Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0699790 (colon cancer)
 28,837 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The etiology of pancreatic cancer is poorly understood, partly because of the inconsistency of findings among case-control studies of pancreatic cancer. Because of the unfavorable prognosis for pancreatic cancer, many case-control studies have been based largely on interviews with next of kin, who are known to report less reliable information on potential risk factors than original respondents. The purpose of this study was to estimate the effects of speculative risk factors such as dietary/nutritional factors and alcohol drinking, as well as those of established risk factors such as cigarette smoking, diabetes mellitus, and family history of pancreatic cancer, on pancreatic cancer risk based solely on direct interviews. This investigation was a population-based case-control study of pancreatic cancer diagnosed in Atlanta (GA), Detroit (MI), and ten New Jersey counties from August 1986 through April 1989. Direct interviews were conducted with 526 incident cases and 2,153 population controls. This study revealed a significant interaction between body mass index and caloric intake that was consistent by both race and gender. Subjects with elevated body mass index and caloric intake had increased risk, whereas those with elevated values for one of these factors but not the other experienced no increased risk. This finding suggests that energy balance may play a major role in pancreatic carcinogenesis. Diabetes mellitus was also a risk factor for pancreatic cancer, as well as a possible complication of the tumor. Our data are consistent with a key role for hyperinsulinemia in pancreatic carcinogenesis, particularly among non-diabetics with an elevated body mass index. A three-fold risk of pancreatic cancer among first-degree relatives of affected individuals was apparent. An increased risk also was associated with a family history of colon, endometrial, ovary, and breast cancer, suggesting a possible link to hereditary non-polyposis colon cancer. Our findings support a causal role for cigarette smoking in pancreatic carcinogenesis. Alcohol drinking at levels typically consumed by the general population of the United States did not appear to be a risk factor for pancreatic cancer, although heavy drinking may be related to risk, particularly in blacks.
 ...
PMID:Risk factors for pancreatic cancer: a case-control study based on direct interviews. 1113 18

Alcohol consumption is one of the top-10 risks for worldwide burden of disease. The International Agency for Research for Cancer affirmed that there was evidence for the carcinogenicity of ethanol in animals and classified alcohol consumption as carcinogenic for humans. Alcohol consumption causes cancers of the oral cavity, pharynx, larynx, oesophagus, colorectum, liver, pancreas and female breast. Most alcohol-induced diseases increases in a linear fashion as intake increases: oral, oesophagus and colon cancer fall into this pattern: very little is known about safe margins of alcohol consumption. Given the linear dose-response relation between alcohol intake and risk of cancer, control of heavy drinking remains the main target for cancer control. European Code Against Cancer recommends keeping daily consumption within two drinks (20 g [corrected] of alcohol/day) for man and one drink for women and US Department of Health and Human Services suggest as a low risk, a maximum of 10 g [corrected] of alcohol a day in man and half of this in women.
 ...
PMID:Human carcinogenesis and alcohol in hepato-gastroenterology. 2269 79

Many epidemiological studies have demonstrated a correlation between alcohol intake and the occurrence of cancer in humans. All types of alcoholic beverages are associated with an increased risk which suggests that ethanol itself is the crucial compound which causes that effect.The International Agency for Research for Cancer classified alcohol consumption and acetaldehyde associated with alcohol consumption as carcinogenic for humans (group 1): oral cavity, pharynx, larynx, esophagus, colorectal, liver and female breast.THE MECHANISMS BY WHICH ALCOHOL CONSUMPTION EXERTS ITS CARCINOGENIC EFFECT HAVE NOT BEEN DEFINED FULLY, ALTHOUGH PLAUSIBLE EVENTS INCLUDE: a genotoxic effect of acetaldehyde; increased estrogen concentration, which is important for breast carcinogenesis; a role as solvent of tobacco carcinogens; production of reactive oxygen species and nitrogen species; and change in folate metabolism.Most alcohol-induced diseases increases in a linear fashion as intake increases: oral, esophagus and colon cancer fall into this pattern: very little is known about safe margins of alcohol consumption. Given the linear dose-response relation between alcohol intake and risk of cancer, control of heavy drinking remains the main target for cancer control.In healthy subjects, European Code Against Cancer recommends keeping daily consumption within two drinks for man and one drink for women.In our opinion, there are not enough data to support the actually safe intake of alcohol. Any level of alcohol consumption increase the risk of developing an alcohol related cancer. The level of risk increases in line with the level consumption.
 ...
PMID:The burden of cancer attributable to alcohol consumption. 2287 47