Bo Chen

Overweight, obesity and gastric cancer risk: Results from a meta-analysis of cohort studies

The relationship between excess body weight and gastric cancer risk has not been well studied to date. We therefore carried out a systematic review and meta-analysis of published cohort studies to evaluate the association between excess body weight and gastric cancer risk. An electronic search of the MEDLINE, PubMed, EMBASE and Academic Search Premier (EBSCO) databases, which contain articles published from 1950 onwards, was conducted in order to select studies for this meta-analysis. Ten studies with a total number of 9492 gastric cancer cases and a studied population of 3,097,794 were identified. Overall, excess body weight [body mass index (BMI)25] was associated with an increased risk of gastric cancer [odds ratio (OR)=1.22; 95% confidence intervals (CIs)=1.06-1.41]. Specifically, a stratified analysis showed that excess body weight was associated with an increased risk of cardia gastric cancer [overweight and obese (BMI 25), OR=1.55, 95% CIs=1.31-1.84] and gastric cancer among non-Asians (overweight and obese, OR=1.24, 95% CIs=1.14-1.36); however, the stratified analysis also showed that there was no statistically significant link between excess body weight and gastric cancer in the following subgroups: males (overweight and obese, OR=1.22, 95% CIs=0.96-1.55), females (overweight and obese, OR=1.13, 95% CIs=0.65-1.94), non-cardia gastric cancer (overweight and obese, OR=1.18, 95% CIs=0.96-1.45) and Asians (overweight and obese, OR=1.17, 95% CIs=0.88-1.56). The combined results of this meta-analysis, however, do indicate that overweight and obesity are associated with an increased risk of gastric cancer. The strength of the association also increases with increasing BMI.

Safety and Efficacy of Fish Oil–Enriched Parenteral Nutrition Regimen on Postoperative Patients Undergoing Major Abdominal Surgery A Meta-Analysis of Randomized Controlled Trials

BACKGROUND To evaluate the safety and efficacy of a fish oil-enriched parenteral nutrition regimen in patients undergoing major abdominal surgery, a meta-analysis of randomized controlled trials was conducted. METHODS An electronic search of PubMed, MEDLINE, EMBASE, Academic Search Premier, and China National Knowledge Infrastructure databases was performed in March 2009. RevMan 5.0 was used for statistical analysis. RESULTS The combined analysis showed that a fish oil-enriched parenteral nutrition regimen had a positive treatment effect on length of hospital stay (weighed mean difference = -2.98, P < .001), length of intensive care unit stay, postoperative infection rate (odds ratio = 0.56, P = .04), and serum levels of aspartate aminotransferase, alanine aminotransferase, and alpha-tocopherol on postoperative day 6 in these patients. The regimen increased the plasma levels of eicosapentaenoic acid (standardized mean difference = 3.11, P < .001) and docosahexaenoic acid and upregulated the leukotriene B(5) production in leukocytes on postoperative day 6. No significant differences were found between the 2 groups in postoperative mortality; incidence of postoperative cardiac complications; serum levels of bilirubin, triglyceride, or arachidonic acid; or the liberation of leukotriene B(4). No serious adverse events related to fish oil treatment were reported. CONCLUSIONS Based on the meta-analysis, fish oil-supplemented parenteral nutrition was safe, improved clinical outcomes, and altered the fatty acid pattern as well as leukotriene synthesis. More laboratory parameters should be considered in future meta-analyses.

Cyclin D1 (CCND1) G870A gene polymorphism is an ethnicity-dependent risk factor for digestive tract cancers: A meta-analysis comprising 20,271 subjects

Published data on the association between Cyclin D1 (CCND1) G870A gene polymorphism and digestive tract cancers (DTC) are inconclusive. We carried out a meta-analysis of published case-control studies to derive a more precise estimation of the association. Relevant studies were identified from PubMed, EMBASE, and China National Knowledge Infrastructure up to February 1st, 2011. Crude odds ratios (OR) and 95% confidence intervals (CI) were used to investigate the strength of the association. Data were available from a total of 33 case-control studies with 8534 cases and 11,737 controls. The combined results based on all studies showed that there was a statistically significant link between CCND1 G870A polymorphism and DTC risk (GG vs. AA: OR=0.83, 95%CI=0.71-0.96). In the analysis of ethnic groups, we found the A allele carriers had a significantly increased DTC susceptibility among Caucasians, but not among Asians. When stratified for tumor location, the results based on all studies only showed the variant allele 870A might have a significantly increased risk of colorectal cancer (CRC), especially of rectal cancer (GG vs. AA: OR=0.71, 95%CI=0.58-0.89). When stratifying by the stage and histological differentiation of CRC, we only observed that patients had a significantly higher frequency of CCND1 870 AA than non-cancer patients among Caucasians. The A allele carriers (hetero- or homozygotes) were significantly more common in cases with a family history of CRC than in controls. There was no evidence of publication bias for CCND1 G870A polymorphism with DTC risk. In summary, this meta-analysis demonstrates that the CCND1 G870A polymorphism may be an ethnicity-dependent risk factor for DTC. And this genetic variant may increase the risk of rectal cancer, but not colon cancer.

CDH1 -160C>A gene polymorphism is an ethnicity-dependent risk factor for gastric cancer.

The associations between E-cadherin (CDH1) gene polymorphisms and gastric cancer (GC) susceptibility are still controversial. Given this uncertainty, we carried out a meta-analysis of published case-control studies to derive more precise estimations of these relationships. Relevant studies were identified from PubMed and EMBASE up to March 2011. Seventeen studies with 3511 GC cases and 4826 controls were selected. Crude odds ratios (OR) and 95% confidence intervals (CI) were used to investigate the strength of the associations. No associations between CDH1 (+54T>C, -160C>A, -347G>GA, -616G>C, -2076C>T and -3159T>C) gene polymorphisms and GC risk for all genetic models were found. As for CDH1 -160C>A polymorphism, subgroup analyses by country, gender, study design, smoking status, Helicobacter pylori infection, and the Lauren classification of GC did not change the results. When stratified by ethnicity, we found the A allele carriers had a significantly increased risk of GC among Caucasians (AA vs. CA+CC: OR=1.50, 95% CI=1.03-2.19, P=0.03), but not among Asians (AA vs. CA+CC: OR=0.87, 95% CI=0.56-1.37, P=0.56). No publication bias was found in the present study. This meta-analysis suggests that CDH1 -160C>A gene polymorphism may contribute to increased risk of GC among Caucasians.

Glutathione S-transferase M1 Gene Polymorphism and Gastric Cancer Risk: An Updated Analysis

BACKGROUND AND AIMS Studies investigating the association between glutathione S-transferase M1 (GSTM1) gene polymorphism and gastric cancer (GC) risk have reported conflicting results. In order to clarify the effect of GSTM1 genotype on the GC risk, we performed an updated meta-analysis of published case-control and cohort studies to better compare results between studies. METHODS Published literature from PubMed, EMBASE, and China National Knowledge Infrastructure (CNKI) were retrieved, and the literature search was updated on June 15, 2010. 49 studies with 7746 cases of GC and 13,230 controls were selected. A fixed- or random-effects model was used to calculate pooled effect estimates depending on statistical heterogeneity. RESULTS The combined analyses showed that there was a significant difference in genotype distribution between GC cases and controls among Asians, but not among Caucasians. Stratified analyses according to control sources also showed the positive association between GSTM1 null genotype and increased risk of GC. However, smoking and Helicobacter pylori infection did not modify the association between this polymorphism and GC susceptibility (p = 0.56 and 0.31, respectively). When stratifying by the location, Laurens classification, and histological differentiation of GC, we observed no statistically significant differences in genotype distribution. A strong correlation between increased GC risk and the combined GSTM1 and GSTT1 null genotype was observed. CONCLUSIONS This meta-analysis demonstrated that the GSTM1 gene polymorphism might be a risk factor for GC among Asians (especially, in some Eastern countries). Smoking, Helicobacter pylori infection status did not modify the association between GSTM1 null genotype and GC risk.

Genetic polymorphism of glutathione S-transferase T1 and the risk of colorectal cancer: A meta-analysis

BACKGROUND Studies investigating the association between genetic polymorphism of glutathione S-transferase T1 (GSTT1) and risk of colorectal cancer have reported conflicting results. In order to clarify the effect of GSTT1 polymorphism on the risk of developing colorectal cancer, we carried out a meta-analysis using published data to obtain more precise estimates of risk. METHODS Electronic searches of PubMed and EMBASE were conducted to select studies for this meta-analysis. Papers were included if they were observational studies investigating the association between GSTT1 polymorphism and colorectal cancer risk. The principal outcome measure was the odds ratio (OR) with 95% confidence interval (CI) for the risk of colorectal cancer associated with GSTT1 null genotype. RESULTS We identified 30 eligible studies, which included 7635 cases and 12,911 controls. The combined results based on all studies showed that there was a statistically significant link between GSTT1 null genotype and colorectal cancer risk (OR=1.20, 95% CI=1.03-1.40). In the analysis of ethnic groups, we observed distinct differences associated with GSTT1 null genotype, the pooled odds ratios for the GSTT1 polymorphism were 1.32 in Caucasians (95% CI=1.09-1.58) and 1.03 in Asians (95% CI=0.81-1.32). As far as concerned the interaction between GSTT1 genotype and colorectal cancer risk in relation to smoking history, there was no increase in risk for smokers or nonsmokers with the GSTT1 null genotype (smokers: OR=1.13, 95% CI=0.80-1.60, nonsmokers: OR=0.99, 95% CI=0.71-1.38). When stratifying by the location of colorectal cancer, we found that there was a statistically significant link in rectal cancer (OR=1.50, 95% CI=1.09-2.07), but not in colon cancer (OR=1.33, 95% CI=0.94-1.88). No associations could be detected between null GSTT1 polymorphism and age, sex, tumor stage and differentiation. CONCLUSION Our current study demonstrates that GSTT1 null genotype is associated with an increased risk of colorectal cancer, specifically, among Caucasians.

Glutathione S-transferase T1 gene polymorphism and colorectal cancer risk: An updated analysis

BACKGROUND AND OBJECTIVE The association between glutathione S-transferase T1 (GSTT1) gene polymorphisms and colorectal cancer (CRC) susceptibility is still controversial. In order to clarify the effect of GSTT1 genotype on the CRC risk, we carried out an updated meta-analysis of published case-control studies to provide more precise evidence. METHODS Two investigators independently searched the databases of Pubmed, EMBASE and China National Knowledge Infrastructure (CNKI) up to October 15, 2012. Crude odds ratios (OR) and 95% confidence intervals (CI) were calculated to investigate the strength of the association in a fixed- or random-effects model depending on statistical heterogeneity. RESULTS Forty-six case-control studies with 15,373 colorectal cancer cases and 21,238 controls were included. Overall, the pooled results indicated that GSTT1 null genotype was significantly associated with increased CRC risk (OR=1.21, 95% CI=1.10-1.33). When stratifying for ethnicity and control sources, we also observed positive association between GSTT1 null genotype and increased risk of CRC. When stratifying by the location, we found there was a statistically significant association in the rectal cancer (OR=1.28, 95% CI=1.01-1.64), but not in colon cancer (OR=1.27, 95% CI=0.94-1.73). Subgroup analyses for Dukes stage, histological differentiation of CRC and smoking habit did not reveal any significant differences in genotype distribution. In addition, we observed a strong correlation between increased CRC risk and the combined GSTM1 and GSTT1 null genotype. CONCLUSIONS This meta-analysis suggests that the GSTT1 null genotype may contribute to increased risk of colorectal cancer. More well-designed studies based on larger population are needed to confirm our results.

Efficacy and safety evaluation of two doses of imatinib for the treatment of advanced gastrointestinal stromal tumors (GISTs)

BACKGROUND AND OBJECTIVE Imatinib is approved worldwide for use in gastrointestinal stromal tumours (GISTs). To evaluate the efficacy and safety of two dose of imatinib treatment for patients with GISTs, a meta-analysis was performed. METHODS Electronic search of the PubMed and EMBASE, which have articles published between 1980 and February 2012, was conducted to select studies for this meta-analysis. RESULTS Five articles with a total number 1861 of advanced GISTs patients were involved in this meta-analysis. There was a slight but significant 2-year PFS advantage with high-dose group (OR=1.25, 95% CIs=1.03-1.52, P=0.03), but not in the 2-year OS (OR=1.02, 95% CIs=0.84-1.24, P=0.87), CR (OR=1.02, 95% CIs=0.66-1.58, P=0.93), and PR (OR=1.13, 95% CIs=0.94-1.36, P=0.20). In safety, the high-dose group increased the incidence of above grade 3 toxicity (OR=2.05, 95% CIs=1.70-2.48, P<0.00001), particular in the blood toxicity, skin disorders, nausea and so on. CONCLUSIONS This analysis confirms a slight 2-year PFS advantage of high-dose imatinib, but imatinib dose escalation could not lead to any other major clinical benefits, and brought more toxic effects for patients.