Nutrient intakes and adenocarcinoma of the esophagus and distal stomach

Human Nutrition Research Center on Aging, Tufts University, Boston, MA 02111, USA.
Nutrition and Cancer (Impact Factor: 2.47). 02/2002; 42(1):33-40. DOI: 10.1207/S15327914NC421_5
Source: PubMed

ABSTRACT We studied the relationship between nutrient intakes and adenocarcinoma of the esophagus and distal stomach among 124 esophageal adenocarcinoma cases, 124 distal stomach cancer cases, and 449 controls in a population-based case-control study in eastern Nebraska. The residual method was used to adjust nutrient intake quartiles or tertiles for energy intake. We observed significant inverse associations with risk of esophageal adenocarcinoma for dietary intakes of total vitamin A [highest vs. lowest quartile, multivariate odds ratio (OR) = 0.5, P for trend = 0.05], beta-cryptoxanthin (OR = 0.5, P = 0.05), riboflavin (OR = 0.5, P = 0.01), folate (OR = 0.5, P = 0.03), zinc (OR = 0.5, P = 0.05), dietary fiber (OR = 0.5, P = 0.05), protein (OR = 0.5, P = 0.02), and carbohydrate (OR = 0.4, P = 0.02). For distal stomach cancer, only vitamin C (OR = 0.6, P = 0.04), dietary fiber (OR = 0.4, P = 0.007), and carbohydrate (OR = 0.4, P = 0.004) were inversely associated with risk. Our analyses showed significant interaction between dietary fat intake, but not intakes of other nutrients, and respondent type for both cancer sites. Subgroup analyses among self-respondents revealed positive associations between saturated fat intake and risk of esophageal adenocarcinoma (OR = 1.0, 4.1, and 4.6 for intake tertiles, P for trend = 0.02) and risk of distal stomach cancer (OR = 1.0, 1.2, and 3.6, P = 0.03). However, no such associations were found among proxy respondents. Our data suggest that greater intake of dietary fiber, certain carotenoids, and vitamins may decrease the risk of esophageal adenocarcinoma, whereas greater intake of saturated fat may increase the risk of esophageal adenocarcinoma and distal stomach cancer.

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Available from: Katherine L Tucker, Aug 07, 2015
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    • "a with 538 cases and one population based case - control study ( Chen et al . , 2002 ) on adenocarcinoma with 124 cases . There was one study ( Franceschi et al . , 2000 ) published in 2000 with 304 cases , and two ( Chen et al . , 2002 ; De Stefani et al . , 2006 ) after 2000 with 358 cases . All of the three studies ( Franceschi et al . , 2000 ; Chen et al . , 2002 ; De Stefani et al . , 2006 ) on alpha - carotene intake reported OR less than 1 , however , only one ( De Stefani et al . , 2006 ) suggested statistical association . The heterogeneity was little ( I 2 = 0 . 0% ; P for heterogeneity 0 . 678 ) , and the fixed effect model was adopted . Comparing the highest intake with the lowest , the "
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    ABSTRACT: This meta-analysis was conducted to evaluate the association between intake of carotenoids and risk of esophageal cancer. A systematic search using PubMed, Cochrane Library, Web of Science, Scopus, CNKI, and CBM (updated to 6 May 2012) identified ten articles meeting the inclusion criteria with 1,958 cases of esophageal cancer and 4,529 controls. Higher intake of beta-carotene, alpha-carotene, lycopene, beta-cryptoxanthin, lutein, and zeaxanthin reduced esophageal cancer risk with pooled ORs of 0.58 (95% CI 0.44, 0.77), 0.81 (95% CI 0.70, 0.94), 0.75 (95% CI 0.64, 0.86), 0.80 (95% CI 0.66, 0.97), and 0.71 (95% CI 0.59, 0.87), respectively. In subgroup analyses, beta-carotene showed protective effects against esophageal adenocarcinoma in studies located in Europe and North America. Alpha-carotene, lycopene, and beta-cryptoxanthin showed protection against esophageal squamous cell cancer. This meta-analysis suggested that higher intake of carotenoids (beta-carotene, alpha- carotene, lycopene, beta-cryptoxanthin, lutein, and zeaxanthin) is associated with lower risk of esophageal cancer. Further research with large-sample studies need to be conducted to better clarify the potentially protective mechanisms of carotenoid associations risk of different types of esophageal cancer.
    Asian Pacific journal of cancer prevention: APJCP 03/2013; 14(3):1911-8. DOI:10.7314/APJCP.2013.14.3.1911 · 2.51 Impact Factor
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    • "methylation and thus to alter the expression of tumor suppressor genes (Choi and Mason, 2000; Kim, 2004; Blount et al., 2007). Previous epidemiologic studies have shown that folate deficiency could increase the risk of human cancers (Yang, 2000; Mayne et al., 2001; Chen et al., 2002). However, the role of dietary folate in esophageal cancers is still controversial and the studies in Chinese population were scarce till now. "
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    ABSTRACT: An epidemiological study was conducted based on an esophageal cancer patient's cohort to investigate the association of folate intake and MTHFR C677T polymorphism with the prognosis of esophageal cancer in a Chinese population. 167 patients aged 37-75 years who had histological confirmed diagnosis of esophageal squamous cell cancer were collected from Jan. 2006 to Jan. 2008. MTHFR genotypes at the C677T site were analyzed by PCR-based RFLP methods, and the folate intake was computed by multiplying the food intake (in grams) and the folate content (per gram) of food in our questionnaire. We found associations between the prognosis of esophageal cancer and smoking status, T and N stages. Individuals carrying the MTHFR 677CT and TT genotypes showed a shorter survival time than with the CC genotype, with adjusted HRs (95% CI) of 1.20 (0.56-2.15) and 2.29 (1.30-4.28), respectively. Similarly, those carrying MTHFR 677T allele had a 1.86-fold risk of death. A higher folate concentration showed a significant decreased risk of death, with an HR (95% CI) of 0.45 (0.18-0.87). Individuals with high folate intake and the MTHFR 677CC genotype showed a significant decreased risk of esophageal cancer (0.43, 0.25-0.89). Our findings supports the hypothesis that high folate intake and active MTHFR C677T polymorphism may exert protective roles in the prognosis of esophageal cancer in the Chinese population.
    Asian Pacific journal of cancer prevention: APJCP 02/2012; 13(2):647-51. DOI:10.7314/APJCP.2012.13.2.647 · 2.51 Impact Factor
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    • "). Previous epidemiologic studies have shown that folate deficiency could increase the carcinogenesis of esophageal cancer(CS 2000; Mayne et al., 2001; Chen et al., 2002). E x c e p t f o r a n i n a d e q u a t e f o l a t e i n t a k e , Methylenetetrahydrofolate reductase (MTHFR), functional polymorphisms in folate metabolism, may also play a role in the susceptibility of esophageal cancer risk. "
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    ABSTRACT: Genetic and environmental factors may play roles in the pathogenesis of esophageal cancer and susceptibility may be modified by functional polymorphisms in folate metabolic genes, such as methylenetetrahydrofolate reductase (MTHFR). We here evaluated associations of the MTHFR C677T polymorphism and folate intake with esophageal cancer. A matched hospital-based case-control study with 155 esophageal cancer and 310 non-cancer controls was conducted in Southern of China with gene-environment interactions evaluated between the MTHFR C667T polymorphism and drinking and smoking, as well as folate intake. Individuals carrying MTHFR 667CT [adjusted odds ratio (OR), 1.95; 95% confidence interval (CI), 1.23-2.62] and TT [adjusted odds ratio (OR), 3.36; 95% confidence interval (CI), 1.46-8.74] had significantly increased esophageal cancer risk compared with those with MTHFR 667CC genotype. Folate intake was seen to have non-significant preventive effect. In former, moderate and heavy drinkers, a high esophageal cancer risk was observed for those with an MTHFR 677T allele genotype [ORs: 5.0(1.29-18.88), 3.70(1.83-7.66) and 5.77(2.11-15.72), respectively]. Significant interaction was found for moderate-heavy drinking and the MTHFR 677T allele genotype for esophageal cancer risk (p<0.05). Significant increased risk was also found in moderate and heavy smokers with the two genotypes [ORs: 3.58(1.64-7.80) and 4.51(1.15-17.78), respectively]. High folate intake and MTHFR 677TT was associated with a non-significant tendency for decreased esophageal cancer risk. Our finding supports the hypothesis that MTHFR C667T polymorphisms play a role in pathogenesis of esophageal cancer in the Chinese population.
    Asian Pacific journal of cancer prevention: APJCP 01/2011; 12(8):2019-23. · 2.51 Impact Factor
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