食管癌前病变研究进展

食管癌前病变研究进展河北省肿瘤研究所陈志峰侯波（指导）高发区流行病学研究表明Ｅ’］：细胞学诊断的食管上皮细胞重度均生（重增）或组织清理学确诊的食管粘膜上皮不典型增生是食管癌前病变．对癌前病变的阻断阻治疗，是食管癌１１级预防一个重要内容．本文概括的总结...     

河南省林州市2004与1980年食管癌前病变和食管癌患病率的比较研究

目的:评估河南省林州市当前食管癌的发病率。方法:按1980年普查的自然村分布,以及居民性别、年龄组的构成,选择其匹配的检查对象,进行内镜与活检组织学检查。结果:2004年普查958例,食管炎占43·53%(417/958),明显低于1980年的64·33%(339/527),差异有统计学意义,z=7·67,P<0·001;基底细胞增生占38·52%(369/958);非典型性增生占9·50%(91/958),与1980年的7·97%(42/527)相比差异无统计学意义,z=0·987,P>0·05;2004年食管癌占3·34%(32/958),与1980年的1·90%(10/527)相比差异无统计学意义,z=1·605,P>0·05。结论:2004年林州高危人群食管癌前病变与癌的患病率未见降低。     

盐亭县核黄素强化盐干预试验人群食管癌前病变与转归的研究

目的:研究核黄素强化盐对食管癌高发人群食管癌前状态的影响.方法:用食管脱落细胞学检查方法,比较分析在食管癌高发区四川盐亭县开展核黄素强化营养盐干预5年的前后,试验组与对照组食管上皮增生的检出率、食管正常者的进展率和食管增生者的逆转率,评价核黄素强化盐对人群的食管癌前病变的干预效果.结果:干预试验前,试验组和对照组的食管上皮增生检出率,男性分别为19.6%(47/240)和10.9%(24/222),女性分别为15.5%(36/233)和13.6%(29/213);干预5年后,试验组男性和女性食管上皮增生检出率分别为12.5%(30/240)和12.9%(30/233),比对照组分别降低49/6%(X2=11.55,P<0.01)和57.0%(X219.68,P<0.01).与对照相比,试验组男性和女性食管增生转归的比数比分别为3.8(95%CI为1.1～13.2,P<0.05)和10.0(95%CI为2.6～37.9,P<0.01);而在正常人群中,试验组男性和女性食管向癌变进展的比数比分别为0.42(95%CI为0.24～0.76,P<0.01)和0.38(95%CI为0.21～0.68,P<0.01).结论:在食管癌高发区人群中实施核黄素强化营养盐的干预措施能延缓和逆转食管癌前病变的发展进程,有益于降低食管癌的发病率.     

食管多原发癌及食管贲门重复癌：附13例报告

我院自１９８６年１月～１９９７年１２月，在９５２例经手术治疗的食管癌病例中，发现食管多原发癌５例及食管贲门重复癌８例，共计１３例，均经手术和（或）病理证实。报告如下。临床资料作者单位：３１０００９浙江医科大学附属第二医院心胸外科本组１３例中，男性１１...     

保留贲门结肠代食管治疗食管癌的初步探讨

我科自1992年10月至1996年9月利用横结肠代食管保留贲门重建食管手术,治疗颈段和胸中、上段食管癌39例,报告如下.     

食管癌高发区的内镜普查研究

目的　通过内镜普查了解食管癌高发区人群食管及贲门癌和其他各级病变的分布情况。方法 :河北省肿瘤研究所于 2 0 0 1年 12月 - 2 0 0 2年 5月在河北省磁县进行了碘染色内镜普查 ,普查结果采用SPSS10 0处理。结果 :食管癌高发区人群中 ,轻、中、重度食管炎的组织学检出率分别是 34 9%、1 6 %、0 2 % ,基底细胞增生、轻、中、重度不典型增生的组织学检出率分别是 0 9%、8 6 %、7 8%、2 6 % ,原位癌、黏膜内癌、浸润性鳞癌的组织学检出率分别是 2 5 %、0 2 %、0 7% ;贲门黏膜非萎缩性胃炎、萎缩性胃炎的组织学检出率分别是 36 3%、11 5 % ,轻、重度不典型增生的组织学检出率分别是2 5 %、0 8% ,黏膜内腺癌、浸润性腺癌的组织学检出率分别是 0 1%、0 8% ;内镜普查食管癌的早期发现率为 79 4 % ,普查率达 73 8%。结论 :本次普查为食管及贲门早期癌的治疗及癌前病变的阻断治疗提供了组织学诊断 ,为今后提高食管癌、贲门癌的治愈率 ,降低食管癌、贲门癌的发病率及死亡率打下了基础     

食管癌高发区的内镜普查研究

目的 通过内镜普查了解食管癌高发区人群食管及贲门癌和其他各级病变的分布情况。方法：河北省肿瘤研究所于2001年12月-2002年5月在河北省磁县进行了碘染色内镜普查，普查结果采用SPSS10．0处理。结果：食管癌高发区人群中，轻、中、重度食管炎的组织学检出率分别是34．9％、1．6％、0．2％，基底细胞增生、轻、中、重度不典型增生的组织学检出率分别是0．9％、8．6％、7．8％、2．6％，原位癌、黏膜内癌、浸润性鳞癌的组织学检出率分别是2．5％、0．2％、0．7％；贲门黏膜非萎缩性胃炎、萎缩性胃炎的组织学检出率分别是36．3％、11．5％，轻、重度不典型增生的组织学检出率分别是2．5％、0．8％，黏膜内腺癌、浸润性腺癌的组织学检出率分别是0．1％、0．8％；内镜普查食管癌的早期发现率为79．4％，普查率达73．8％。结论：本次普查为食管及贲门早期癌的治疗及癌前病变的阻断治疗提供了组织学诊断，为今后提高食管癌、贲门癌的治愈率，降低食管癌、贲门癌的发病率及死亡率打下了基础。     

食管和贲门癌癌变多阶段演进机制

食管和贲门上皮癌变是一个多阶段、进行性演进过程。上皮细胞增生异常是食管和贲门癌易患人群最早期变化特征。食管上皮细胞增生异常的形态表现为基底细胞过度增生(basal cell hyperplasia,BCH)、间变(dysplasia,DYS)和原位癌(carcinoma in situ,CIS);贲门上皮细胞增生异常的形     

食管和贲门癌及癌前病变患者血清中多个自身抗体的检测及其临床意义

目的:探讨食管和贲门癌及癌前病变患者血清中多个肿瘤相关自身抗体的变化特征及其在食管和贲门癌高危人群筛查和早期诊断中的意义。方法:应用间接酶联免疫反应法和肿瘤相关抗原微阵列(包含8个重组的癌抗原蛋白:C-myc、p53、cyclinB1、p16、p62、Koc、IMP1和Survivin)检测376例食管和贲门各级病变患者(正常、癌前病变和癌)血清中的自身抗体。结果:在所检测的八种抗原中,p53、C-myc、cyclinB1、IMP1和p62从正常食管到癌前病变及癌患者血清中和p53、C-myc、p16、p62在正常贲门到癌前病变及癌患者血清中阳性百分率均具有线性升高趋势。单一抗体对食管和贲门癌检出率较低,p53在癌血清中的表达阳性率在所有抗原中最高,在食管癌和贲门癌患者中分别为23%(13/57)和21%(9/43)。但是,当应用8个抗原分析时,至少有1个反应为阳性时,其检出阳性率明显增高,食管和贲门癌的阳性检出率分别提高到63%(36/57)和61%(26/43),上述检测指标在正常食管和贲门与相应各级癌前病变和癌患者阳性表达率差异有统计学意义,P<0·05。结论:联合应用多个肿瘤相关抗原比应用单个肿瘤相关抗原分析食管和贲门癌及癌前病变患者血清中的自身抗体变化能够提高癌和癌前病变患者的检出率。食管和贲门癌多个相关抗原微阵列的进一步优化有可能成为临床上食管和贲门癌和高危人群检测和早期诊断的非侵袭性方法。     

Antigen MG7 in gastric cancer and gastric precancerous lesions

Earlydetectionandearlydiagnosisofgastriccancerareessentialtodecreasethemortalityandincreasesurvivalrateofgastriccancer.TheZhuangheregioninLiaoningProvinceisahighriskareaofgastriccancerandanimportantresearchbaseforgastriccancerpreventionandtreatmentinChina[1].AlargescalescreeningofgastriccancerinthisareawascarriedoutbytheCancerInstituteofChinaMedicalUniversitypreviously.Inthepresentstudy,thegastricmucosasamplesfromthescreeningwereusedtoinvestigatethedynamicexpressionofgastriccancer-associat…     

Association between oral health and gastric precancerous lesions

Although recent studies have suggested that tooth loss is positively related to the risk of gastric non-cardia cancer, the underlying oral health conditions potentially responsible for the association remain unknown. We investigated whether clinical and behavioral measures of oral health are associated with the risk of gastric precancerous lesions. We conducted a cross-sectional study of 131 patients undergoing upper gastrointestinal endoscopy. Cases were defined as those with gastric precancerous lesions including intestinal metaplasia or chronic atrophic gastritis on the basis of standard biopsy review. A validated structured questionnaire was administered to obtain information on oral health behaviors. A comprehensive clinical oral health examination was performed on a subset of 91 patients to evaluate for periodontal disease and dental caries experience. A total of 41 (31%) cases of gastric precancerous lesions were identified. Compared with non-cases, cases were significantly more likely to not floss their teeth [odds ratio (OR) = 2.89, 95% confidence interval (CI): 1.09-7.64], adjusting for age, sex, race, body mass index, smoking status, educational attainment and Helicobacter pylori status in serum. Among participants who completed the oral examination, cases (n = 28) were more likely to have a higher percentage of sites with gingival bleeding than non-cases [OR = 2.63, 95% CI: 1.37-5.05 for a standard deviation increase in bleeding sites (equivalent to 19.7%)], independent of potential confounders. Our findings demonstrate that specific oral health conditions and behaviors such as gingival bleeding and tooth flossing are associated with gastric precancerous lesions.     

Secondary prevention of esophageal cancer--intervention on precancerous lesions of the esophagus

In 1983, intervention of precancerous lesion of esophagus was undertaken in the high risk area of esophageal cancer, Heshun Village, Linxian County. It had been expected that cancerous degeneration rate of esophageal dysplasia should be reduced by 50% so as the prevention of esophageal cancer could become possible. 6758 subjects of the general population aging from 40 to 65 were examined by esophageal exfoliative cytology, 1729 had marked dysplasia and 2411 had mild dysplasia of esophageal epithelium. Those with marked dysplasia were randomized into 3 groups to take their respective medication: antitumor B (Chinese herbs); retinamide (4-Ethoxycarbophenylretinamide) and placebo. The subjects with mild dysplasia were divided randomly into 2 groups for treatment by riboflavin and placebo. 95% of the subjects had taken 90% or more of the total medication for 3 years, at the end of which they were reexamined by esophageal exfoliative cytology. The reexamination rate was 94.1%. The incidence of esophageal cancer in the antitumor B group (3.9%) was reduced by 53% as compared with that of the placebo group (8.3%). This difference had statistical significant (means 2 = 7.672, P less than 0.05). The incidence of esophageal cancer in retinamide and riboflavin groups were reduced by 33.7% and 19% as compared with those of the control groups. The regression rate of dysplasia in the treatment groups were increased than that of the control groups. The above results showed that our hypothesis about the secondary prevention of esophageal cancer is correct. The intervention of precancerous lesion of the esophagus is effective in the prevention of esophageal cancer.(ABSTRACT TRUNCATED AT 250 WORDS)     

A meta-analysis on alcohol drinking and esophageal and gastric cardia adenocarcinoma risk

BackgroundIn order to provide a precise quantification of the association between alcohol drinking and esophageal and gastric cardia adenocarcinoma risk, we conducted a meta-analysis of available data.Patients and methodsWe identified 20 case–control and 4 cohort studies, including a total of 5500 cases. We derived meta-analytic estimates using random-effects models, taking into account correlation between estimates, and we carried out a dose–risk analysis using nonlinear random-effects meta-regression models.ResultsThe relative risk (RR) for drinkers versus nondrinkers was 0.96 [95% confidence interval (CI) 0.85–1.09] overall, 0.87 (95% CI 0.74–1.01) for esophageal adenocarcinoma and 0.89 (95% CI 0.76–1.03) for gastric cardia adenocarcinoma. Compared with nondrinkers, the pooled RRs were 0.86 for light (≤1 drink per day), 0.90 for moderate (1 to <4 drinks per day), and 1.16 for heavy (≥4 drinks per day) alcohol drinking. The dose–risk model found a minimum at 25 g/day, and the curve was <1 up to 70 g/day.ConclusionsThis meta-analysis provides definite evidence of an absence of association between alcohol drinking and esophageal and gastric cardia adenocarcinoma risk, even at higher doses of consumption.     

Abdominal obesity and the risk of esophageal and gastric cardia carcinomas

BACKGROUND: Esophageal adenocarcinoma is rapidly increasing in incidence. Body mass index (BMI) is a risk factor, but its distribution does not reflect the demographic distribution of the cancer (which is highest among White men). Abdominal obesity patterns may explain this discordance, but no studies exist to date. METHODS: Nested case-control study within 206,974 members of the Kaiser Permanente multiphasic health checkup cohort; subjects received detailed questionnaires, a standardized examination including BMI and anthropometric measurements, and follow-up of esophageal and cardia cancers using registry data. RESULTS: 101 incident esophageal adenocarcinomas, 105 cardia adenocarcinomas, and 144 esophageal squamous cell carcinomas were detected (BMI data available for all cases; abdominal measurements for a subset). Increasing abdominal diameter was strongly associated with an increased risk of esophageal adenocarcinoma [odds ratio (OR), 3.47; 95% confidence interval (95% CI), 1.29-9.33; abdominal diameter, > or =25 versus <20 cm]. Adjustment for BMI did not diminish this association (BMI-adjusted OR, 4.78; 95% CI, 1.14-20.11). The association was also not diminished by adjustment for gastroesophageal reflux-type symptoms, although reflux-type symptoms were separately associated with both abdominal diameter and cancer risk. Abdominal diameter was not associated with the risk of cardia adenocarcinomas (OR, 1.28; 95% CI, 0.38-4.25; diameter, > or =25 versus <20 cm) or esophageal squamous cell carcinomas (OR, 0.78; 95% CI, 0.32-1.92). CONCLUSIONS: Increasing abdominal diameter was associated with an increased risk of esophageal adenocarcinoma, independent of BMI. Cancer risk was not substantially mediated through gastroesophageal reflux-type symptoms, although symptoms may imperfectly measure reflux severity. Given abdominal obesity is more common among males, these findings suggest that increases in obesity may disproportionately increase the risk of esophageal adenocarcinoma in males.