Regular colonoscopy could prevent 40% of colorectal cancers

Association of Metabolic Syndrome With Proximal and Synchronous Colorectal Neoplasm

Association of dietary insulinemic potential and colorectal cancer risk in men and women

Pharmacoepidemiology and Drug SafetyVolume 5, Issue 6 p. 415-418 ISPE Notice Common Language Alexander M. Walker, Corresponding Author Alexander M. Walker Harvard School of Public Health, USAA. M. Walker, Department of Epidemiology, Harvard School of Public Health, 677 Huntington Avenue, Boston MA 02115 USA, e-mail: amwalker@episun1.harvard.edu.Search for more papers by this author Alexander M. Walker, Corresponding Author Alexander M. Walker Harvard School of Public Health, USAA. M. Walker, Department of Epidemiology, Harvard School of Public Health, 677 Huntington Avenue, Boston MA 02115 USA, e-mail: amwalker@episun1.harvard.edu.Search for more papers by this author First published: November 1996 https://doi.org/10.1002/(SICI)1099-1557(199611)5:6<415::AID-PDS254>3.0.CO;2-HCitations: 2AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat Citing Literature Volume5, Issue6November 1996Pages 415-418 RelatedInformation

Journal of Food ScienceVolume 38, Issue 7 p. 1255-1255 MONOSODIUM GLUTAMATE INGESTION AND THIRST PRODUCTION PAUL E. ARAUJO, PAUL E. ARAUJO Dept. of Nutrition, Harvard School of Public Health, 665 Huntington Ave., Boston, MA 02115Search for more papers by this authorDENIS HOURIHAN, DENIS HOURIHAN Dept. of Nutrition, Harvard School of Public Health, 665 Huntington Ave., Boston, MA 02115Search for more papers by this authorJEAN MAYER, JEAN MAYER Dept. of Nutrition, Harvard School of Public Health, 665 Huntington Ave., Boston, MA 02115Search for more papers by this author PAUL E. ARAUJO, PAUL E. ARAUJO Dept. of Nutrition, Harvard School of Public Health, 665 Huntington Ave., Boston, MA 02115Search for more papers by this authorDENIS HOURIHAN, DENIS HOURIHAN Dept. of Nutrition, Harvard School of Public Health, 665 Huntington Ave., Boston, MA 02115Search for more papers by this authorJEAN MAYER, JEAN MAYER Dept. of Nutrition, Harvard School of Public Health, 665 Huntington Ave., Boston, MA 02115Search for more papers by this author First published: November 1973 https://doi.org/10.1111/j.1365-2621.1973.tb07252.x This work was supported in part by N.I.H. Grant NB 01941 and Grant AM 02911 and from the Fund for Research and Teaching. Dept. of Nutrition, Harvard School of Public Health. AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL No abstract is available for this article. Volume38, Issue7November 1973Pages 1255-1255 RelatedInformation

Cyclin D1 (CCND1) plays a key role in cell cycle control, particularly in the transition from G1 to S phase, which is regulated by cyclin-dependent kinases. A common adenine to guanine polymorphism (A870G) in the CCND1 gene has been associated with a longer-life protein and an increased risk of colorectal cancer and adenoma in some studies. Among subjects with hereditary nonpolyposis colorectal cancer, the A870G polymorphism has also been associated with a younger age of onset of colorectal cancer. We analysed 181 colorectal cancer cases and 475 matched controls and 524 adenoma cases and 517 matched controls within women in the Nurses’ Health Study (NHS) cohort, 171 colorectal cancer cases and 347 matched controls and 372 adenoma cases and 712 matched controls nested within men in the Health Professionals’ Follow-Up Study (HPFS) cohort, and 258 colorectal cancer cases and 415 matched controls within men in the Physicians’ Health Study (PHS) cohort to assess the risk associated with the CCND1 A870G genotype. Moreover, we assessed whether CCND1 genotype modified the effect of a sporadic (nonsyndromic) family history of colorectal cancer as well as the effect of other dietary and lifestyle risk factors for colorectal cancer and adenoma. In all cohorts combined, the CCND1 polymorphism did not show statistically significant associations to risk of colorectal cancer (odds ratio (OR) for A allele carriers, 1.04; 95% confidence interval (95% CI), 0.82–1.32) or adenoma (OR, 0.96; 95% CI, 0.79–1.18). The CCND1 A870G genotype was associated with a modest, although nonsignificantly elevated risk of colorectal cancer (OR, 1.59; 95% CI, 0.98–2.57) in women. In contrast, the polymorphism was not associated with increased risk of adenoma in either men or women. Among participants with the A870G genotype, a family history of colorectal cancer conferred a substantially greater risk of colorectal cancer in the women (P for interaction=0.06) and adenoma in the men (P for interaction=0.02). Current postmenopausal hormone (PMH) use was associated with a significant reduction in the risk of colorectal cancer and adenoma among women with the A870G genotype, whereas there was no effect of PMH use among those with the GG genotype. The CCND1 polymorphism appeared to confer a modest elevation in the risk of colorectal cancer among women. Moreover, the A870G genotype may enhance the protective effect of postmenopausal oestrogen use on the development of colorectal neoplasia.

Colonoscopy is widely recommended for colorectal cancer (CRC) screening, but evidence to guide the optimal frequency of repeat screening examination is limited. We examined the duration and magnitude of the risk of developing CRC, following a negative colonoscopy in those at average risk and those with a first-degree family history of CRC. A cohort of Utah residents aged 50-80 years who had a negative colonoscopy between 1 January 2001 and 31 December 2011 was identified using the Utah Population Database. Patients were followed from the time of the index colonoscopy until diagnosis of CRC, death, migration out of state, repeat colonoscopy, or end of the study period. CRC incidence after the index colonoscopy was compared with that of the state population by standardized incidence ratios (SIRs). A cohort of 131,349 individuals at average risk with a negative colonoscopy was identified. Compared with the state population, a negative colonoscopy was associated with SIRs of 0.15 (95% confidence interval (CI): 0.08-0.23) at 1 year, 0.26 (95% CI: 0.19-0.32) at 2-5 years, 0.33 (95% CI: 0.22-0.43) at 5-6 years, and 0.60 (95% CI: 0.44-0.76) at 7-10 years for CRC following the index colonoscopy. In a secondary analysis involving only patients with a first-degree relative with CRC, patients had a significantly lower incidence of CRC only for the first 5 years of follow-up (SIR 0.39, 95% CI: 013-0.64). There was also a difference in the risk of proximal (SIR 0.72, 95% CI: 0.45-0.98) and distal (SIR 0.51, 95% CI: 0.30-0.72) colon cancers at 7-10 years following a negative colonoscopy. The risk of developing CRC remains decreased for at least 10 years following the performance of a negative colonoscopy. However, the lower incidence of CRC in those with a family history of CRC differed in magnitude and timing being limited primarily to the first 5 years of follow-up and of lesser magnitude than that in the overall cohort.

This investigation was performed as a tandem to the Veterans Affairs (VA) Cooperative Study 380, which compared the results of colonoscopy screening with the estimated results of screening with flexible sigmoidoscopy in a mostly male population. The study population for this series consisted of asymptomatic women referred for routine colorectal cancer screening whose colonoscopy was complete to the cecum. Estimates of diagnoses with flexible sigmoidoscopy were made by assuming that advanced lesions in the distal colon (defined as the rectum and the sigmoid colon) would be detected and that small adenomas in the distal colon, which were concurrent with advanced neoplasia in the proximal colon, would have triggered colonoscopy and therefore a correct diagnosis. All asymptomatic women 50 to 79 years of age at average risk for developing colorectal cancer who were screened at one of 4 military centers between July 1999 and December 2002 were eligible for the study. In addition, women with an elevated risk for colorectal cancer (first-degree relative with colon cancer) who were 40 years of age or older were included. Colonoscopy was complete to the cecum in 1463 participants, including 230 (15.7%) who had an elevated risk for colorectal cancer. Neoplastic lesions were identified in 299 women. Seventy-two (4.9%) patients were diagnosed with advanced neoplasia, including 46 women with tubular adenoma 1 cm or more in size, 26 with villous adenoma, 9 who had an adenoma with high-grade dysplasia, and one woman with invasive colorectal cancer. Advanced neoplasia was present in 16 (7.0%) of the 230 high-risk participants. Small or nonadvanced adenomas were seen in 227 women, including 60 high-risk patients. Older women were the most likely to have advanced disease. Nearly 12% (19 of 162) of those 70 to 79 years of age had advanced neoplasia compared with 3.3% (26 of 786) of women in the 50- to 59-year-old group (P = .002). In the 60- to 69-year age group, 5.5% (23 of 420) participants had advanced lesions. Of the 72 women with advanced lesions, 25 (34.7%) had neoplasia in the distal colon, which would have been identified by flexible sigmoidoscopy screening. Forty-seven women positive for advanced neoplasia in the proximal colon had no lesions in the distal colon (65.3%) and would have been missed with sigmoidoscopy. In the entire screening population, 1.7% (25 of 1463) women would have been diagnosed correctly with advanced neoplasias, and 3.2% (47 of 1463) would have been undetected if screening had been performed with flexible sigmoidoscopy. Stratification according to age or family history did not affect the estimated yield of sigmoidoscopy screening. When the distal colon was defined as the rectum and sigmoid colon, a total of 6.3% of participants had neoplastic lesions in the distal colon. Among the 1367 women with no lesions in the distal colon, 47 (3.4%) had advanced disease in the proximal colon and would not have been detected with flexible sigmoidoscopy done to the junction of the sigmoid and descending colon. The incidence of advanced neoplasia in the proximal colon with no lesions in the distal colon was similar for women with and without a family member with colorectal cancer (3.1% and 3.9%, respectively). Among high-risk patients, more advanced lesions were seen in the proximal colon in women with no neoplasia in the distal colon than in women with disease in the distal colon (5.2% vs. 0%, P = .32). When the definition of the distal colon was further expanded to include the descending colon as well as the rectum and sigmoid colon, no neoplasia was found in the distal colon of 1324 (90.6%) women, and small adenomas or advanced neoplasia were seen in 138 (9.4%) patients. Under this definition, 36 (2.7%) women had advanced lesions in the proximal colon but no lesions in the distal colon. Only 3 women (2.2%) had disease in both the proximal and distal colon. The results of this study were compared with the data from the men in the VA Cooperative Study 380. Men under 70 years of age with a negative occult blood test and negative family history who underwent colonoscopy screening were diagnosed with advanced neoplasia nearly twice as often as their female counterparts (15.5% vs. 7.9%). However, in the older age range, 70 to 79 years, the rate of advanced lesions was greater in women than in men (11.8% vs. 10.6%). Overall, the rate of advanced neoplasia was 8.6% in men and 4.5% in women. Screening with flexible sigmoidoscopy would have correctly identified two thirds (126 of 190, 66.3%) of all men with advanced neoplasia. In contrast, sigmoidoscopy screening would not have detected advanced disease in nearly two thirds of all women (64.8%, 10 of 54) who had advanced neoplasia in the proximal colon.

Hypomethylation in long interspersed nucleotide element-1 (LINE-1) and high-degree microsatellite instability (MSI-high) in colorectal cancer (CRC) have been associated with inferior and superior survival, respectively; however, it remains uncertain whether the prognostic association of LINE-1 hypomethylation differs by MSI status. We hypothesized that the adverse prognostic association of LINE-1 hypomethylation might be stronger in MSI-high CRCs than in microsatellite stable (MSS) CRCs. Utilizing 1211 CRCs in the Nurses' Health Study and the Health Professionals Follow-up Study, we examined patient survival according to LINE-1 hypomethylation status in strata of MSI status. A Cox proportional hazards model was used to compute multivariable CRC-specific mortality hazard ratios (HRs) for a 10% decrease in LINE-1 methylation level (range = 23.1-93.1%), adjusting for potential confounders, including CpG island methylator phenotype, and KRAS, BRAF, and PIK3CA mutations. Statistical tests (log-rank test, chi-square test, and likelihood ratio test) were two-sided. In MSI-high cancers, the association of LINE-1 hypomethylation with higher mortality (HR = 2.45, 95% confidence interval [CI] = 1.64 to 3.66, P < .001) was stronger than that in MSS cancers (HR = 1.10, 95% CI = 0.98 to 1.24, P = .11) (P interaction < .001, between LINE-1 and MSI statuses). In MSI-high cases with CRC family history, the association of LINE-1 hypomethylation with higher mortality (HR = 5.13, 95% CI = 1.99 to 13.2; P < .001) was stronger than that in MSI-high cases without CRC family history (HR = 1.62, 95% CI = 0.89 to 2.94, P = .11) (P interaction = .02, between LINE-1 and CRC family history statuses). The association of LINE-1 hypomethylation with inferior survival is stronger in MSI-high CRCs than in MSS CRCs. Tumor LINE-1 methylation level may be a useful prognostic biomarker to identify aggressive carcinomas among MSI-high CRCs.

International Journal of DermatologyVolume 19, Issue 3 p. 168-170 Schistosomiasis Markley H. Boyer M.D., M.P.H., Corresponding Author Markley H. Boyer M.D., M.P.H. From the Department of Tropical Public Health, Harvard School of Public Health, Boston, MassachusettsAddress for reprints: Markley H. Boyer, M.D., Department of Tropical Public Health, Harvard School of Public Health, 665 Huntington Avenue, Boston, MA 02115.Search for more papers by this author Markley H. Boyer M.D., M.P.H., Corresponding Author Markley H. Boyer M.D., M.P.H. From the Department of Tropical Public Health, Harvard School of Public Health, Boston, MassachusettsAddress for reprints: Markley H. Boyer, M.D., Department of Tropical Public Health, Harvard School of Public Health, 665 Huntington Avenue, Boston, MA 02115.Search for more papers by this author First published: April 1980 https://doi.org/10.1111/j.1365-4362.1980.tb00289.xCitations: 1AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat Citing Literature Volume19, Issue3April 1980Pages 168-170 RelatedInformation

Sugar-sweetened beverage and sugar consumption and colorectal cancer incidence and mortality according to anatomic subsite

Individuals with a family history of colorectal cancer may be more susceptible to adverse effects of alcohol consumption. We investigated whether the association between alcohol consumption and colon cancer risk differed by family history of colorectal cancer. We conducted prospective studies in women and men in the Nurses' Health Study and Health Professionals Follow-Up Study, respectively. Alcohol consumption was first assessed in 1980 in women and in 1986 in men. During a follow-up of 26 y among 87,861 women and 20 y among 47,290 men, we documented 1801 cases of colon cancer (1094 women and 707 men). Higher alcohol consumption was associated with an elevated risk of colon cancer, although the association was significant only for the highest intake category of ≥30 g/d, with no significant linear trend. The association between alcohol consumption and colon cancer risk differed by family history of colorectal cancer; in comparison with nondrinkers, the pooled multivariate RRs for alcohol consumption of ≥30 g/d were 1.23 (95% CI: 0.96, 1.57; NS) among those with no family history and 2.02 (95% CI: 1.30, 3.13) among those with a family history of colorectal cancer (P value test for difference = 0.05). In comparison with nondrinkers with no family history, the RR for colon cancer was 2.80 (95% CI: 2.00, 3.91) for individuals who consumed ≥30 g/d and who had a family history of colorectal cancer. Reducing alcohol consumption may decrease the incidence of colon cancer, especially among those with a family history of colorectal cancer.

&lt;p&gt;Supplementary Figure S4: Antibiotics use in relation to survival outcomes in stage I-III colorectal cancer (crude and completecase multivariable analyses). (A) Antibiotics use in relation to overall survival. (B) Antibiotics use in relation to cancer-specific survival. Prediagnostic antibiotics use was categorized as no use, any use, low use (1-10 days), moderate use (11-60 days), high use (61-180 days) and very high use (&gt;180 days), based on defined daily doses. Antibiotics use during one year before colorectal cancer diagnosis was excluded to account for potential use due to undiagnosed but clinically manifest colorectal cancer. CI = confidence interval; HR = Hazard Ratio. Model 0 is crude or univariable Cox analysis. Model 1 is a Cox proportional hazard model including main demographic and socioeconomic factors (age and calendar year of diagnosis and prediagnostic Charlson comorbidity index as continuous variables, and sex, place of birth, county of residence, marital status, level of education, income status and family history of colorectal cancer as categorical variables). Model 2 includes tumour sites and tumour stage in addition to the covariates in model 1. Model 3 includes therapy-related variables such as operation type, preoperative chemotherapy (yes/no) and preoperative radiotherapy (yes/no) in addition to covariates in model 2. Variable definitions and categorization for the covariates in models 1-3 are as presented in Table 1. For each multivariable model, variables violating the proportional hazard assumption were controlled for by stratification in the respective models. They were age at diagnosis (&lt;/≥ 50 years), sex (men/women), prediagnostic Charlson comorbidity index (CCI) (no/any comorbidity), income status (quartile categories) and family history of colorectal cancer (0/1/≥2 first degree relatives) for model 1; age at diagnosis, prediagnostic CCI, family history of colorectal cancer, tumour sites (proximal colon, distal colon, rectum, unspecified) and tumour stage (stage I-III) for model 2, age at diagnosis, prediagnostic CCI, type of surgery 2 (elective/emergency), tumour sites and tumour stage for model 3. For age at diagnosis and prediagnostic CCI (continuous variables), binary variable types (age at diagnosis: &lt;/≥ 50 years, prediagnostic CCI: no/any CCI) were used and continuous variable types were also adjusted to account for residual confounding in each stratum.&lt;/p&gt;&lt;/p&gt;

&lt;p&gt;Supplementary Figure S4: Antibiotics use in relation to survival outcomes in stage I-III colorectal cancer (crude and completecase multivariable analyses). (A) Antibiotics use in relation to overall survival. (B) Antibiotics use in relation to cancer-specific survival. Prediagnostic antibiotics use was categorized as no use, any use, low use (1-10 days), moderate use (11-60 days), high use (61-180 days) and very high use (&gt;180 days), based on defined daily doses. Antibiotics use during one year before colorectal cancer diagnosis was excluded to account for potential use due to undiagnosed but clinically manifest colorectal cancer. CI = confidence interval; HR = Hazard Ratio. Model 0 is crude or univariable Cox analysis. Model 1 is a Cox proportional hazard model including main demographic and socioeconomic factors (age and calendar year of diagnosis and prediagnostic Charlson comorbidity index as continuous variables, and sex, place of birth, county of residence, marital status, level of education, income status and family history of colorectal cancer as categorical variables). Model 2 includes tumour sites and tumour stage in addition to the covariates in model 1. Model 3 includes therapy-related variables such as operation type, preoperative chemotherapy (yes/no) and preoperative radiotherapy (yes/no) in addition to covariates in model 2. Variable definitions and categorization for the covariates in models 1-3 are as presented in Table 1. For each multivariable model, variables violating the proportional hazard assumption were controlled for by stratification in the respective models. They were age at diagnosis (&lt;/≥ 50 years), sex (men/women), prediagnostic Charlson comorbidity index (CCI) (no/any comorbidity), income status (quartile categories) and family history of colorectal cancer (0/1/≥2 first degree relatives) for model 1; age at diagnosis, prediagnostic CCI, family history of colorectal cancer, tumour sites (proximal colon, distal colon, rectum, unspecified) and tumour stage (stage I-III) for model 2, age at diagnosis, prediagnostic CCI, type of surgery 2 (elective/emergency), tumour sites and tumour stage for model 3. For age at diagnosis and prediagnostic CCI (continuous variables), binary variable types (age at diagnosis: &lt;/≥ 50 years, prediagnostic CCI: no/any CCI) were used and continuous variable types were also adjusted to account for residual confounding in each stratum.&lt;/p&gt;&lt;/p&gt;

&lt;p&gt;Supplementary Figure S4: Antibiotics use in relation to survival outcomes in stage I-III colorectal cancer (crude and completecasemultivariable analyses).(A) Antibiotics use in relation to overall survival. (B) Antibiotics use in relation to cancer-specific survival.Prediagnostic antibiotics use was categorized as no use, any use, low use (1-10 days), moderate use (11-60days), high use (61-180 days) and very high use (&gt;180 days), based on defined daily doses. Antibiotics useduring one year before colorectal cancer diagnosis was excluded to account for potential use due toundiagnosed but clinically manifest colorectal cancer. CI = confidence interval; HR = Hazard Ratio. Model 0 iscrude or univariable Cox analysis. Model 1 is a Cox proportional hazard model including main demographic andsocioeconomic factors (age and calendar year of diagnosis and prediagnostic Charlson comorbidity index ascontinuous variables, and sex, place of birth, county of residence, marital status, level of education, incomestatus and family history of colorectal cancer as categorical variables). Model 2 includes tumour sites andtumour stage in addition to the covariates in model 1. Model 3 includes therapy-related variables such asoperation type, preoperative chemotherapy (yes/no) and preoperative radiotherapy (yes/no) in addition tocovariates in model 2. Variable definitions and categorization for the covariates in models 1-3 are as presentedin Table 1. For each multivariable model, variables violating the proportional hazard assumption werecontrolled for by stratification in the respective models. They were age at diagnosis (&lt;/≥ 50 years), sex(men/women), prediagnostic Charlson comorbidity index (CCI) (no/any comorbidity), income status (quartilecategories) and family history of colorectal cancer (0/1/≥2 first degree relatives) for model 1; age at diagnosis,prediagnostic CCI, family history of colorectal cancer, tumour sites (proximal colon, distal colon, rectum,unspecified) and tumour stage (stage I-III) for model 2, age at diagnosis, prediagnostic CCI, type of surgery2(elective/emergency), tumour sites and tumour stage for model 3. For age at diagnosis and prediagnostic CCI (continuous variables), binary variable types (age at diagnosis: &lt;/≥ 50 years, prediagnostic CCI: no/any CCI) were used and continuous variable types were also adjusted to account for residual confounding in each stratum.&lt;/p&gt;&lt;/p&gt;

Challenges With Colorectal Cancer Family History Assessment—Motivation to Translate Polygenic Risk Scores Into Practice