Dietary patterns and colorectal cancer risk: a meta-analysis.

Association of obesity, serum glucose and lipids with the risk of advanced colorectal adenoma and cancer: A case-control study in Korea

To evaluate the relationship between the use of proton pump inhibitors (PPI) and the risk of gastric cancer and colorectal cancer by using meta-analysis. Computer search PUBMED, EMBASE, Cochrane Library, CNKI and Wanfang database to obtain relevant literature on the use of PPI and the risk of gastric cancer and colorectal cancer, extract relevant data, and use Stata14.0 for Meta-analysis. A total of 24 articles were included, including 12 articles for gastric cancer and 12 articles for colorectal cancer. A total of 5 313 749 persons were included in the study and analysis. Meta-analysis results showed that the risk of gastric cancer in PPI users was significantly increased [risk ratio (RR) = 2.04, 95% confidence interval (CI) (1.33-2.75)], and the regional subgroup analysis results showed that in Europe [RR = 2.01, 95% CI (0.92, 3.09), P < 0.05] and Asia [RR = 2.15, 95% CI (1.16, 3.14), P < 0.05] This risk is higher, and Asia is higher than Europe. The risk of colorectal cancer is slightly increased [RR = 1. 22, 95% CI (1.03, 1.40, P < 0.05], and the regional subgroup analysis results show that in Europe [RR = 1.05 95% CI (0.98, 1.12), P < 0.05] and Asia [RR = 1.18, 95% CI (1.10, 1.27), P < 0.05]. This risk is low, but Asia is higher than Europe. The use of PPI significantly increases gastric cancer However, the risk of colorectal cancer is not significantly increased. The risk of gastric cancer and colorectal cancer in the population using PPI in Asia is higher than that in Europe.

Association of Metabolic Syndrome With Proximal and Synchronous Colorectal Neoplasm

Dose-response of serum 25-hydroxyvitamin D in association with risk of colorectal cancer: A meta-analysis

Cigarette Smoking and Colorectal Cancer Risk: A Burning Issue

Guidelines on genetic evaluation and management of Lynch syndrome: A consensus statement by the U.S. Multi-Society Task Force on Colorectal Cancer

BackgroundThe mouse double minute 2 (MDM2) gene encodes a phosphoprotein that interacts with P53 and negatively regulates its activity. The SNP309 polymorphism (T-G) in the promoter of MDM2 gene has been reported to be associated with enhanced MDM2 expression and tumor development. Studies investigating the association between MDM2 SNP309 polymorphism and colorectal cancer (CRC) risk reported conflicting results. We performed a meta-analysis of all available studies to explore the association of this polymorphism with CRC risk.MethodsAll studies published up to July 2013 on the association between MDM2 SNP309 polymorphism and CRC risk were identified by searching electronic databases PubMed, EMBASE, and Chinese Biomedical Literature database (CBM) databases. The association between the MDM2 SNP309 polymorphism and CRC risk was assessed by odds ratios (ORs) together with their 95% confidence intervals (CIs).ResultsA total of 14 case-control studies including 4460 CRC cases and 4828 controls were identified. We did not find a significant association between the MDM2 SNP309 polymorphism and CRC risk in all genetic models in overall population. However, in subgroup analysis by ethnicity, significant associations were found in Asians (TG vs. TT: OR = 1.197, 95% CI = 1.055–1.358, P=0.005; GG+TG vs. TT: OR = 1.246, 95% CI = 1.106–1.404, P=0.000) and Africans. When stratified by HWE in controls, significantly increased risk was also found among the studies consistent with HWE (TG vs. TT: OR = 1.166, 95% CI = 1.037–1.311, P= 0.010). In subgroup analysis according to p53 mutation status, and gender, no any significant association was detected.ConclusionsThe present meta-analysis suggests that the MDM2 is a candidate gene for CRC susceptibility. The MDM2 SNP309 polymorphism may be a risk factor for CRC in Asians.

The effect of vitamin A (VA) and vitamin E (VE) on colorectal cancer (CRC) risk is controversial. The aim of this study is to examine the association between serum concentrations and dietary intakes of VA and VE and the risk of CRC in Guangdong, China. A total of 535 cases and 552 sex and age-matched (5-year interval) controls were recruited during July 2010 to September 2014. Dietary information was assessed by face-to-face interviews using a validated food frequency questionnaire. Concentrations of VA and VE were measured by high-performance liquid chromatography. Multivariable logistic regression was used to estimate the odds ratios (ORs) and 95% confidence interval (CI) after adjusting for various potential confounders. A higher intake of VA and VE was found to be associated with 52 and 43% reduction in CRC risk. The ORs of the highest quartile compared with the lowest quartile intake were 0.48 (95% CI: 0.31, 0.73, Ptrend<0.01) for VA and 0.57 (95% CI: 0.37, 0.88, Ptrend<0.01) for VE. An inverse association was also found between serum retinol and CRC risk, with an adjusted OR (95% CI) of 0.28 (0.19-0.43) (Ptrend<0.01). However, no statistically significant association was found between serum α-tocopherol and CRC risk. Stratified analysis by sex showed that serum retinol and dietary VA and VE were inversely associated with CRC risk in both sexes. This study supported the hypothesis that lower serum levels of retinol and lower intakes of VA and VE were associated with the risk of CRC in a Chinese population.

Introduction: Early-onset colorectal cancer (CRC), as defined by CRC diagnosed before age 50, has been increasing in the past 2 decades, with unidentified reasons. Type 2 diabetes increases risk of CRC with average age of onset, however, epidemiological data linking type 2 diabetes and risk of early-onset CRC is thus far limited. Methods: To examine the association between type 2 diabetes and risk of early-onset CRC, we conducted a nested case-control study of early-onset CRC among participants aged 18-50 years with at least 2 years and 3 months of continuous enrollment in the IBM® MarketScan® Research Databases (2006-2015), the largest database that covers healthcare claims from over 150 million privately insured adults in the US. Incident CRC cases were identified using ICD-9-CM diagnosis codes on pathologists' claims. For cases, the index dates were set at the first pathologist date. Controls without CRC were identified using 1:8 frequency matching on age, sex, and geographical region, duration of insurance enrollment, and Rx coverage. Type 2 diabetes within 2 years of the index dates were identified through the ICD-9-CM and confirmed by Klabunde algorithm. Multivariate logistic regression was used to estimate the odds ratios (ORs) and 95% confidence intervals (CIs). Results: A total of 5986 early-onset CRC cases were identified. Type 2 diabetes was significantly associated with an increased risk of early-onset CRC (prevalence in cases/controls: 7.2% vs 4.3%; OR: 1.40, 95% CI 1.24-1.56), after adjusting for the matching factors, health care utilization, Charlson Comorbidity Index, obesity, inflammatory bowel disease (IBD), colonoscopy and fecal occult blood test (FOBT), and family history of gastrointestinal neoplasm. Notably, the association between type 2 diabetes and early onset-CRC was similar for colon (OR: 1.44, 95% CI 1.25-1.64) and rectal cancer (OR: 1.30, 95% CI 1.18-1.56) (Pheterogeneity = 0.41). These associations remain similar while we restricted the analyses to individuals without IBD, endoscopy/FOBT, or early symptoms, respectively. In addition, the findings were also similar for women and men, as well as CRC diagnosed before and after age 45. Conclusions: Type 2 diabetes was associated with increased risk of early-onset CRC with similar strength of associations for colon and rectal cancer. Citation Format: Zitong Li, Xiaobin Zheng, Katelin B. Nickel, Hanyu Chen, Andrew Tipping, Long H. Nguyen, Andrew T. Chan, Ryan C. Fields, Nicholas O. Davidson, Edward Giovannucci, Margaret A. Olsen, Peter T. Campbell, Graham A. Colditz, Yin Cao. Diabetes and risk of early-onset colorectal cancer [abstract]. In: Proceedings of the Annual Meeting of the American Association for Cancer Research 2020; 2020 Apr 27-28 and Jun 22-24. Philadelphia (PA): AACR; Cancer Res 2020;80(16 Suppl):Abstract nr 2351.

The study aimed to examine the association between a dietary index for gut microbiota (DI-GM) and the risk of incident colorectal cancer (CRC). Clarifying the role of diet-induced alterations in the composition and function of gut microbiota on the development of CRC can contribute to prevention efforts. Participants from the Prostate, Lung, Colorectal, and Ovarian Cancer Screening trial enrolled in the intervention arm and who completed baseline assessments were included in the analysis (n = 55,685). The DI-GM is a literature-derived index used to score diet quality in terms of maintaining healthy gut microbiota. A time-dependent Cox model stratified by follow-up years (<5 and ≥5 person-years) was used to evaluate the relationships between the dietary patterns and risk of incident CRC. A total of 735 incident CRC were identified over 650,470 person-years of follow-up. During < 5 years of follow-up, those with higher diet quality (DI-GM scores above 67th percentile) had an 18% lower risk of incident CRC (HRadjusted = 0.82, 95% CI: 0.63, 1.07) compared with those with lower diet quality (DI-GM scores below the 67th percentile), though effect estimates were imprecise. During ≥ 5 years of follow-up, there was no association between incident CRC and DI-GM (HRadjusted = 1.01, 95% CI: 0.80, 1.26). Diet quality measured using the DI-GM was associated with the risk of CRC in the first five years of follow-up in a large prospective cohort study. A diet that enhances the composition and function of gut microbiota may contribute to reduction in CRC risk.

BackgroundSubstantial evidence supports an association between use of menopausal hormone therapy and decreased colorectal cancer (CRC) risk, indicating a role of exogenous sex hormones in CRC development. However, findings on endogenous oestrogen exposure and CRC are inconsistent.MethodsWe used a Mendelian randomisation approach to test for a causal effect of age at menarche and age at menopause as surrogates for endogenous oestrogen exposure on CRC risk. Weighted genetic risk scores based on 358 single-nucleotide polymorphisms associated with age at menarche and 51 single-nucleotide polymorphisms associated with age at menopause were used to estimate the association with CRC risk using logistic regression in 12,944 women diagnosed with CRC and 10,741 women without CRC from three consortia. Sensitivity analyses were conducted to address pleiotropy and possible confounding by body mass index.ResultsGenetic risk scores for age at menarche (odds ratio per year 0.98, 95% confidence interval: 0.95–1.02) and age at menopause (odds ratio 0.98, 95% confidence interval: 0.94–1.01) were not significantly associated with CRC risk. The sensitivity analyses yielded similar results.ConclusionsOur study does not support a causal relationship between genetic risk scores for age at menarche and age at menopause and CRC risk.

BackgroundThe proportion of screening colonoscopic examinations performed by a physician that detect one or more adenomas (the adenoma detection rate) is a recommended quality measure. However, little is known about the association between this rate and patients' risks of a subsequent colorectal cancer (interval cancer) and death.MethodsUsing data from an integrated health care delivery organization, we evaluated the associations between the adenoma detection rate and the risks of colorectal cancer diagnosed 6 months to 10 years after colonoscopy and of cancer-related death. With the use of Cox regression, our estimates of attributable risk were adjusted for the demographic characteristics of the patients, indications for colonoscopy, and coexisting conditions.ResultsWe evaluated 314,872 colonoscopies performed by 136 gastroenterologists; the adenoma detection rates ranged from 7.4 to 52.5%. During the follow-up period, we identified 712 interval colorectal adenocarcinomas, including 255 advanced-stage cancers, and 147 deaths from interval colorectal cancer. The unadjusted risks of interval cancer according to quintiles of adenoma detection rates, from lowest to highest, were 9.8, 8.6, 8.0, 7.0, and 4.8 cases per 10,000 person-years of follow-up, respectively. Among patients of physicians with adenoma detection rates in the highest quintile, as compared with patients of physicians with detection rates in the lowest quintile, the adjusted hazard ratio for any interval cancer was 0.52 (95% confidence interval [CI], 0.39 to 0.69), for advanced-stage interval cancer, 0.43 (95% CI, 0.29 to 0.64), and for fatal interval cancer, 0.38 (95% CI, 0.22 to 0.65). Each 1.0% increase in the adenoma detection rate was associated with a 3.0% decrease in the risk of cancer (hazard ratio, 0.97; 95% CI, 0.96 to 0.98).ConclusionsThe adenoma detection rate was inversely associated with the risks of interval colorectal cancer, advanced-stage interval cancer, and fatal interval cancer. (Funded by the Kaiser Permanente Community Benefit program and the National Cancer Institute.)

BackgroundObservational studies have shown that milk consumption is inversely associated with colorectal, bladder, and breast cancer risk, but positively associated with prostate cancer. However, whether the associations reflect causality remains debatable. We investigated the potential causal associations of milk consumption with the risk of colorectal, bladder, breast, and prostate cancer using a genetic variant near the LCT gene as proxy for milk consumption.MethodsWe obtained genetic association estimates for cancer from the UK Biobank (n = 367,643 women and men), FinnGen consortium (n = 135,638 women and men), Breast Cancer Association Consortium (n = 228,951 women), and Prostate Cancer Association Group to Investigate Cancer Associated Alterations in the Genome consortium (n = 140,254 men). Milk consumption was proxied by a genetic variant (rs4988235 or rs182549) upstream of the gene encoding lactase, which catalyzes the breakdown of lactose.ResultsGenetically proxied milk consumption was associated with a reduced risk of colorectal cancer. The odds ratio (OR) for each additional milk intake increasing allele was 0.95 (95% confidence interval [CI] 0.91–0.99; P = 0.009). There was no overall association of genetically predicted milk consumption with bladder (OR 0.99; 95% CI 0.94–1.05; P = 0.836), breast (OR 1.01; 95% CI 1.00–1.02; P = 0.113), and prostate cancer (OR 1.01; 95% CI 0.99–1.02; P = 0.389), but a positive association with prostate cancer was observed in the FinnGen consortium (OR 1.07; 95% CI 1.01–1.13; P = 0.026).ConclusionsOur findings strengthen the evidence for a protective role of milk consumption on colorectal cancer risk. There was no or limited evidence that milk consumption affects the risk of bladder, breast, and prostate cancer.

Background: Recent research suggests that in addition to advanced adenomas, sessile serrated polyps (SSPs) may be important precursors for proximal colon cancer. In this study, we conducted the first large cohort study to evaluate the risk of colorectal cancer (CRC) in patients diagnosed with SSPs through usual care. Methods: The University of Washington Medical Center (UWMC) uses a comprehensive electronic medical records (EMR) system to track patient demographics and health-related information, including diagnoses and procedures for all patients. We used procedure codes to identify a cohort of patients receiving colonoscopies at UWMC from 2003-2013. Natural language processing of text in the final diagnosis section of the pathology report was used to characterize the type of polyps present at each colonoscopy procedure, including non-advanced conventional adenomas, advanced conventional adenomas (defined as having villous histology, high-grade dysplasia, or a diameter ≥ 10 mm), and sessile serrated polyps. These colonoscopy records were then linked to the Puget Sound Surveillance, Epidemiology, and End Results Cancer Registry (SEER) and subsequent EMR data to identify incident CRCs occurring through December 31, 2014 within this cohort. Those who lived outside of the SEER catchment area or who had prior colectomy, inflammatory bowel disease, or CRC were excluded from analyses. Cox proportional hazards regression models were used to calculate adjusted hazard ratios (HRs) and 95% confidence intervals (CIs) comparing the risk of CRC in each polyp group to those who were polyp-free at an index colonoscopy. HR estimates were adjusted for age, sex, race/ethnicity, smoking status, and body mass index. Results: From 2003 through 2013, 32,136 colonoscopies were performed at UWMC, and 17,424 colonoscopies from 14,846 patients met the study inclusion criteria. Of these patients, 8,908 were polyp-free, 4,145 had only non-advanced conventional adenomas, 927 had advanced conventional adenomas and no SSPs, 314 had ≥1 SSP and ≥1 conventional adenoma, and 552 had SSPs and no conventional adenomas at an index colonoscopy. Median follow-up time in the study cohort was 5.8 years, and 66 incident colorectal cancers occurred during the follow-up period. The risk of incident CRC in those with advanced conventional adenomas at their index colonoscopy was significantly higher than those who were polyp-free (HR=3.9; CI: 1.9-7.7). However, there was not a statistically significant difference in the risk of incident CRC between those who were polyp-free at their index colonoscopy and those who had only non-advanced conventional adenomas (HR=1.5; CI: 0.8-2.6), SSPs with conventional adenomas (HR=2.0; CI: 0.5-8.7), or SSPs without conventional adenomas (HR=1.3; CI: 0.3-5.5). Discussion: Despite recent evidence from cross-sectional studies suggesting that SSPs are high-risk precursors for a subset of colorectal cancers, our results indicate that the risk of CRC in patients with clinically-diagnosed SSPs is similar to the risk of CRC in those with non-advanced adenomas. Additional longitudinal studies of SSPs diagnosed through usual care are needed to inform guidelines for the surveillance of patients with SSPs. This abstract is also being presented as Poster B01. Citation Format: Andrea Burnett-Hartman, Polly A. Newcomb, Chan X. Zeng, Yingye Zheng, John M. Inadomi, Christine Fong, Melissa P. Upton, William M. Grady. Using medical informatics to evaluate the risk of colorectal cancer in patients with clinically diagnosed sessile serrated polyps. [abstract]. In: Proceedings of the AACR Special Conference on Colorectal Cancer: From Initiation to Outcomes; 2016 Sep 17-20; Tampa, FL. Philadelphia (PA): AACR; Cancer Res 2017;77(3 Suppl):Abstract nr PR05.

POLYMORPHISMS OF BIOTRANSFORMATION AND DNA REPAIR GENES, DIETARY AND RISK OF COLORECTAL CANCER IN TAIWAN