222 research outputs found
A Comparison of Different Approaches to Determine the Acceleration of Components due to Random Vibration Loads
No full textCohort profile: The Colon Cancer Family Registry Cohort (CCFRC)
No full textMark A Jenkins, Aung Ko Win, Allyson S Templeton, Maggie S Angelakos, Daniel D Buchanan, Michelle Cotterchio, Jane C Figueiredo, Stephen N Thibodeau, John A Baron, John D Potter, John L Hopper, Graham Casey, Steven Gallinger, Loic Le Marchand, Noralane M Lindor, Polly A Newcomb, and Robert W Haile, Colon Cancer Family Registry Cohort Investigators (Joanne Young
Alcohol consumption and pancreatic cancer: a pooled analysis in the International Pancreatic Cancer Case-Control Consortium (PanC4)
No full textBACKGROUND: Heavy alcohol drinking has been related to pancreatic cancer, but the issue is still unsolved. METHODS: To evaluate the role of alcohol consumption in relation to pancreatic cancer, we conducted a pooled analysis of 10 case-control studies (5585 cases and 11,827 controls) participating in the International Pancreatic Cancer Case-Control Consortium. We computed pooled odds ratios (ORs) by estimating study-specific ORs adjusted for selected covariates and pooling them using random effects models. RESULTS: Compared with abstainers and occasional drinkers (< 1 drink per day), we observed no association for light-to-moderate alcohol consumption (≤ 4 drinks per day) and pancreatic cancer risk; however, associations were above unity for higher consumption levels (OR = 1.6, 95% confidence interval 1.2-2.2 for subjects drinking ≥ 9 drinks per day). Results did not change substantially when we evaluated associations by tobacco smoking status, or when we excluded participants who reported a history of pancreatitis, or participants whose data were based upon proxy responses. Further, no notable differences in pooled risk estimates emerged across strata of sex, age, race, study type, and study area. CONCLUSION: This collaborative-pooled analysis provides additional evidence for a positive association between heavy alcohol consumption and the risk of pancreatic cancer.E. Lucenteforte, C. La Vecchia, D. Silverman, G. M. Petersen, P. M. Bracci, B. T. Ji, C. Bosetti, D. Li, S. Gallinger, A. B. Miller, H. B. Bueno-de-Mesquita, R. Talamini, J. Polesel, P. Ghadirian, P. A. Baghurst, W. Zatonski, E. Fontham, W. R. Bamlet, E. A. Holly, Y. T. Gao, E. Negri, M. Hassan, M. Cotterchio, J. Su, P. Maisonneuve, P. Boffetta, and E. J. Duel
Risk of colorectal cancer for people with a mutation in both a MUTYH and a DNA mismatch repair gene
No full textPublished online: 23 July 2015The base excision repair protein, MUTYH, functionally interacts with the DNA mismatch repair (MMR) system. As genetic testing moves from testing one gene at a time, to gene panel and whole exome next generation sequencing approaches, understandin g the risk associated with co-existence of germline mutations in these genes will be important for clinical interpretation and management. From the Colon Cancer Family Registry, we identified 10 carriers who had both a MUTYH mutation (6 with c.1187G>A p.(Gly396Asp), 3 with c.821G>A p.(Arg274Gln), and 1 with c.536A>G p.(Tyr179Cys)) and a MMR gene mutation (3 in MLH1, 6 in MSH2, and 1 in PMS2), 375 carriers of a single (monoallelic) MUTYH mutation alone, and 469 carriers of a MMR gene mutation alone. Of the 10 carriers of both gene mutations, 8 were diagnosed with colorectal cancer. Using a weighted cohort analysis, we estimated that risk of colorectal cancer for carriers of both a MUTYH and a MMR gene mutation was substantially higher than that for carriers of a MUTYH mutation alone [hazard ratio (HR) 21.5, 95% confidence interval (CI) 9.19-50.1; p < 0.001], but not different from that for carriers of a MMR gene mutation alone (HR 1.94, 95% CI 0.63-5.99; p = 0.25). Within the limited power of this study, there was no evidence that a monoallelic MUTYH gene mutation confers additional risk of colorectal cancer for carriers of a MMR gene mutation alone. Our finding suggests MUTYH mutation testing in MMR gene mutation carriers is not clinically informative.Aung Ko Win, Jeanette C. Reece, Daniel D. Buchanan, Mark Clendenning, Joanne P. Young, Sean P. Cleary, Hyeja Kim, Michelle Cotterchio, James G. Dowty, Robert J. MacInnis, Katherine M. Tucker, Ingrid M. Winship, Finlay A. Macrae, Terrilea Burnett, Loı, c Le Marchand, Graham Casey, Robert W. Haile, Polly A. Newcomb, Stephen N. Thibodeau, Noralane M. Lindor, John L. Hopper, Steven Gallinger, Mark A. Jenkin
Public Health Rep
No full textTo evaluate the effectiveness of a food manager training and certification program in increasing compliance with restaurant sanitary codes.|Using routine sanitary inspection records, the authors compared pre- and post-training inspection scores for 94 restaurants falling into three groups: a "mandatory" group (managers' attendance was mandated for these restaurants); a "voluntary" group (managers attended the training voluntarily); and a control group (no staff attended the training program).|Restaurants for which managers were mandated to attend a training and certification program demonstrated a significant improvement in inspection scores, an improvement that was sustained over a two-year follow-up period. The mean inspection scores for a control group did not change significantly over time. However, improvements were not noted in all areas of food safety.|Food manager training and certification programs may be an effective way to improve the sanitary conditions of restaurants and reduce the spread of foodborne illnesses.9672577PMCnul
Risk of extracolonic cancers for people with biallelic and monoallelic mutations in MUTYH
No full textGermline mutations in the DNA base excision repair gene MUTYH are known to increase a carrier's risk of colorectal cancer. However, the risks of other (extracolonic) cancers for MUTYH mutation carriers are not well defined. We identified 266 probands (91% Caucasians) with a MUTYH mutation (41 biallelic and 225 monoallelic) from the Colon Cancer Family Registry. Mutation status, sex, age and histories of cancer from their 1,903 first- and 3,255 second-degree relatives were analyzed using modified segregation analysis conditioned on the ascertainment criteria. Compared with incidences for the general population, hazard ratios (HRs) (95% confidence intervals [CIs]) for biallelic MUTYH mutation carriers were: urinary bladder cancer 19 (3.7-97) and ovarian cancer 17 (2.4-115). The HRs (95% CI) for monoallelic MUTYH mutation carriers were: gastric cancer 9.3 (6.7-13); hepatobiliary cancer 4.5 (2.7-7.5); endometrial cancer 2.1 (1.1-3.9) and breast cancer 1.4 (1.0-2.0). There was no evidence for an increased risk of cancers at the other sites examined (brain, pancreas, kidney or prostate). Based on the USA population incidences, the estimated cumulative risks (95% CI) to age 70 years for biallelic mutation carriers were: bladder cancer 25% (5-77%) for males and 8% (2-33%) for females and ovarian cancer 14% (2-65%). The cumulative risks (95% CI) for monoallelic mutation carriers were: gastric cancer 5% (4-7%) for males and 2.3% (1.7-3.3%) for females; hepatobiliary cancer 3% (2-5%) for males and 1.4% (0.8-2.3%) for females; endometrial cancer 3% (2%-6%) and breast cancer 11% (8-16%). These unbiased estimates of both relative and absolute risks of extracolonic cancers for people, mostly Caucasians, with MUTYH mutations will be important for their clinical management.Aung Ko Win, Jeanette C. Reece, James G. Dowty, Daniel D. Buchanan, Mark Clendenning, Christophe Rosty, Melissa C. Southey, Joanne P. Young, Sean P. Cleary, Hyeja Kim, Michelle Cotterchio, Finlay A. Macrae, Katherine M. Tucker, John A. Baron, Terrilea Burnett, Loïc Le Marchand, Graham Casey, Robert W. Haile, Polly A. Newcomb, Stephen N. Thibodeau, John L. Hopper, Steven Gallinger, Ingrid M. Winship, Noralane M. Lindor, and Mark A. Jenkin
Risk of colorectal cancer for carriers of mutations in MUTYH, with and without a family history of cancer
No full textWe studied 2332 individuals with monoallelic mutations in MUTYH among 9504 relatives of 264 colorectal cancer (CRC) cases with a MUTYH mutation. We estimated CRC risks through 70 years of age of 7.2% for male carriers of monoallelic mutations (95% confidence interval [CI], 4.6%-11.3%) and 5.6% for female carriers of monoallelic mutations (95% CI, 3.6%-8.8%), irrespective of family history. For monoallelic MUTYH mutation carriers with a first-degree relative with CRC diagnosed by 50 years of age who does not have the MUTYH mutation, risks of CRC were 12.5% for men (95% CI, 8.6%-17.7%) and 10% for women (95% CI, 6.7%-14.4%). Risks of CRC for carriers of monoallelic mutations in MUTYH with a first-degree relative with CRC are sufficiently high to warrant more intensive screening than for the general population.Aung Ko Win, James G. Dowty, Sean P. Cleary, Hyeja Kim, Daniel D. Buchanan, Joanne P. Young, Mark Clendenning, Christophe Rosty, Robert J. MacInnis, Graham G. Giles, Alex Boussioutas, Finlay A. Macrae, Susan Parry, Jack Goldblatt, John A. Baron, Terrilea Burnett, Loïc Le Marchand, Polly A. Newcomb, Robert W. Haile, John L. Hopper, Michelle Cotterchio, Steven Gallinger, Noralane M. Lindor, Katherine M. Tucker, Ingrid M. Winship, Mark A. Jenkin
Cigar and pipe smoking, smokeless tobacco use and pancreatic cancer: An analysis from the International Pancreatic Cancer Case-Control Consortium (PanC4)
No full textBackground: Cigarette smoking is the best-characterized risk factor for pancreatic cancer. However, data are limited for other tobacco smoking products and smokeless tobacco. Materials and methods: We conducted a pooled analysis of cigar and pipe smoking and smokeless tobacco use and risk of pancreatic cancer using data from 11 case-control studies (6056 cases and 11 338 controls) within the International Pancreatic Cancer Case-Control Consortium (PanC4). Pooled odds ratios (OR) and the corresponding 95% confidence intervals (CI) were estimated by unconditional multiple logistic regression models adjusted for study center and selected covariates. Results: Compared with never tobacco users, the OR for cigar-only smokers was 1.6 (95% CI: 1.2-2.3), i.e. comparable to that of cigarette-only smokers (OR 1.5; 95% CI 1.4-1.6). The OR was 1.1 (95% CI 0.69-1.6) for pipeonly smokers. There was some evidence of increasing risk with increasing amount of cigar smoked per day (OR 1.82 for ≥ 10 grams of tobacco), although not with duration. The OR for ever smokeless tobacco users as compared with never tobacco users was 0.98 (95% CI 0.75-1.3). Conclusion: This collaborative analysis provides evidence that cigar smoking is associated with an excess risk of pancreatic cancer, while no significant association emerged for pipe smoking and smokeless tobacco use. © The Author 2011. Published by Oxford University Press on behalf of the European Society for Medical Oncology. All rights reserved
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