Intestine Cancer

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Erich V. Kliewer - One of the best experts on this subject based on the ideXlab platform.

  • Associations between small Intestine Cancer and other primary Cancers: an international population-based study.
    International journal of cancer, 2006
    Co-Authors: Ghislaine Scelo, Paolo Boffetta, Kari Hemminki, Eero Pukkala, Jørgen H. Olsen, Aage Andersen, Elizabeth Tracey, David H. Brewster, Mary L. Mcbride, Erich V. Kliewer
    Abstract:

    Cancer of the small Intestine is a rare neoplasm, and its etiology remains poorly understood. Analysis of other primary Cancers in individuals with small Intestine Cancer may help elucidate the causes of this neoplasm and the underlying mechanisms. We included 10,946 cases of first primary small Intestine Cancer from 13 Cancer registries in a pooled analysis. The observed numbers of 44 types of second primary Cancer were compared to the expected numbers derived from the age-, gender- and calendar period-specific Cancer incidence rates in each registry. We also calculated the standardized incidence ratios (SIR) for small Intestine Cancer as a second primary after other Cancers. There was a 68% overall increase in the risk of a new primary Cancer after small Intestine carcinoma (SIR = 1.68, 95% confidence interval [CI] = 1.47-1.71), that remained constant over time. The overall SIR was 1.18 (95% CI = 1.05-1.32) after carcinoid, 1.29 (1.01-1.63) after sarcoma, and 1.27 (0.78-1.94) after lymphoma. Significant (p < 0.05) increases were observed for Cancers of the oropharynx, colon, rectum, ampulla of Vater, pancreas, corpus uteri, ovary, prostate, kidney, thyroid gland, skin and soft tissue sarcomas. Small Intestine Cancer as a second primary was increased significantly after all these Cancers, except after oropharyngeal and kidney Cancers. Although some of the excess may be attributable to overdiagnosis, it is plausible that most additional cases of second primary Cancers were clinically relevant and were due to common genetic (e.g., defects in mismatch or other DNA repair pathways) and environmental (e.g., dietary) factors.

Paolo Boffetta - One of the best experts on this subject based on the ideXlab platform.

  • body mass tobacco smoking alcohol drinking and risk of Cancer of the small Intestine a pooled analysis of over 500 000 subjects in the asia cohort consortium
    Annals of Oncology, 2012
    Co-Authors: Paolo Boffetta, W D Hazelton, Yu Chen, Rashmi Sinha, Manami Inoue, Yu Tang Gao, Woonpuay Koh, Xiaoou Shu, Eric J Grant, Ichiro Tsuji
    Abstract:

    ABSTRACT Background The evidence for a role of tobacco smoking, alcohol drinking, and body mass index (BMI) in the etiology of small Intestine Cancer is based mainly on case–control studies from Europe and United States. Subjects and methods We harmonized the data across 12 cohort studies from mainland China, Japan, Korea, Singapore, and Taiwan, comprising over 500 000 subjects followed for an average of 10.6 years. We calculated hazard ratios (HRs) for BMI and (only among men) tobacco smoking and alcohol drinking. Results A total of 134 incident cases were observed (49 adenocarcinoma, 11 carcinoid, 46 other histologic types, and 28 of unknown histology). There was a statistically non-significant trend toward increased HR in subjects with high BMI [HR for BMI >27.5 kg/m2, compared with 22.6–25.0, 1.50; 95% confidence interval (CI) 0.76–2.96]. No association was suggested for tobacco smoking; men drinking >400 g of ethanol per week had an HR of 1.57 (95% CI 0.66–3.70), compared with abstainers. Conclusions Our study supports the hypothesis that elevated BMI may be a risk factor for small Intestine Cancer. An etiologic role of alcohol drinking was suggested. Our results reinforce the existing evidence that the epidemiology of small Intestine Cancer resembles that of colorectal Cancer.

  • Associations between small Intestine Cancer and other primary Cancers: an international population-based study.
    International journal of cancer, 2006
    Co-Authors: Ghislaine Scelo, Paolo Boffetta, Kari Hemminki, Eero Pukkala, Jørgen H. Olsen, Aage Andersen, Elizabeth Tracey, David H. Brewster, Mary L. Mcbride, Erich V. Kliewer
    Abstract:

    Cancer of the small Intestine is a rare neoplasm, and its etiology remains poorly understood. Analysis of other primary Cancers in individuals with small Intestine Cancer may help elucidate the causes of this neoplasm and the underlying mechanisms. We included 10,946 cases of first primary small Intestine Cancer from 13 Cancer registries in a pooled analysis. The observed numbers of 44 types of second primary Cancer were compared to the expected numbers derived from the age-, gender- and calendar period-specific Cancer incidence rates in each registry. We also calculated the standardized incidence ratios (SIR) for small Intestine Cancer as a second primary after other Cancers. There was a 68% overall increase in the risk of a new primary Cancer after small Intestine carcinoma (SIR = 1.68, 95% confidence interval [CI] = 1.47-1.71), that remained constant over time. The overall SIR was 1.18 (95% CI = 1.05-1.32) after carcinoid, 1.29 (1.01-1.63) after sarcoma, and 1.27 (0.78-1.94) after lymphoma. Significant (p < 0.05) increases were observed for Cancers of the oropharynx, colon, rectum, ampulla of Vater, pancreas, corpus uteri, ovary, prostate, kidney, thyroid gland, skin and soft tissue sarcomas. Small Intestine Cancer as a second primary was increased significantly after all these Cancers, except after oropharyngeal and kidney Cancers. Although some of the excess may be attributable to overdiagnosis, it is plausible that most additional cases of second primary Cancers were clinically relevant and were due to common genetic (e.g., defects in mismatch or other DNA repair pathways) and environmental (e.g., dietary) factors.

Stanley Teleka - One of the best experts on this subject based on the ideXlab platform.

Fung Chang Sung - One of the best experts on this subject based on the ideXlab platform.

  • increased incidence of gastrointestinal Cancers among patients with pyogenic liver abscess a population based cohort study
    Gastroenterology, 2014
    Co-Authors: Hsueh Chou Lai, Chechen Lin, Ken Sheng Cheng, Jung Ta Kao, Jen Wei Chou, Chengyuan Peng, Shihwei Lai, Peichun Chen, Fung Chang Sung
    Abstract:

    Background & Aims The relationship between pyogenic liver abscess (PLA) and gastrointestinal (GI) Cancer was first reported more than 20 years ago, yet little is known about this connection. We evaluated this association in a population-based, retrospective, cohort study. Methods Using Taiwan National Health Insurance claims data, we collected data on a cohort of 14,690 patients with PLA diagnosed from 2000 to 2007. A reference cohort of 58,760 persons without PLA (controls) was selected from the same database, frequency matched by age, sex, and index year. Both cohorts were followed up until the end of 2009, and incidences of GI Cancer were calculated. Results The incidence of GI Cancer was 4.30-fold higher among patients with PLA compared with controls (10.8 vs 2.51/1000 person-years). Site-specific analysis showed that the highest incidence of colorectal Cancer was among patients with PLA and diabetes mellitus, followed by patients with PLA without diabetes and controls with diabetes (9.58, 5.76, and 1.49/10,000 person-years, respectively). The PLA cohort also had a high risk of small Intestine Cancer (adjusted hazard ratio [aHR], 12.7; 95% confidence interval [CI], 5.79–27.7) and biliary tract Cancer (aHR, 9.56; 95% CI, 6.68–13.7). Their risk of pancreatic Cancer (aHR, 2.51; 95% CI, 1.68–3.76) was also significant. However, patients with PLA did not have an increased risk of gastric Cancer compared with controls. Conclusions In a population-based study, we found that the incidence of GI Cancer is increased more than 4-fold among patients with PLA compared with controls. PLA might therefore be an indicator of GI Cancer. Patients with PLA had the highest incidence of colorectal Cancer, followed by Cancers of the biliary tract, pancreas, and small Intestine.

Meir J Stampfer - One of the best experts on this subject based on the ideXlab platform.

  • unrestrained eating behavior and risk of digestive system Cancers a prospective cohort study
    The American Journal of Clinical Nutrition, 2021
    Co-Authors: Yin Zhang, Mingyang Song, Andrew T Chan, Eva S Schernhammer, Brian M Wolpin, Meir J Stampfer
    Abstract:

    Background Unrestrained eating behavior, as a potential proxy for diet frequency, timing, and caloric intake, has been questioned as a plausible risk factor for digestive system Cancers, but epidemiological evidence remains sparse. Objectives We investigated prospectively the associations between unrestrained eating behavior and digestive system Cancer risk. Methods Participants in the Nurses' Health Study who were free of Cancer and reported dietary information in 1994 were followed for ≤18 y. Cox models were used to estimate HRs and 95% CIs for unrestrained eating (eating anything at any time, no concern with figure change, or both) and risk of digestive system Cancers. Results During follow-up, 2064 digestive system Cancer cases were documented among 70,450 eligible participants in analyses of eating anything at any time, In total, 2081 digestive system Cancer cases were documented among 72,468 eligible participants in analyses of no concern with figure change. In fully adjusted analyses, women with the behavior of eating anything at any time had a higher risk of overall digestive system Cancer (HR: 1.22; 95% CI: 1.10, 1.35), overall gastrointestinal tract Cancer ((HR: 1.33; 95% CI: 1.18, 1.50), buccal cavity and pharynx Cancer (HR: 1.50; 95% CI: 1.02, 2.21), esophageal Cancer (HR: 1.62; 95% CI: 1.01, 2.62), small Intestine Cancer (HR: 1.92; 95% CI: 1.02,3. 59), and colorectal Cancer (HR: 1.20; 95% CI: 1.04, 1.38), and a non-statistically significant increased risk of stomach Cancer (HR: 1.54; 95% CI: 0.96,2.48), compared with women without this behavior. No statistically significant association was observed for pancreatic Cancer and liver and gallbladder Cancer. The combined effect of eating anything at any time and having no concern with figure change was associated with a significantly increased risk of overall digestive system Cancer (HR: 1.27; 95% CI: 1.10, 1.46), overall gastrointestinal tract Cancer (HR: 1.45; 95% CI: 1.23, 1.71), and colorectal Cancer (HR: 1.34; 95% CI: 1.11, 1.63), compared with women exhibiting the opposite. Conclusions Unrestrained eating behavior was independently associated with increased risk of gastrointestinal tract Cancers. The potential importance of unrestrained eating behavior modification in preventing gastrointestinal tract Cancers should be noted.