There has been marked improvement in leukemia survival, particularly among children in recent time. However, the long-term trends in survival among adult leukemia patients and the associated sex and racial survival disparities are not well understood. We, therefore, evaluated the secular trends in survival improvement of leukemia patients from 1973 through 2014, using Surveillance Epidemiology and End-Result Survey Program (SEER) data. ICD-O-3 morphology codes were used to group leukemia into four types: acute lymphoblastic leukemia (ALL), acute myeloid leukemia (AML), chronic lymphocytic leukemia (CLL), chronic myeloid leukemia (CML). Survival analysis for each leukemia type stratified by race/ethnicity, age, sex was performed to generate relative survival probability estimates for the baseline time period of 1973 through 1979. Hazard ratios (HR) and respective 95% confidence intervals (CIs) for survival within subsequent 10-year time periods by race, age and sex were calculated using Cox proportional hazard models. Of the 83,255 leukemia patients for the current analysis, the 5-year survival of patients with ALL, AML, CLL, and CML during 1973–1979 were 42.0%, 6.5%, 66.5%, and 20.9%, respectively. Compared to the baseline, there were substantial improvements of leukemia-specific survival in 2010–2014 among African-American (81.0%) and Asian (80.0%) patients with CML and among 20–49 year of age with CLL (96.0%). African-American patients, those with AML and those older than 75 years of age had the lowest survival improvements. Asians experienced some of the largest survival improvements during the study period. Others, including African-American and the elderly, have not benefited as much from advances in leukemia treatment.

Experimental studies have shown that dietary isothiocyanates reduced cellular proliferative marker Ki-67 and increased apoptotic markers caspase-3 and terminal deoxynucleotidyl transferase–mediated dUTP nick end labeling (TUNEL) in animals, but human data are lacking. The present study was to assess whether sulforaphane would stop/reverse the progression of bronchial histopathology, reduce the Ki-67 index, and/or increase caspase-3 and TUNEL indices in humans. A randomized clinical trial (NCT03232138) was conducted in former smokers. Forty-three subjects were randomly assigned to the placebo or the treatment with a potential daily dose of 95 μmol sulforaphane for 12 months. The endpoints were the changes in histopathology scores and Ki-67, caspase-3, and TUNEL indices in post- versus pretreatment bronchial biopsies. Thirty-seven participants (17 in the sulforaphane and 20 in the placebo group) completed the study. Supplementation of sulforaphane did not show significant impact on bronchial histopathology but significantly reduced the Ki-67 index with a 20% decrease in the sulforaphane group and a 65% increase in the placebo (P = 0.014). The difference was even greater in high-density (3+) positive Ki-67, with a 44% decrease in the sulforaphane group compared with a 71% increase in the placebo (P = 0.004). Higher bioavailability of sulforaphane was correlated with greater reduction of the Ki-67 index (P for trend = 0.019). Sulforaphane treatment had no impact on the caspase-3 or TUNEL index in bronchial biopsies. No severe adverse event was observed in the study participants. The findings of oral sulforaphane that significantly reduced the Ki-67 index in bronchial tissue support further development as a potential chemopreventive agent against lung cancer development. Prevention Relevance: High intake of cruciferous vegetables and their sulforaphane is associated with lower incidence of lung cancer in humans and animal models. This clinical trial has demonstrated that oral supplementation of sulforaphane for 12 months significantly reduced the Ki-67 index, a potential surrogate endpoint of biomarkers for lung cancer risk.

Limited data are reported on the association between low-carbohydrate diet (LCD) score, a comprehensive measure of dietary pattern according to sources of carbohydrate, fat, and protein, and risk of hepatocellular carcinoma (HCC). We evaluated this score with HCC risk in the Singapore Chinese Health Study, a prospective cohort of 63,275 middle-aged and elderly Chinese living in Singapore and recruited during 1993–1998 period. LCD scores were derived from the semi-quantitative food frequency questionnaire at baseline. A nested case–control study involved 197 HCC cases and 465 controls was also constructed among 28,346 participants who provided blood samples. Cox proportional hazard regression method was used to calculate HRs and 95% confidence intervals (CI) for HCC with different levels of LCD scores. Conditional logistic regression was performed for the case–control study analysis. After 17.6 years of follow-up with 819,573 person-years, 561 participants developed primary HCC. Although there was a null association between total LCD score and HCC risk (HRper-SD increment = 1.07; 95% CI, 0.98–1.16; Ptrend = 0.06), there was a positive association between animal-based LCD and the risk of HCC (HRper-SD increment = 1.11; 95% CI, 1.02–1.21; Ptrend = 0.01). Furthermore, this association was present in both HBsAg-negative and HBsAg-positive individuals in the case–control study. In stratified analysis for the entire cohort, this positive association was only present in those who consumed alcoholic beverages monthly or less frequent but not in weekly or daily drinker (Pinteraction = 0.79). In summary, a diet with lower carbohydrate, higher animal fat and protein was significantly associated with higher risk of HCC among Chinese Singaporeans. Prevention Relevance: In a large cohort study of more than 63,000 Chinese Singaporeans, we found that a diet with lower carbohydrate and higher animal fat and protein was associated with increased risk of HCC, suggesting that dietary modification could be an effective strategy in primary prevention to reduce the HCC burden.

Background: Data on the association between the plant-based diet and pancreatic cancer are sparse. We, therefore, examined associations for plant-based dietary indices (PDI), healthy PDI (hPDI), and unhealthy PDI (uPDI) with pancreatic cancer risk. Methods: We used data from the Singapore Chinese Health Study, a prospective cohort study of 63,275 participants, ages 45 to 74 years, living in Singapore who were recruited during 1993 to 1998. The three plant-based dietary scores were calculated from the semiquantitative food frequency questionnaire that was collected at the baseline. We identified pancreatic cancer cases using record linkage with the Singapore Cancer Registry. A Cox proportional hazard regression method was used to generate HRs and 95% confidence intervals (CI) for pancreatic cancer in relation with PDI, hPDI, and uPDI scores, adjusted for potential confounders. Results: After 17.6 years of follow-up, we identified 316 pancreatic cancer cases. uPDI was associated with increased risk of pancreatic cancer with a dose–response trend (HRper-SD increment = 1.20; 95% CI, 1.06–1.37). The adjusted HRs (95% CIs) for quartiles 2, 3, and 4 relative to quartile 1 of uPDI were 1.32 (0.94–1.86), 1.22 (0.86–1.71), and 1.68 (1.18–2.39), respectively (Ptrend = 0.01). Null association was found for PDI and hPDI with pancreatic cancer risk. Conclusions: We showed that uPDI was associated with increased risk of pancreatic cancer. Impact: Our results have public health implications for primary prevention against pancreatic cancer development, one of the deadliest malignancies worldwide.

Background/Objectives: Lycopene, a red lipophilic carotenoid hydrocarbon pigment found primarily in tomatoes and other red/pink fruits and vegetables, has anti-inflammatory, anticarcinogenic and cardioprotective properties. There is a lack of evidence regarding the effect of lycopene intake on gastric cancer risk in the Asian population. We, thus, evaluate the association between lycopene intake and gastric cancer risk in a hospital-based case–control study, including 1182 incident cases of gastric cancer and 2995 controls in Vietnam. Methods: Lycopene intake was derived from a semi-quantitative, validated food frequency questionnaire. An unconditional logistic regression model was performed to estimate the odds ratios (ORs) and 95% confidence intervals (CIs) for gastric cancer risk in relation to lycopene intake, adjusted for potential confounding factors. Results: Overall, there was a dose–response inverse association between lycopene intake and gastric cancer risk (OR_{per-SD increment} = 0.88, 95% CI: 0.81–0.95; P_trend = 0.002). Compared with quintile 1 (the lowest quintile), the ORs and 95% CIs of gastric cancer for quintiles 2, 3, 4 and 5 of the lycopene intakes were 0.63 (0.51–0.79), 0.64 (0.51–0.80), 0.65 (0.52–0.81) and 0.62 (0.50–0.78), respectively. A similar pattern of inverse association between lycopene intake and gastric cancer risk was seen only in females, ever alcohol drinkers, and individuals with H. pylori negative status, without type 2 diabetes and with blood group B (all P_{heterogeneity} > 0.05). Conclusions: We observed a reduced risk of gastric cancer in individuals with higher lycopene intake in the Vietnamese population, regardless of BMI or smoking status. Our results have great implications for a healthy dietary pattern (i.e., lycopene with major sources from fruits and vegetables) for strategies in the prevention and control programs of gastric cancer in low-and middle-income countries.

Background: Iron is one of the essential elements for human life. Prior studies provided inconclusive results about the association between dietary iron intake and gastric cancer risk. We determined the association between dietary iron intake and the risk of gastric cancer in a case–control study of 1,182 incident gastric cancer cases and 2,965 controls in Vietnam. Methods: We used a validated, semiquantitative food frequency questionnaire to obtain dietary information, including dietary iron intake. An unconditional regression model was used to calculate OR and 95% confidence intervals (95% CI) of gastric cancer in relation to dietary iron intake, adjusted for potential confounders. Results: We observed a U-shaped association between dietary iron intake and gastric cancer risk. Compared with category 2 (reference group), the ORs and 95% CIs of category 1 (lowest intake) and categories 3, 4, 5, and 6 were 1.64 (1.27–2.12), 1.17 (0.90–1.53), 1.35 (1.01–1.82), 1.65 (1.18–2.31), and 2.00 (1.36–2.95; Ptrend < 0.001), respectively. This U-shaped association was also observed in both sexes, in all types of dietary iron intake (i.e., heme and nonheme), and among individuals with noncardia gastric cancer. This pattern was more apparent among individuals with a body mass index < 23 kg/m2 (Pheterogeneity = 0.02), never smokers (Pheterogeneity = 0.02), those without a family history of cancer (Pheterogeneity = 0.99), and individuals with blood group O (Pheterogeneity = 0.98) but showed up in both alcohol and coffee drinkers. Conclusions: We found a U-shaped association between dietary iron intake and gastric cancer risk. Impact: Results from our study also provide evidence for a tailored dietary intervention program that would benefit specific populations and those living in similar settings.