Gastric signet ring cell carcinoma (GSRC) is a distinctive type of gastric cancer. It is a mucus-secreting adenocarcinoma that may progress to distant metastasis at an early stage. Because of poor differentiation, aggressive invasion, rapid progression, and other high-risk characteristics, early surgical intervention should be prioritized.

To explore the clinical efficacy of fluorouracil (5-FU) combined with paclitaxel and oxaliplatin for the treatment of advanced GSRC.

A total of 85 patients with advanced GSRC were selected between January 2020 and June 2021 and randomly divided into a control group (n = 42, receiving standard chemotherapy) and a treatment group (n = 43, receiving monotherapy with oxaliplatin, 5-FU, and paclitaxel). Patients in the treatment group received a 135 mg/m2 infusion of paclitaxel for 3 hours, a 400 mg/m2 infusion of calcium folate (or 200 mg/m2 of levocalcium folate) for 2 hours, and an 85 mg/m2 infusion of oxaliplatin for 2 hours. This was followed by a continuous intravenous infusion of 2200-2400 mg/m2 5-FU for 46 hours using a portable pump.

The treatment group showed a median survival time of 11.7 months and an objective response rate (ORR) of 32.5%, significantly higher than the control group (P < 0.05). Serum carcinoembryonic antigen (CEA), carbohydrate antigen 19-9 (CA19-9), and albumin levels were correlated with treatment effectiveness in advanced GSRC (P < 0.01), but total serum protein was not correlated (P > 0.05). Safety and survival were assessed in all patients. Short-term efficacy was evaluated in 66 patients, with a disease control rate of 89.4% and an ORR of 48.5%. Median progression-free survival was 7.0 months (95% confidence interval [CI]: 6.85-7.15), and median overall survival was 10.6 months (95%CI: 9.86-11.3). Primary grade III/IV adverse events included neutropenia (22.1%) and peripheral neurotoxicity (10.3%).

This treatment regimen is more effective for patients with advanced GSRC. Serum levels of CEA, CA19-9, and albumin predicted chemotherapy efficacy, while total protein concentration correlated minimally and insignificantly.

Gastric cancer is one of the leading malignancies worldwide. B vitamins play important roles in DNA synthesis and methylation because they are considered co-enzymes in one-carbon metabolism. There is inconclusive evidence regarding the associations between dietary vitamins B1, B2, and B6 with the risk of gastric cancer in different epidemiologic studies. We, therefore, investigated such associations in a hospital-based case-control study comprising 1182 incident cases of gastric cancer and 2995 controls in Vietnam.

Dietary vitamins B1, B2, and B6 were derived from a semi-quantitative validated food frequency questionnaire. An unconditional logistic regression model was used to calculate the odds ratios (ORs) and 95% confidence intervals (CIs) for the risk of gastric cancer in relation to dietary intake of vitamins B1, B2, and B6.

Overall, dietary vitamins B1 (ORper-SD increment = 0.83; 95% CI: 0.78-0.89; Ptrend < 0.001) and B6 (ORper-SD increment = 0.88; 95% CI: 0.81-0.94; Ptrend < 0.001) were associated with a reduced risk of gastric cancer. Compared with the lowest quintile, the ORs (95% CIs) of gastric cancer for quintiles 2, 3, 4, and 5 of the vitamin B1 intake were 0.64 (0.51-0.79), 0.54 (0.43-0.69), 0.57 (0.44-0.74), and 0.42 (0.31-0.55), respectively; for vitamin B6 intake, quintiles 2, 3, 4, and 5 were 0.53 (0.42-0.66), 0.54 (0.42-0.70), 0.61 (0.46-0.81), and 0.46 (0.33-0.63), respectively. This inverse association was not different across sex, BMI, and smoking statuses. No association was found between dietary vitamin B2 and gastric cancer risk.

Dietary vitamins B1 and B6 were associated with a reduced risk of gastric cancer in the Vietnamese population. Future studies are warranted to replicate our findings, which also have great implications for gastric cancer prevention and control programs in low- and middle-income countries.

Polyunsaturated fatty acids (PUFAs) are fatty acids, containing more than one double bond and have both anti-inflammatory properties and inhibit tumor progression effects as well as carcinogenic properties. There is inconclusive evidence regarding the effect of PUFA intake on gastric cancer in diverse populations. We, therefore, aimed to determine the association between PUFA intake and risk of gastric cancer in a hospital-based case-control study comprising 1182 incident cases of gastric cancer and 2965 controls in Vietnam. A semiquantitative validated food frequency questionnaire was used to derive PUFA intake. Unconditional logistic regression model was applied to calculate the odds ratios (ORs) and 95% confidence intervals (CIs) for the risk of gastric cancer in relation to PUFA intake. Overall, there was a dose-response inverse association between PUFA intake and gastric cancer risk (ORper-SD increment = 0.72, 95% CI: 0.65-0.79; Ptrend < 0.001). Compared with quintile 1 (the lowest quintile), the ORs and respective 95% CIs of gastric cancer for quintiles 2, 3, 4, and 5 of the PUFA intake were 0.65 (0.52-0.80), 0.51 (0.41-0.64), 0.47 (0.37-0.59), and 0.37 (0.28-0.48), respectively. A similar pattern was observed in both sexes and individuals aged <60 years and those aged 60 years or older. In summary, we found a risk reduction of gastric cancer in individuals with a higher intake of PUFA in the Vietnamese population, regardless of sex or age. Our findings have great implications for the prevention and control programs against gastric cancer in low-middle-income countries and similar limited-resource settings.

Cancer incidence in young adults or those aged 15-49 years old has increased during the past decade. Knowledge about the risk factors for cancer-related deaths in young adults is limited, particularly in low- and middle-income countries (LMICs).

This analysis was based on the Hanoi Prospective Cohort Study, an ongoing study of 39,401 participants aged 15 or older in Northern Vietnam in the 2007-2019 period. A Cox proportional hazard regression model was used to calculate the hazard ratio (HR) and 95% confidence intervals (95% CIs) for the association between potential factors and the risk of cancer-related deaths.

With a median follow-up of 11.01 years, we identified 164 deaths in young adults out of 554 total deaths. Overall, family history of cancer (HR = 7.34; 95% CI: 3.30-16.36), drinking alcohol (HR = 1.82; 95% CI: 1.18-2.81), and smoking (HR = 2.22; 95% CI: 1.36-3.63) were found to be risk factors, while drinking coffee was found to be a protective factor (HR = 0.49; 95% CI: 0.24-1.00) for cancer-related deaths in young adults. Young male adults were found to be at a higher risk due to excessive cigarette smoking (HR = 1.91; 95% CI: 1.00-3.68) and alcohol consumption (HR = 2.15; 95% CI: 1.32-3.53) than those aged 50 years and older (HR = 1.36 and 95% CI: 0.96-1.93 and 1.27 and 95% CI: 0.97-1.67, respectively). The risk of death from cancer in women compared with men in the young population was twice as high as that in the older population (HR = 1.18 and 95% CI: 0.72-1.94 vs. 0.47 and 95% CI: 0.35-0.63, respectively).

Our data suggest that the young Vietnamese population is vulnerable to the risk of cancer-related deaths and that cancer in women will increase rapidly in the future.

There is inconclusive evidence on the role of dietary intake of vitamin B12 in cancer. We evaluated the association between vitamin B12 intake and cancer risk in a hospital-based case-control study, comprising 3,758 cancer cases and 2,995 controls in Vietnam. Vitamin B12 intake was derived from the validated food frequency questionnaire. Unconditional logistic regression model was used to calculate the odds ratios (ORs), and respective 95% confidence intervals (CIs) for the association between vitamin B12 and cancer risk. There was a U-shaped association between vitamin B12 intake and overall risk of cancer. Individuals with intakes lower than the median intake had a 6% (OR = 1.06, 95% CI: 0.86-1.31)-107% (OR = 2.07, 95% CI: 1.58-2.71), increased risk of cancer (Ptrend<0.001), whereas those with higher intakes than the median intake had a 20% (OR = 1.20, 95% CI: 0.97-1.48)-52% (OR = 1.52, 95% CI: 1.22-1.89) increased risk of cancer (Ptrend<0.04). The excess risk of cancer associated with low intakes of vitamin B12 was observed among esophageal, lung, and breast cancer patients, whereas with high intakes of vitamin B12 among gastric cancer patients. In summary, a U-shaped association between vitamin B12 intake and increased cancer risk was observed in the Vietnamese population.

While selenium is a cofactor of several antioxidant enzymes against cancer and is essential for human health, its excess intake may also be harmful. Though a safe intake of selenium has recently been recommended, it is not well understood in the Asian population. We aimed to determine the association between dietary intake of selenium and cancer risk in a case-control study of 3758 incident cancer cases (i.e., stomach, colon, rectum, lung cancers, and other sites) and 2929 control subjects in Vietnam. Daily intake of selenium was derived from a semiquantitative food frequency questionnaire. The unconditional logistic regression model was used to calculate the odds ratios (ORs) and 95% confidence intervals (CIs) for the association between selenium intake and cancer risk. We observed a U-shaped association between selenium intake and cancer risk. A safe intake ranged from 110.8 to 124.4 µg/day (mean 117.8 µg/day). Compared to individuals with the safe intake of selenium, individuals with the lowest intake (i.e., 27.8-77.2 µg/day) were associated with an increased risk of cancer (OR = 3.78, 95% CI 2.89-4.95) and those with the highest intake (169.1-331.7 µg/day) also had an increased cancer risk (OR = 1.86, 95% CI 1.45-2.39). A U-shaped pattern of association between selenium intake and cancer risk was stronger among participants with body mass index (BMI) < 23 kg/m2 and never smokers than BMI ≥ 23 kg/m2 and ever smokers (P'sheterogeneity = 0.003 and 0.021, respectively) but found in both never and ever-drinkers of alcohol (Pheterogeneity = 0.001). A U-shaped association between selenium intake and cancer risk was seen in cancer sites of the stomach, colon, rectum, and lung cancers. In summary, we found a U-shaped association between selenium intake and cancer risk and a safe selenium intake (mean: 117.8 µg/day) in the Vietnamese population. Further mechanistic investigation is warranted to understand better a U-shaped association between selenium intake and cancer risk.

Pancreatic cancer is a leading cause of cancer-related death worldwide. Tryptophan plays a vital role in cell growth and maintenance as a building block of protein and coordination of organismal responses to environmental and dietary cues. Animal model study showed that dietary tryptophan improved treatment response in those who received chemotherapy or immune checkpoint inhibitors. Limited data are available assessing the association between tryptophan intake and risk of pancreatic cancer. We aimed to evaluate this association in a case-control study in Vietnam.

We analyzed data from a case-control study, including 3759 cancer cases and 2995 control subjects of whom 37 with pancreatic cancer cases. Tryptophan intake was derived from food frequency questionnaire. Unconditional logistic regression was used to calculate odds ratios (ORs) and 95% confidence intervals (CIs) for different levels of tryptophan intake with pancreatic cancer risk.

Overall, tryptophan intake was inversely associated with pancreatic cancer risk in a dose-dependent manner. The ORs and 95% CIs of pancreatic cancer were 0.51 (0.29-0.92) for continuous scale, 0.27 (0.10-0.73) for tertile 2 and 0.34 (0.11-1.06) for tertile 3, compared with tertile 1 (the lowest intake) ( Ptrend = 0.02). In stratified analysis, this inverse association pattern was present among those with BMI < 23 kg/m 2 and ever drinkers.

A diet with a higher intake of tryptophan was significantly associated with a lower incidence of pancreatic cancer among Vietnamese population. These suggest that dietary modification may be an effective strategy for primary prevention of pancreatic cancer development.