Advances in Prevention and Diagnosis of Pancreatic Cancer

Advances in Prevention and Diagnosis of Pancreatic Cancer

European Gastroenterology Review 2007 - December 2007
Published: October 2008
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Pancreatic cancer is the fifth leading cause of cancer deaths in the Western world. Ninety-five per cent of all pancreatic malignancies are ductal adenocarcinomas. Pancreatic cancer is one of the most lethal cancers, as indicated by a mortality incidence ratio of 98%. Five-year survival rates are less than 2% in all patients, 10–15% in ‘curatively’ operated patients and 20–25% after resection and adjuvant chemotherapy.1,2 Since only a small minority of patients present with potentially resectable tumours at the time of diagnosis, prevention and early detection are the most promising options to improve on the poor outcome of the disease.

Prevention
In prospective studies, a carcinogenetic role has been confirmed for only a minority of environmental factors despite previous evidence from retrospective epidemiological studies. The strongest association with pancreatic cancer was found for smoking. Since the first description of an association between smoking and pancreatic cancer in 1977,3 many case control and cohort studies have confirmed a relative risk of more than two.4 According to a computer-based calculation, the incidence rate of pancreatic cancer in the EU could be reduced by 15% if all smokers would stop immediately. A reduced risk was described for people who quit smoking; however, this occured only after 10 years.5 Among putative nutritional risk factors, alcohol and coffee are the most frequently studied nutrients. Studies investigating alcohol intake and the risk of pancreatic cancer yielded conflicting results. Most studies did not detect an increased risk for alcohol drinkers. If any, the excess risk for pancreatic cancer among alcohol drinkers is small and is possibly confounded by smoking.6 Plenty of epidemiological studies exist investigating a potential role of coffee. The scientific community, as an intense coffee consumer, was obviously alarmed by a study reporting an increased risk among coffee drinkers.7 The majority of subsequent cohort studies reassured them that there is little evidence for a positive association between coffee intake and pancreatic cancer.4

A high consumption of fruit and vegetables may reduce the risk.8 However, data from case-control studies on pancreatic cancer are difficult to interpret because of methodological flaws. Thus, definite statements regarding the risk or benefit of a specific diet are not possible.9 Similarly, there is no convincing evidence to support an aetiological role of occupational agents in pancreatic cancer. In recent years, various cohort studies have demonstrated an elevated risk among overweight and obese subjects. A meta-analysis of 14 case-control and cohort studies on obesity and pancreatic cancer yielded an odds ratio of 1.19 (95% confidence interval [CI] 1.10–1.29) for a body mass index (BMI) of 30 versus 22kg/m2.10 Weight loss in women and moderate to strenuous physical activity in men may reduce the risk. Insulin resistance has been suggested to be the link between obesity, physical activity and the risk of pancreatic cancer. Support for this hypothesis comes from studies showing an association between type II diabetes and increased pancreatic cancer risk. As pancreatic tumours may also lead to diabetes, there was doubt about the causal nature of this relationship. In a metaanalysis of 20 studies with data on the duration of diabetes prior to the diagnosis of pancreatic cancer, subjects who had diabetes for five or more years had a two-fold increased risk of pancreatic cancer compared with individuals without diabetes, or those with diabetes for fewer than five years.11 It has been concluded that diabetes that develops 10 or more years prior to cancer diagnosis is causally related to pancreatic cancer.

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