Nutrition and stomach cancer

Kono, Suminori; Hirohata, Tomio

doi:10.1007/bf00115637

Cited by 196 publications

(143 citation statements)

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“…26 Helicobacter pylori infection, salt intake and smoking and dietary mutagens such as nitrosamines intake were known factors of developing pre-cancerous lesions and well-differentiated type of gastric adenocarcinoma. 1,2,29,30 In our study, the frequency of the CYP2A6 homozygote deletion was higher among well-differentiated adenocarcinoma cases and this increase admitted statistical significance (OR ϭ 4.91, 95% CI 1.17-20.52). The result considered that the CYP2A6 homozygote deletion genotype was one of the risk factors of developing well-differentiated type of gastric adenocarcinoma.…”

Section: Discussionsupporting

confidence: 53%

“…Epidemiological and experimental evidence have indicated that excess salt intake, which promotes cell replication, increases gastric cancer risk. 1,2 There is considerable evidence to support the view that carcinogenic N-nitrosamine derivatives are important factors in human cancer, including gastric cancer. The chemical mechanisms of carcinogenesis by these nitrosamines in humans are therefore of considerable interest.…”

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confidence: 99%

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Effects of cytochrome P450 (CYP) 2A6 gene deletion and CYP2E1 genotypes on gastric adenocarcinoma

Tsukino

Kuroda

Qiu

et al. 2002

Intl Journal of Cancer

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Cytochrome P450 (CYP) 2A6 and CYP2E1 are enzymes with a high ability to activate a nitrosamine, 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK), to its potent and ultimate carcinogens. The polymorphic CYP2A6 and CYP2E1 have been implicated in increased susceptibility to certain malignancies. In our study, 120 Japanese patients with gastric adenocarcinoma and 158 healthy controls were compared for frequencies of CYP2A6 and CYP2E1 genotypes. The frequency with which the subjects carried homozygotes of the CYP2A6 gene deletion allele, which causes lack of the enzyme activity, was significantly higher in the gastric cancer patients than in the healthy control subjects (OR ‫؍‬ 3.14, 95% confidence interval (95% CI) ‫؍‬ 1.05-9.41). Subdividing gastric adenocarcinoma according to tumor differentiation, patients with the well-differentiated type were 4. Although gastric cancer incidence has fallen markedly over the past 50 years in industrialized nations, it remains the second leading cause of cancer death in Japan. Epidemiological and experimental evidence have indicated that excess salt intake, which promotes cell replication, increases gastric cancer risk. 1,2 There is considerable evidence to support the view that carcinogenic N-nitrosamine derivatives are important factors in human cancer, including gastric cancer. The chemical mechanisms of carcinogenesis by these nitrosamines in humans are therefore of considerable interest. 3,4 Numerous studies have shown that several cytochrome P450 (CYP) enzymes, particularly cytochrome P4502A6 (CYP2A6) and cytochrome P4502E1 (CYP2E1), catalyze metabolic activation of nitrosamine derivatives, including N-nitroso-dialkyiamines and tobacco-smoke-related nitrosamine. [5][6][7][8] Genetic polymorphisms for CYP2A6 have been described and 2 variant alleles associated with reduced activity have been identified. Variant 1 (CYP2A6*2) and Variant 2 (CYP2A6*3) are the results of amino acid exchanged for wildtype (CYP2A6*1). Recently, Kitagawa et al. 9 revealed that a novel deletion genotype variant of the CYP2A6 gene was one of the major polymorphic genes in Japanese lacking CYP2A6 activity.In addition, CYP2E1 represents a major CYP isoform in the human liver and is also expressed in extrahepatic tissue. This enzyme can be induced by certain chemicals, such as ethanol and large interindividual variations have been observed, suggesting that the variation may be due to genetic polymorphism. It was reported that RsaI polymorphism, which is located in the 5Ј-flanking region of CYP2E1 gene, has been shown to be associated with the transcriptional regulation of gene expression, resulting in different expression levels of the CYP2E1 mRNA. 6 CYP2E1 participated in the metabolic activation of various N-nitrosamines, including a potent tobacco-specific carcinogen, 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone. 8,10 Several recent reports have investigated the role of CYP2A6 genetic polymorphisms in tobacco dependence and lung cancer risk, with conflicting results. [11][12][13][14][15] Less ...

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Section: Discussionsupporting

confidence: 53%

mentioning

confidence: 99%

Effects of cytochrome P450 (CYP) 2A6 gene deletion and CYP2E1 genotypes on gastric adenocarcinoma

Tsukino

Kuroda

Qiu

et al. 2002

Intl Journal of Cancer

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“…The relative risks reported ranged from 1.5 to 6.7 for various measures of salt intake [14]. In several other case-control studies no association was reported for (total) salt or sodium intake [43][44][45], salted foods [11,13,43,46], for use of table salt [10,47] or salt added to food [8,13,15,16,47], preference of foods with a salty taste [8,12,13,15].…”

Section: Discussionmentioning

confidence: 99%

“…Numerous epidemiological studies have investigated the association between stomach cancer risk and salt or sodium intake (e.g., [2][3][4]), salted foods (e.g., [5][6][7]), salt added during cooking or at table (e.g., [8][9][10]) and preference of salty taste (e.g., [11][12][13]). In many case-control studies a positive association was reported between an indicator of high salt intake and stomach cancer risk, but in nearly all cohort studies no association was observed [14].…”

Section: Introductionmentioning

confidence: 99%

Untitled

Brandt

Botterweck

Goldbohm

2003

Cancer Causes and Control

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Objective: Many case-control studies have reported that salt and cured meat intake are positively, and refrigerator use is inversely, associated with stomach cancer risk. In the current prospective study these associations were evaluated. Methods: The Netherlands Cohort Study consisted of 120,852 men and women ages 55-69 years at baseline in 1986. Salt exposure was measured by calculating mean daily sodium intake (dietary salt) from 150 food items and by specific salt questions. After 6.3 years of follow-up, 282 incident stomach cancer cases were available for analyses. Case-cohort analyses were based on the 282 cases and 3123 subcohort members. Results: In multivariate analyses adjusted for age, sex, smoking, education, stomach disorders, history of stomach cancer in the family, rate ratios (RR) for increasing quintiles of energy-adjusted intake of dietary salt were 1.00, 1.49, 1.03, 1.54 and 1.18, respectively (p trend ¼ 0.43). An inverse association was found between stomach cancer and salt added at the hot meal (p trend ¼ 0.04). For salt added to home-made soup, use of salt at the table, salt preference and duration of refrigerator use, no associations were observed. Positive associations were found for bacon (RR highest/lowest intake ¼ 1.33; 95% CI ¼ 1.03-1.71) and other sliced cold meat (RR highest/lowest intake ¼ 1.29; 95% CI ¼ 0.96-1.72), but not for smoked sausage, total cold meats, rashers/bacon, boiled ham and smoked beef/pork loin roll. Separate analyses among subjects with self-reported stomach disorders revealed higher RR of stomach cancer for dietary salt and several types of cured meat. Conclusion: The present findings suggest that intake of dietary salt and several types of cured meat were weakly positively associated with stomach cancer risk.Abbreviations: CI -confidence interval; RR -rate ratio

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“…There is a distinct familial risk for gastric cancer, and studies have demonstrated that the risk is higher for siblings than for parents and offspring 4. A high salt intake has been identified as a risk factor for gastric cancer in case‐control studies 5. Red and processed meat intake was associated with a 43% increase in the risk for gastric cancer 6.…”

Section: Risk Factors For Gastric/gej Cancersmentioning

confidence: 99%

Identifying and targeting cancer stem cells in the treatment of gastric cancer

Bekaii‐Saab

El‐Rayes²

2017

Cancer

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Current treatment regimens for gastric cancer are not adequate. Cancer stem cells (CSCs) may be a key driving factor for growth and metastasis of this tumor type. In contrast to the conventional clonal evolution hypothesis, CSCs can initiate tumor formation, self‐renew, and differentiate into tumor‐propagating cells. Because gastric cancer can originate from CSCs, it is necessary to review current targets of signaling pathways for CSCs in gastric cancer that are being studied in clinical trials. These pathways are known to regulate the self‐renewal and differentiation process in gastric CSCs. A better understanding of the clinical results of trials that target gastric CSCs will lead to better outcomes for patients with gastric cancer. Cancer 2017;123:1303–1312. © 2017 The Authors. Cancer published by Wiley Periodicals, Inc. on behalf of American Cancer Society. This is an open access article under the terms of the Creative Commons Attribution NonCommercial License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.

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Nutrition and stomach cancer

Cited by 196 publications

References 83 publications

Effects of cytochrome P450 (CYP) 2A6 gene deletion and CYP2E1 genotypes on gastric adenocarcinoma

Effects of cytochrome P450 (CYP) 2A6 gene deletion and CYP2E1 genotypes on gastric adenocarcinoma

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Identifying and targeting cancer stem cells in the treatment of gastric cancer

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