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Background/objectives To assess the association between processed meat and the risk of selected digestive tract and laryngeal cancers. Subjects/methods We conducted a series of case-control studies between 1985 and 2007 in Italy. The studies included a total of 1475 cases of cancer of the oral cavity and pharynx, 1077 of the larynx, 716 of the esophagus, 999 of the stomach, 684 of the liver, 159 of the biliary tract, 688 of the pancreas, and a total of 9720 controls. Odds ratios (ORs), and the corresponding 95% confidence intervals (CIs), were estimated by unconditional logistic regression models, including terms for socio-demographic factors, tobacco smoking, and alcohol intake. Results Compared to the lowest tertile of processed meat consumption, the ORs for subjects in the highest one were 1.18 (95% CI 0.98–1.43) for oral cavity and pharyngeal, 1.51 (95% CI 1.18–1.91) for esophageal, 1.19 (95% CI 0.96–1.47) for laryngeal, 0.98 (95% CI 0.81–1.18) for stomach, 0.85 (95% CI 0.51–1.40) for biliary tract, 1.20 (95% CI 0.94–1.54) for liver, and 1.46 (95% CI 1.15–1.85) for pancreatic cancers. Conclusions Our findings support the hypothesis that high processed meat consumption increases esophageal and pancreatic cancers risk. Residual confounding by socio-demographic factors, tobacco smoking, and alcohol intake may, partly or largely, account for these associations. We found no overall association with other digestive tract and laryngeal cancers.

Objective Yeast cell-free extracts and supernatants contain several compounds such as β-glucan, mannan, chitin, and mannoprotein with potent antitumor and other health-promoting activities. Candida albicans have been frequently and widely isolated from different habitats compared to other yeasts. The supernatant extracted from this yeast also contains β-glucan, chitin, and mannan compounds. This study investigates the anticancer, apoptosis-inducing, and downregulation of proinflammatory gene expression activities in normal and drug-resistant human stomach cancer cells (EPG and RDB cell lines) after 24 and 48 h treatment. Results We found that Candida albicans supernatant-induced apoptosis suppressed the survivin gene expression in both cell lines and suppressed the expression of IL-8 and NF- ƙ B genes in normal stomach cancer cells. IC 50 for EPG cells were 1599 µg/mL and 1040 µg/mL after 24 and 48 h treatment, respectively; and for RDB cells were 877 µg/mL and 675 µg/mL after 24 and 48 h treatment, respectively. Consequently, this work suggests that Candida albicans supernatant can potentially protect against and treat human stomach cancer.

The current nutritional guidelines for stomach cancer survivors (SCSs) mainly focus on the influence of the surgical resection of the stomach, with limited guidance regarding a wider range of food options. We aimed to investigate the factors associated with healthier dietary changes in Korean adult SCSs. This cross-sectional study assessed dietary pattern changes after cancer treatment for 11 food categories, using a self-administered questionnaire. A ‘healthier dietary change’ was operationally defined as a reduced consumption of red and processed meat, grains, salt, and burnt food, and an increased consumption of poultry, fish, vegetables, fruits, legumes, and dairy products. Among a total of 624 SCSs, approximately 60% of participants reported dietary changes in a healthier direction in three or more food categories, while 9.1% reported no changes. There was no significant difference in dietary habit changes between surgery types. Multivariable adjusted analysis showed that elderly and long-term survivors were inversely associated with a healthier dietary change. SCSs with a higher level of educational achievement and income were more likely to make healthier changes in their intake of processed meat, vegetables, fruits, burnt food, or salt. SCSs with higher levels of fear of cancer recurrence, anxiety, or depression were more likely to follow healthier dietary changes regarding fish, meat, fruits, grains, or burnt food. Change in dietary pattern varied across different food items, and was associated with various characteristics of SCSs. It is crucial to repeatedly provide SCSs with information about healthier dietary patterns, considering their sociodemographic, clinical, and psychological characteristics.

GC/MS coupled metabolomics analysis, using a simplified and much less expensive silylation process with trimethylsilyl cyanide (TMSCN), was conducted to investigate metabolic abnormalities in stomach cancer cells. Under optimized conditions for derivatization by TMSCN and methanol extraction, 228 metabolites were detected using GC/MS spectrometry analysis, and 89 metabolites were identified using standard compounds and the NIST database. Ten metabolite levels were found to be lower in stomach cancer cells relative to normal cells. Among those ten metabolites, four metabolites—ribose, proline, pyroglutamic acid, and glucose—were known to be linked to cancers. In particular, pyroglutamic acid level showed a drastic reduction of 22-fold in stomach cancer cells. Since glutamine and glutamic acid are known to undergo cyclization to pyroglutamic acid, the 22-fold reduction might be the actual reduction in the levels of glutamine and/or glutamic acid—both known to be cancer-related. Hence, the marked reduction in pyroglutamic acid level might serve as a biomarker to aid early detection of stomach cancer.

Using the gastric cancer cell line SGC7901, we constructed a cell line that overexpressed octamer-binding protein 4 (Oct4) and SRY-box 2 (Sox2) to explore the stem cell oncological and biological characteristics of these cells and to elucidate the mechanisms of Oct4 and Sox2 in cancer. A lentiviral vector containing the Sox2 gene was constructed and transfected into a gastric cancer cell line overexpressing Oct4 (SGC7901-Oct4) to obtain a stably transfected cell line (SGC7901-Oct4-Sox2). Oct4 and Sox2 expression was detected by RT-PCR and Western blotting. The proliferation, drug resistance, migration, and invasion abilities of the cells were assessed using in vitro (3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium), drug resistance, scratch-wound migration, transwell migration, transwell invasion, and spherical clone formation assays, and their tumorigenic ability was assessed using a tumor formation experiment in mice. Compared with the control group, the expression of Oct4, Sox2, CD44, and E-cadherin was significantly higher in the group that overexpressed Oct4 and Sox2, while the expression of c-Myc and Klf4 did not significantly change. The proliferation, drug resistance, migration, and invasion abilities were significantly enhanced in the overexpression group, and the tumorigenic ability in mice was also significantly enhanced, with significantly increased tumor size and weight. The proliferation, drug resistance, migration, invasion, and tumorigenic abilities of SGC7901 cells overexpressing Oct4 and Sox2 were significantly improved. Oct4 and Sox2 play important roles in the proliferation, migration, invasion, and tumorigenicity of gastric cancer cells, and the two genes may be synergistic to a certain degree.

Although there is a clear relationship between family history (FH) and the risk of gastric cancer (GC), quantification is still needed in relation to different histological types and anatomical sites, and in strata of covariates. The objective was to analyze the risk of GC according to first-degree FH in a uniquely large epidemiological consortium of GC. This investigation includes 5946 cases and 12,776 controls from 17 studies of the Stomach Cancer Pooling (StoP) Project consortium. Summary odds ratios (OR) and the corresponding 95% confidence intervals (CIs) were calculated by pooling study-specific ORs using fixed-effect model meta-analysis techniques. Stratified analyses were carried out by sex, age, tumor location and histological type, smoking habit, socioeconomic status, alcohol intake and fruit consumption. The pooled OR for GC was 1.84 (95% CI: 1.64–2.04; I2 = 6.1%, P heterogeneity = 0.383) in subjects with vs. those without first-degree relatives with GC. No significant differences were observed among subgroups of sex, age, geographic area or study period. Associations tended to be stronger for non-cardia (OR = 1.82; 95% CI: 1.59–2.05 for subjects with FH) than for cardia GC (OR = 1.38; 95% CI: 0.98–1.77), and for the intestinal (OR = 1.92; 95% CI: 1.62–2.23) than for the diffuse histotype (OR = 1.62; 95% CI: 1.28–1.96). This analysis confirms the effect of FH on the risk of GC, reporting an approximately doubled risk, and provides further quantification of the risk of GC according to the subsite and histotype. Considering these findings, accounting for the presence of FH to carry out correct prevention and diagnosis measures is of the utmost importance.

Acetaldehyde (ACH) associated with alcoholic beverages is Group 1 carcinogen to humans (IARC/WHO). Aldehyde dehydrogenase (ALDH2), a major ACH eliminating enzyme, is genetically deficient in 30-50% of Eastern Asians. In alcohol drinkers, ALDH2-deficiency is a well-known risk factor for upper aerodigestive tract cancers, i.e., head and neck cancer and esophageal cancer. However, there is only a limited evidence for stomach cancer. In this study we demonstrated for the first time that ALDH2 deficiency results in markedly increased exposure of the gastric mucosa to acetaldehyde after intragastric administration of alcohol. Our finding provides concrete evidence for a causal relationship between acetaldehyde and gastric carcinogenesis. A plausible explanation is the gastric first pass metabolism of ethanol. The gastric mucosa expresses alcohol dehydrogenase (ADH) enzymes catalyzing the oxidation of ethanol to acetaldehyde, especially at the high ethanol concentrations prevailing in the stomach after the consumption of alcoholic beverages. The gastric mucosa also possesses the acetaldehyde-eliminating ALDH2 enzyme. Due to decreased mucosal ALDH2 activity, the elimination of ethanol-derived acetaldehyde is decreased, which results in its accumulation in the gastric juice. We also demonstrate that ALDH2 deficiency, proton pump inhibitor (PPI) treatment, and L-cysteine cause independent changes in gastric juice and salivary acetaldehyde levels, indicating that intragastric acetaldehyde is locally regulated by gastric mucosal ADH and ALDH2 enzymes, and by oral microbes colonizing an achlorhydric stomach. Markedly elevated acetaldehyde levels were also found at low intragastric ethanol concentrations corresponding to the ethanol levels of many foodstuffs, beverages, and dairy products produced by fermentation. A capsule that slowly releases L-cysteine effectively eliminated acetaldehyde from the gastric juice of PPI-treated ALDH2-active and ALDH2-deficient subjects. These results provide entirely novel perspectives for the prevention of gastric cancer, especially in established risk groups.