METHODS: We will acquire eligible studies through a systematic search of MEDLINE, EMBASE, the Cochrane Central Registry of Controlled Trials, CINAHL plus, IPA and clinicaltrials.gov website. The Cochrane Risk of Bias Tool will be used to assess the quality of included studies. The primary outcomes are the incidence of CRC, the incidence/recurrence of any adenoma or change in polyp burden (number or size). Quantitative synthesis or meta-analysis will be considered. We will also construct a network meta-analysis (NMA) to improve precision of the comparisons among chemo-preventive interventions by combining direct and indirect evidence. The probability of each treatment being the best and/or safest, the number-needed-to-treat [NNT; 95% credible interval (CrIs)], and the number-needed-to-harm (NNH; 95% CrIs) will be calculated to provide measures of treatment efficacy. The GRADE approach will be used to rate the quality of evidence of estimates derived from NMA.
RESULTS: This protocol has been registered (registration number: CRD42015025849) with the PROSPERO (International Prospective Register of Systematic Reviews). The procedures of this systematic review and NMA will be conducted in accordance with the PRISMA-compliant guideline. The results of this systematic review and NMA will be submitted to a peer-reviewed journal for publication.
CONCLUSIONS: To the best of our knowledge, this study will be the first NMA to identify the comparative effectiveness of interventions for the prevention of CRC. The results of our study will update evidence for chemoprevention of CRC, identify key areas for future research, and provide a framework for conducting large systematic reviews involving indirect comparisons.
Methods: A multi-centred matched case control study was conducted in five local hospitals. A total of 140 histologically confirmed CRC cases were matched with 280 cancer free controls. Mean value and prevalence of the components of metabolic syndrome between cases and controls were measured based on the three definitions. A multiple variable analysis using Cox regression was conducted to measure the strength of the association between the definitions of MetS, components of MetS and risk of CRC.
Results: Multiple variable analyses showed that metabolic syndrome significantly and independently increased the risk of CRC, with an odds ratio ranging from 1.79 to 2.61. This study identified that the definition of metabolic syndrome by the International Diabetes Federation is the most sensitive in predicting the risk of CRC, compared to metabolic syndrome as defined by the World Health Organization and National Cholesterol Education Program Adults Treatment Panel III. Abdominal obesity, low HDL-cholesterol, and hypertension were identified as the three core risk factors, which promote inflammatory signals that contribute to metabolic syndrome and an increased risk of CRC.
Conclusions: These data hypothesized that simple measurement of abdominal obesity, abnormal BP and HDL-cholesterol especially using International Diabetes Federation (IDF) definition of MetS for South Asians for to detect individuals at CRC risk may have higher clinical utility than applying other universal complex MetS definitions.
Methods: We reviewed the records of colorectal cancer patients treated in Hospital Tuanku Ja'afar Seremban, Malaysia from 2008 to 2012. Survival analysis at five years was performed using the Kaplan-Meier method. Cox proportional hazard regression analysis was carried out to determine the predictors of 5-year colorectal cancer survival.
Results: Of the 275 patients, 43.3% were colon cancers, 51.8% were rectal cancers. Only 2.2% were diagnosed in Stage I. 28.7%, 33.1%, and 16.7% were in Stage II, III and IV respectively; 62/79 (78%) of Stage II patients were in Stage IIb; 15.7% of patients were below the age of 50 and fewer of them presented early (P=0.002). The overall 5-year survival was 46.5%. It was 67.9%, 50.5% and 12.8% for Stage I&II, III and IV patients respectively. Early stage of cancer (P<0.001) and age below the mean (P=0.01) were the most significant factor in predicting better survival. Gender and ethnic group were not associated with late presentation nor survival. Neither was there a difference between colon and rectum cancers nor patients who received elective surgical treatment compared to patients receiving other treatment first (P=0.085).
Conclusions: Late presentation is the most important predictor for poor outcome for colorectal cancer in Seremban. Patients under the age of 50 years present late more often, but do not have poorer survival.
METHODS: Single-nucleotide polymorphisms (SNPs) associated with exposures and outcomes were sourced from the Integrative Epidemiology Unit (IEU) Open Genome-Wide Association Study (GWAS) database. Specifically, the data of GBC comprised 907 East Asians (pathological results of all cases were registered into Biobank Japan) and 425,707 SNPs; T2D comprised 655,666 Europeans with 5,030,727 SNPs; AIF comprised 462,346 Europeans and 9,851,867 SNPs; AAM comprised 243,944 Europeans and 9,851,867 SNPs. The measurement of exposure traits is collected uniformly from the UK Biobank (UKB) database and presented in the form of standard deviation (SD) or the logarithmic form of the odds ratio (logOR). We employed a two-sample Mendelian randomization (MR) analysis to discern the causalities between T2D, AIF, AAM, and GBC. Sensitivity analyses were conducted to identify and address potential heterogeneity, horizontal pleiotropy, and outliers.
RESULTS: Our findings indicated that T2D reduced GBC risk [odds ratio (OR) =0.044; 95% confidence interval (CI): 0.004-0.55; P=0.015, inverse variance-weighted (IVW)]. However, no causal relationship was observed between AIF (OR =0.158; 95% CI: 5.33E-05 to 466.84; P=0.65, IVW), AAM (OR =0.19; 95% CI: 0.0003-140.34; P=0.62, IVW), and GBC. Sensitivity analysis revealed no evidence of horizontal pleiotropy, heterogeneity, or outliers, suggesting the robustness and reliability of our conclusions.
CONCLUSIONS: T2D emerged as a potentially protective factor against GBC, whereas neither AIF nor AAM demonstrated a causal relationship with GBC risk. Regulation of glucose metabolism may be one of the methods for preventing GBC.