Risk Of Incident Colorectal Cancer Research Articles

Epidemiology of Vitamin D and Colorectal Cancer

Garland and Garland first hypothesized that better vitamin D status lowered risk of colorectal cancer in 1980. Subsequently, the relation between vitamin D status and colorectal cancer risk has been investigated in epidemiologic studies. Various approaches have been used to estimate vitamin D status, including direct measures of circulating 25(OH)vitamin D levels, surrogates or determinants of vitamin D (including region of residence, intake, and sun exposure estimates, or a combination of these). These measures of vitamin D status have been studied in relation to colorectal adenoma, precursors of cancer, and colorectal cancer incidence and mortality. In general, all lines of inquiry from observational studies indicate that better vitamin D status is associated with lower colorectal cancer risk. While most of the studies have examined vitamin D status in relation to risk of incident colorectal cancer, some evidence suggests that vitamin D may be additionally important for colorectal cancer progression and mortality. Although the influence of confounding factors cannot be entirely excluded, the consistency of the association using various approaches to measure vitamin D, for diverse endpoints and in diverse populations shows high consistency and is strongly suggestive of a causal association. Thus, improving vitamin D status could be potentially beneficial against colorectal cancer incidence and mortality.

The Role of Diabetes and Diabetes Treatments in Colorectal Cancer Mortality, Incidence, and Survival

Type 2 diabetes mellitus (T2DM) and colorectal cancer are major causes of morbidity and mortality worldwide. T2DM and colorectal cancer share common risk factors related to westernized lifestyles, including high body mass index and central adiposity, low physical activity, cigarette smoking, and diets characterized by low intake of fruit and vegetables and high intake of red and processed meats and refined grains and sugars. Epidemiologic studies show that T2DM is quite convincingly associated with higher risk of colorectal cancer incidence and mortality, even after accounting for their shared risk factors. Whether T2DM is related to poorer prognosis after colorectal cancer diagnosis is less understood and controversial, although some larger studies suggest poorer prognosis among patients with T2DM. The impact of diabetes treatments, such as metformin or insulin, on colorectal cancer risk also is characterized poorly. This review describes studies on the association of diabetes and its treatments with colorectal cancer mortality, incidence, and survival. Potential clinical and biological explanations for these associations are explored.

Body Mass Index at Different Adult Ages, Weight Change, and Colorectal Cancer Risk in the National Institutes of Health-AARP Cohort

The authors investigated the relations of body mass index at different ages and adult weight change to incident colorectal cancer risk in the prospective National Institutes of Health-AARP Diet and Health Study (1995-1996), using a subcohort with repeated recall weights (273,679 participants; mean baseline age = 62.8 years). During 2,509,662 person-years follow-up, 4076 incident colorectal cancers were ascertained. For men, an increased risk of colon cancer but not rectal cancer was associated with body mass index at baseline age (per 5-kg/m(2) increase, hazard ratio (HR) = 1.18, 95% confidence interval (CI): 1.11, 1.25), at age 50 years (HR = 1.18, 95% CI: 1.10, 1.26), and at age 35 years (HR = 1.16, 95% CI: 1.07, 1.25) but less so at age 18 years. Weight gained between the ages of 18 and 35 years and between 18 years of age and the baseline age was associated with an increased risk of colon cancer in men (per 0.5-kg/year increase, HR = 1.18, 95% CI: 1.11, 1.25 and HR = 1.29, 95% CI: 1.16, 1.56, respectively). For women, relations throughout were weaker than those observed for men. These findings suggest that weight gains during early to middle adulthood have important influences on colon cancer risk, especially in men.

Contribution of Behavioral Risk Factors and Obesity to Socioeconomic Differences in Colorectal Cancer Incidence

Health behaviors are known risk factors for colorectal cancer and are more common in low socioeconomic status (SES) populations. We evaluated the extent to which behavioral risk factors and body mass index (BMI) explain SES disparities in colorectal cancer incidence, overall and by tumor location. We analyzed prospective National Institutes of Health-AARP Diet and Health Study data on 506 488 participants who were recruited in 1995-1996 from six US states and two metropolitan areas and followed through 2006. Detailed baseline data on risk factors for colorectal cancer, including health behaviors, were obtained using questionnaires. SES was measured by self-reported education and census-tract data. The outcome was primary incident invasive colorectal adenocarcinoma. Poisson regression was used to estimate the association between SES and risk of incident colorectal cancer, with adjustment for age, sex, race and ethnicity, family history, and state of residence. The model estimates were used to derive percentage mediation by behavioral risk factors; bias-corrected 95% confidence intervals were obtained through bootstrap techniques. Seven-thousand six-hundred seventy-six participants developed colorectal cancer during follow-up. SES differences in prevalence of physical inactivity, unhealthy diet, smoking, and unhealthy weight each explained between 11.3% (BMI) and 21.6% (diet) of the association between education and risk of colorectal cancer and between 8.6% (smoking) and 15.3% (diet) of the association between neighborhood SES and risk of colorectal cancer. Health behaviors and BMI combined explained approximately 43.9% (95% CI = 35.1% to 57.9%) of the association of education and 36.2% (95% CI = 28.0% to 51.2%) of the association of neighborhood SES with risk of colorectal cancer. The percentage explained by all factors and BMI combined was largest for right colon cancers and smallest for rectal cancers. A substantial proportion of the socioeconomic disparity in risk of new-onset colorectal cancer, and particularly of right colon cancers, may be attributable to the higher prevalence of adverse health behaviors in low-SES populations.

658 Effect of Colonoscopy on Colorectal Cancer Incidence and Mortality: An Instrumental Variable Analysis

Colonoscopy may reduce the incidence and mortality of colorectal cancer (CRC). Using population-based health services information to estimate the effectiveness of colonoscopy on the risk of CRC incidence and mortality is prone to selection bias, especially since it is difficult to determine whether colonoscopy procedures are performed for screening or for other purposes. The objective of this study was to determine the effect of colonoscopy on CRC incidence and mortality using administrative health data.

Abstract B101: Garlic consumption and colorectal cancer risk in the CPS-II Nutrition Cohort

Abstract Background: The World Cancer Research Fund/American Institute for Cancer Research considers a role for garlic in colorectal cancer prevention to be “probable”. This conclusion is based on supportive preclinical evidence and pooled analyses of high vs low consumption from two prospective cohort (RR=0.72, 95% CI 0.54–0.96) and five case control (RR=0.76, 95% CI 0.58–0.98) studies. The two prospective studies included <300 cases each, and the highest category of garlic consumption considered was ≥1 or ≥2 servings per week compared to none. We examined the association between garlic consumption and risk of colorectal cancer in a large, nationwide prospective cohort study including over 1100 colorectal cancer cases. This large study allowed for a more detailed analysis of garlic intake including at least daily consumption. Methods: In 1999, 43,025 male and 57,043 female participants in the Cancer Prevention Study (CPS)-II Nutrition Cohort with no history of cancer completed food frequency questionnaires in which frequency of garlic consumption was assessed. Garlic supplement use was assessed in 2001. Participants were followed for incident colorectal cancer through mid-2007 via biennial questionnaires and cases were verified by medical record abstraction or linkage to state tumor registries. Cox proportional hazards regression methods were used to estimate hazard rate ratios (HRs) and 95% confidence intervals (CIs). Potential non-dietary and dietary confounders included in the models were age, history of endoscopy, NSAID use, recreational physical activity, body mass index, smoking, HRT use (women), red and processed meat consumption, fruit and vegetable consumption and total calcium intake. Results: Incident colorectal cancer was verified in 595 men and 559 women. Five percent of participants reported garlic consumption (1 clove or 4 shakes) 1 or more times per day in 1999, and in 2001, and 5% reported currently using garlic supplements. Dietary garlic consumption was not related to colorectal cancer risk in men. Among women, compared to consumers of dietary garlic less than once per month, never consumption of garlic was associated with a lower risk of colorectal cancer (RR=0.74, 95% CI 0.57–0.96); similarly, regular consumption of garlic was associated with a lower risk of incident colorectal cancer (HR1 time/wk=0.80, 95% CI 0.60–1.07; HR2–4 times/wk=0.65, 95% CI=0.48–0.87; HR5–6 times/wk=0.61, 95% CI=0.40–0.94 and HR1+ times/day=0.72, 95% CI 0.47–1.10). Garlic supplement use (current use at least once/week vs never) was not related to colorectal cancer risk in men or women. These associations did not vary by colorectal sub-site, BMI or HRT use (among women). Conclusion: This study does not support the hypothesis that garlic intake or supplement use reduces colorectal cancer risk in men, but suggests an inverse association with greater dietary intake among women who consume garlic. The reasons for different associations by sex, and for lower risk in female non-consumers are unclear and deserve further study. Citation Information: Cancer Prev Res 2011;4(10 Suppl):B101.

P2-18 Whole grain consumption and the risk of colorectal cancer: a systematic review and meta-analysis of cohort studies

IntroductionSeveral case-control studies have suggested inverse associations between whole grain intake and colorectal cancer risk, but few cohort studies have been published on the subject. As part of the Continuous...

ABO Blood Group and Risk of Colorectal Cancer

Recent studies have shown an association between non-O blood group and risk of pancreatic cancer. It is unclear whether this association is observed with other gastrointestinal malignancies, including colorectal cancers. We examined the relationship between ABO blood group and the risk of incident colorectal cancer in two large prospective cohorts. We calculated HR using Cox proportional hazard modeling while adjusting for known risk factors of colorectal cancer. During 996,779 person-years of follow-up, we documented 1,025 incident cases of colorectal cancers. Compared to individuals with blood group O, the multivariate-adjusted HR were 1.08 (95% CI, 0.94-1.24) for blood group A, 1.20 (95% CI, 1.00-1.45) for blood group B, and 1.08 (95% CI, 0.85-1.36) for blood group AB. In two large prospective cohorts, we did not observe a statistically significant association between ABO blood group and risk of colorectal cancer. These results do not support an association between ABO blood group and risk of colorectal cancer.

Homocysteine, cysteine and risk of incident colorectal cancer in the Women's Health Initiative Observational Cohort

Inflammatory bowel disease (IBD) is a risk factor for colorectal cancer (CRC), as is low intake of folate. Hyperhomocysteinemia is highly prevalent in patients with IBD and is a marker of low folate status; thus homocysteine may serve as a risk marker for CRC. Cysteine is a metabolic product of homocysteine and a precursor for glutathione, an important intracellular antioxidant. It is unknown if cysteine is associated with CRC. We investigated the associations between homocysteine and cysteine and incident CRC in the Women's Health Initiative Observational Cohort using a nested case-control design. Cases and controls (n=988 per group) were matched for age (mean 67±7 yrs) and ethnicity. Multivariate-adjusted odds ratios (95% CI) for incident CRC were 1.4 (1.0, 1.9) for those subjects in the highest quartile of homocysteine (>9.8 μmol/L) compared with the lowest (≤6.8 μmol/L) (p=0.03), and 0.6 (0.4, 0.8) for those in the highest quartile of cysteine (>308 μmol/L) compared with the lowest (≤259 μmol/L) (p=0.007). The associations were statistically significant for proximal tumors (p≤0.04), but not for distal tumors, and were significant for localized tumors (p≤0.01), but not for metastases. These data indicate that high plasma homocysteine is associated with increased risk of CRC, while high cysteine is associated with decreased risk. Funding: NIH R01 CA120523, NIH N01 WH22110

Body mass index and risk of colorectal cancer in Chinese Singaporeans

The authors chose to examine the association between body mass index (BMI) and incident colorectal cancer across the spectrum of BMI, including underweight persons, because detailed prospective cohort data on this topic in Asians is scarce, as is data on underweight persons (BMI, <18.5 kg/m(2)) in any population. Analysis of the Singapore Chinese Health Study included 51,251 men and women aged 45-74 years enrolled in 1993-1998 and followed through 2007. Incident cancer cases and deaths among cohort members were identified through record linkage, and 980 cases were identified. Cox regression models were used to investigate the association of baseline BMI with risk of incident colorectal cancer during a mean of 11.5 years of follow-up. A significant, U-shaped, quadratic association was observed between BMI and colon cancer risk, with increased risk in BMIs ≥27.5 and <18.5 kg/m(2). The association was more pronounced in never smokers and most prominent when further limiting the sample to those free of diabetes and cases with longer than 5 years of follow-up. Localized cases had a more pronounced association in BMIs ≥27.5, whereas advanced cases had a more pronounced association in BMIs <18.5 kg/m(2) . No association was found in relation to rectal cancer risk. The association was also stronger among patients aged 65 years and older. BMI displays a U-shaped, quadratic association with colon cancer risk in this Chinese population in Southeast Asia.

Abstract A87: Folate and vitamin B6 intake and colorectal cancer risk in the CPS-II Nutrition Cohort

Abstract Background: High folate intake has been inversely associated with incident colorectal cancer risk. However, it is not clear whether folic acid, the synthetic folate added to foods and supplements, is as effective as natural folates. Vitamin B6, which is found in many of the same foods and participates in one-carbon metabolism with folate has also been inversely associated with colorectal cancer risk. Whether the associations between folate and vitamin B6 and risk of colorectal cancer are independent has not been investigated. Methods: The associations of folate and vitamin B6 intakes with colorectal cancer risk were investigated in the American Cancer Society Cancer Prevention Study II (CPS-II) Nutrition Cohort. Of the 43,512 men and 56,011 women who provided detailed dietary information in 1999, 526 men and 497 women were diagnosed with colorectal cancer between 1999 and 2007. Food frequency questionnaire (FFQ) responses, reported multivitamin and other supplement use, and composition values from the USDA were used to quantify intakes of natural folates (in food), dietary folate (natural food folates and folic acid from fortification), folic acid (in foods from fortification and from multivitamins and supplements), total folate (from all sources), dietary vitamin B6 (from food) and total vitamin B6 (from food, multivitamins and supplements). Cox proportional hazards modeling was used to calculate multivariate hazards ratios and 95% confidence intervals. Results: Higher intakes of natural folate (RRQ5vsQ1=0.82; 95% CI; 0.68, 1.01; p-trend=0.07), dietary folate (RRQ5vsQ1=0.83; 95% CI; 0.68, 1.02; p-trend=0.14), folic acid (RRQ5vsQ1=0.88; 95% CI; 0.72, 1.08; p-trend=0.09), and total folate (RRQ5vsQ1=0.79; 95% CI; 0.65, 0.97; p-trend=0.05) were associated with lower colorectal cancer risk, although not all results were statistically significant. Similarly, higher intakes of dietary B6 (RRQ5vsQ1=0.82; 95% CI; 0.67, 1.07; p-trend=0.07) and total vitamin B6 (RRQ5vsQ1=0.82; 95% CI; 0.67, 1.00; p-trend=0.12) also were associated with lower colorectal cancer risk. Exclusion of the first two years of follow-up strengthened the inverse associations with folate measures but attenuated associations with vitamin B6. Controlling for vitamin B6 intake did not substantively change risk estimates for measures of folate intake, although confidence intervals were widened. The associations of dietary and total vitamin B6 with colorectal cancer risk were somewhat attenuated but remained inverse when controlled for either dietary or total folate intake. Conclusions: Our findings add to the epidemiologic evidence which suggests that higher intakes of folate reduce colorectal cancer risk and indicate that synthetic folic acid is as effective as natural folates. The inverse association of vitamin B6 intake with colorectal cancer was somewhat weaker and may be due, at least in part, to the correlated intake of folate. While vitamin B6 intake did not appear to confound associations with folate, further studies with blood levels of these two nutrients might help to disentangle associations of folate and vitamin B6 with colorectal cancer risk. Citation Information: Cancer Prev Res 2010;3(12 Suppl):A87.

Cigarette Smoking and Colorectal Cancer Risk by Molecularly Defined Subtypes

Cigarette smoking is an established risk factor for colorectal cancer. Because colorectal carcinogenesis is a heterogeneous process, we investigated whether cigarette smoking is differentially associated with molecularly defined subtypes of colorectal cancer. We evaluated associations between smoking and incident colorectal cancer, overall and by microsatellite instability (MSI) phenotype (MSI-high vs MSI-low or microsatellite stable), CpG island methylator phenotype (CIMP positive or CIMP negative), and BRAF mutation status (BRAF mutation positive or BRAF mutation negative), among 37 399 participants in a population-based cohort study (the Iowa Women's Health Study). Cigarette smoking (and other exposures) was assessed by self-report at baseline in 1986, including smoking status (never and ever [former or current]), age at initiation, total duration, average number of cigarettes smoked per day, cumulative pack-years, and induction period. Vital status and state of residence were determined by mailed follow-up questionnaires in 1987, 1989, 1992, and 1997 and by linkage to Iowa death certificate records. Nonrespondents were checked via the National Death Index to identify descendants. Participants with newly diagnosed (ie, incident) colorectal cancer were identified through annual linkage with the Iowa Cancer Registry. Archived paraffin-embedded tumor tissue specimens were obtained for 555 patients with colorectal cancer who were diagnosed from January 1, 1986, through December 31, 2002, and MSI status, CIMP status, and BRAF status were determined. Multivariable Cox regression models were fit to estimate relative risks (RRs) and 95% confidence intervals (CIs). Ever-smokers were at moderately increased risk for incident colorectal cancer (RR = 1.19, 95% CI = 1.05 to 1.35) compared with never-smokers. Higher risk estimates were observed for current smokers with MSI-high tumors (RR = 1.99, 95% CI = 1.26 to 3.14), CIMP-positive tumors (RR = 1.88, 95% CI = 1.22 to 2.90), and BRAF mutation-positive tumors (RR = 1.92, 95% CI = 1.22 to 3.02). Other smoking-related variables (ie, age at initiation, total duration, average number of cigarettes smoked per day, cumulative pack-years, and induction period) were also associated with MSI-high, CIMP-positive, and BRAF mutation-positive tumor subtypes. Conversely, cigarette smoking status (ever vs never) was not associated with the MSI-low or microsatellite stable (RR = 1.00, 95% CI = 0.79 to 1.25), CIMP-negative (RR = 1.02, 95% CI = 0.81 to 1.30), or BRAF mutation-negative subtypes (RR = 1.00, 95% CI = 0.65 to 1.27). In this prospective study of older women, cigarette smoking was associated with the MSI-high, CIMP-positive, and BRAF mutation-positive colorectal cancer subtypes, which indicates that epigenetic modification may be functionally involved in smoking-related colorectal carcinogenesis.

Abstract 1841: Diabetes, insulin-use and risk of colorectal cancer in a U.S. cohort study

Abstract Background: Diabetes is associated with a modest increased risk of colorectal cancer (CRC). Evidence also indicates that high endogenous insulin and glucose levels are associated with increased risk of CRC. However, few studies have evaluated whether exogenous insulin, used to treat diabetes, is associated with risk of CRC, and one of these studies reported strongly increased risk among diabetics who had used insulin. Further, few studies have examined the association between diabetes and risk of CRC by gender, tumor phenotype (e.g., sub-site, stage) and other factors, that may be relevant to the etiology of CRC. Methods: The CPS II Nutrition Cohort is a prospective study of cancer incidence including approximately 184,000 U.S. adults aged 50 to 75 at enrollment in 1992-93. At enrollment, participants completed a detailed self-administered questionnaire that included information on demographic, medical, lifestyle, and dietary factors. The questionnaire asked if a participant had been diagnosed by a physician with diabetes mellitus and if the participant was taking insulin to treat the disease. Follow-up questionnaires were sent to cohort members in 1997, and every two years thereafter to update exposure information, including diabetes and insulin-use, and to learn of incident cancers. Colorectal cancer cases in the current study were identified by linkage with the National Death Index (NDI) or by self-reports, subsequently verified by medical record abstraction or linkage with state cancer registries. Results: After exclusions, 73,328 men and 81,670 women remained in the final analytic cohort, of whom 1,444 men and 1,154 women were diagnosed with colon or rectal cancer between enrollment and the end of follow-up in 2007. Among female participants, diabetes and insulin-use were not associated with incident colorectal cancer overall (Relative Risk (RR): 0.98; 95% Confidence Interval (CI): 0.79-1.22 and RR: 0.92; 95% CI: 0.61-1.40, respectively) or when stratified by tumor sub-site in the colon or rectum, stage of disease, or fatality. Among male participants, both diabetes and insulin-use were associated with modestly increased risk of incident colorectal cancer (RR: 1.25; 95% CI: 1.08-1.46 and RR: 1.35; 95% CI: 1.02-1.78, respectively). There were no clear differences in associations with diabetes by subsite or stage. Duration of diabetes was linearly associated with CRC risk among men (p-trend: 0.0002), but not women. Duration of insulin-use was not linearly associated with CRC risk in men or women. Conclusions: Our results from a large U.S. prospective study confirm a modest association between diabetes and colorectal cancer risk among men but not among women. Reasons for these differences are unclear but might be due to sex-differences in hormones or better glucose control among women than men. Our results also suggest that exogenous insulin-use is unlikely to substantially increase risk of colorectal cancer among diabetics. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 1841.

Diabetes and risk of incident colorectal cancer in a prospective cohort of women.

To determine whether accounting for the time dynamics of diabetes exposure will change the risk estimates for colorectal cancer. We analyzed data from the 45, 516 women enrolled in the BCDDP follow-up cohort study. We used proportional hazards regression to obtain multivariable-adjusted risk estimates for incident colorectal cancer for prevalent diabetes at baseline and diabetes as a time-dependent variable. Subjects with diabetes had a statistically significant increased risk of colorectal cancer compared to subjects without diabetes (RR = 1.60, 95% CI 1.18-2.18). When we defined exposure as duration of diabetes exposure at cohort exit, we found that in the first 4 years after diagnosis risk was essentially the same as in those never having had a diagnosis of diabetes. For those who had been diagnosed between 4 and 8 years previously, however, we observed a RR of 2.36 (95% CI 0.96-5.79), while longer duration of exposure was associated with smaller and then no change in risk compared to those without a diagnosis of diabetes. These results are consistent with the theory that hyperinsulinemia can explain, at least in part, the association of diabetes with colorectal cancer, but in a time-dependent manner.

Atrophic gastritis and the risk of incident colorectal cancer

Previous studies evaluating whether risk factors for gastric cancer are also associated with colorectal cancer (CRC) have shown inconsistent results. We prospectively examined the association of atrophic gastritis, a pre-malignant condition for gastric cancer and long-term sequelae common to many exposure factors, and the risk of incident CRC. A total of 20,928 Finnish male smokers, aged 50-69, who were participants in the Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study (ATBC) had serum pepsinogen I (SPGI) levels measured. Participants with low SPGI levels (< 25 microg/l; n = 1,665) were invited for gastroscopy. Of these, 1,059 (63.6%) participants underwent gastroscopy and atrophic gastritis was histologically confirmed in 1,006 (95.0%) participants. We used Cox proportional hazards regression to evaluate the risk of incident CRC. During a mean follow-up of 11.3 years (236,258 person-years), 425 incident CRCs were diagnosed. The incidence rates were 1.82, 1.48, and 1.82 per 1,000 person-years of follow-up for participants with normal SPGI (> or =25 microg/l), low SPGI, and histologically confirmed atrophic gastritis, respectively. Compared to subjects with normal SPGI, there was no increased risk of CRC among subjects with low SPGI (Adjusted Hazard Ratio (HR) = 0.71; 95% CI: 0.47-1.05) and among those with histologically confirmed atrophic gastritis (Adjusted HR = 0.86; 95% CI: 0.55-1.34). Atrophic gastritis is not associated with an increased risk of colorectal cancer among male smokers.

Colorectal Cancer Outcomes, Recurrence, and Complications in Persons With and Without Diabetes Mellitus: A Systematic Review and Meta-Analysis

Diabetes mellitus increases the risk of incident colorectal cancer, but it is less clear if pre-existing diabetes mellitus influences mortality outcomes, recurrence risk, and/or treatment-related complications in persons with colorectal cancer. We performed a systematic review and meta-analysis comparing colorectal cancer mortality outcomes, cancer recurrence, and treatment-related complications in persons with and without diabetes mellitus. We searched MEDLINE and EMBASE through October 1, 2008, including hand-searching references of qualifying articles. We included studies in English that evaluated diabetes mellitus and cancer treatment outcomes, prognosis, and/or mortality. The initial search identified 8,208 titles, of which 15 articles met inclusion criteria. Each article was abstracted by one author using a standardized form and re-reviewed by another author for accuracy. Authors graded quality based on pre-determined criteria. We found significantly increased short-term perioperative mortality in persons with diabetes mellitus. In the meta-analysis of long-term mortality, persons with diabetes mellitus had a 32% increase in all-cause mortality compared to those without diabetes mellitus (95% CI: 1.24, 1.41). Although data on other outcomes are limited, available studies suggest that pre-existing diabetes mellitus predicts increased risk of some post-operative complications as well as 5-year cancer recurrence. In contrast, there is little evidence that diabetes confers increased risk for long-term cancer-specific mortality. Patients with colorectal cancer and pre-existing diabetes mellitus have an increased risk of short- and long-term mortality. Future research should determine whether improvements in prevention and treatment of diabetes mellitus will improve outcomes for colorectal cancer patients.

Fish consumption and the risk of colorectal cancer: the Ohsaki Cohort Study

Background:Evidence from laboratory and animal studies suggests that high fish consumption may reduce the risk of colorectal cancer, but the results of studies in humans have been inconsistent. The objective of this study was to prospectively examine the association between fish consumption and the risk of colorectal cancer incidence in Japan, where fish is widely consumed.Methods:We analysed data from 39 498 men and women registered in the Ohsaki National Health Insurance Cohort Study who were 40–79 years old and free of cancer at the baseline. Fish consumption was assessed at the baseline using a self-administered food frequency questionnaire.Results:During 9 years of follow-up, we identified 566 incident cases of colorectal cancer (379 men and 187 women). The hazard ratios and 95% confidence intervals (CIs) for colorectal cancer incidence in the highest quartile of fish consumption compared with the lowest quartile were 1.07 (95% CIs; 0.78–1.46, P-trend=0.43) for men, and 0.96 (95% CIs; 0.61–1.53, P-trend=0.69) for women.Conclusion:The results of this prospective cohort study revealed no association between fish consumption and the risk of colorectal cancer.

Prospective Study of JC Virus Seroreactivity and the Development of Colorectal Cancers and Adenomas

Infection with JC virus has been proposed as a risk factor for colorectal cancer. A nested case-control study was conducted to evaluate the association between prediagnostic JC virus antibodies and the risk of incident colorectal cancer and adenomas. Two research serum banks were established in Washington County, MD in 1974 and 1989, with the collection of blood samples from >45,000 volunteers. Incident colorectal cancer cases diagnosed through 2006 (n = 611) were identified among participants by linkage to population-based cancer registries, contributing 729 pairs of observations. Cases of adenomatous polyps (n = 123) were identified from participants of the 1989 cohort who reported having a colonoscopy-detected adenoma at follow-up through 2000 with histology confirmed through medical record review. One control was matched to each case on age, sex, race, and date of blood draw, and, for adenoma controls, date of endoscopy. IgG antibodies to JC virus were measured using virus-like particle ELISA. Associations between JC virus seropositivity and colorectal cancer and adenomas were estimated using conditional logistic regression. Overall, there was no association between antibodies to JC virus and colorectal cancer [odds ratio (OR), 0.91; 95% confidence interval (95% CI), 0.71-1.17]. However, a statistically significant positive association between JC virus seropositivity and subsequent adenoma diagnosis was observed among males (OR, 2.31; 95% CI, 1.20-4.46), whereas a statistically significant inverse association was observed among females (OR, 0.31; 95% CI, 0.14-0.67; P for interaction = 0.01), after adjustment for baseline smoking and body mass index. Overall, JC virus seropositivity was not associated with colorectal cancer development up to 31 years later. Future studies are needed to confirm the adenoma findings.

Serum Pepsinogen Level, Atrophic Gastritis and the Risk of Incident Colorectal Cancer – a Long-Term Prospective Study

Serum Pepsinogen Level, Atrophic Gastritis and the Risk of Incident Colorectal Cancer – a Long-Term Prospective Study

Fish Consumption and Colorectal Cancer Prevention: Is There a Catch?

Fish Consumption and Colorectal Cancer Prevention: Is There a Catch?