significant linear trend towards an increased odds ratios (OR) for the development of PC with a higher level of smoking was seen (P<0.001). Diabetes mellitus (DM) also exhibited an increased risk (OR: 2.84; P<0.01), while this risk still existed among those patients who had a diabetic history of more than 3 years. Among 129 histologically established PC patients, smoking remained as a risk factor for PC, while the linear trend with an increasing OR with increasing levels of smoking was confirmed again (P<0.01). DM, particularly over the long-term, was also a risk factor for those histologically established PC patients. In summary, cigarette smoking and existing diabetes mellitus are probable risk factors for the development of pancreatic cancer in Taiwan.