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Worldwide, over 200000 people die annually of pancreatic cancer. The highest incidence and mortality rates of pancreatic cancer are found in developed countries. In the United States, pancreatic cancer is the 4(th) leading cause of cancer death, and in Europe it is the 6th. Because of high fatality rates, pancreatic cancer incidence rates are almost equal to mortality rates. Pancreatic cancer is diagnosed late in the natural history of the disease, given the few early indicators of illness, and the lack of screening tests for this disease. Treatment has not improved substantially over the past few decades and has little effect on prolonging survival time. Therefore, prevention could play an important role in reducing pancreatic cancer mortality. International variations in rates and time trends suggest that environmental factors are likely to play a role in the etiology of pancreatic cancer. Variations in rates are substantial and occur even within industrialized nations. While rates have been stabilizing over the past 2 decades in many countries where they are already high, they continue to increase in countries where rates were relatively low 4 decades ago, such as Japan. In the US, the highest rates of pancreatic cancer incidence and mortality are observed among blacks, who have some of the highest rates in the world. A known cause of pancreatic cancer is tobacco smoking. This risk factor is likely to explain some of the international variations and gender differences. A number of studies observed a reduction in pancreatic cancer risk within a decade after smoking cessation, when compared to current smokers. With tobacco smoking as an exception, risk factors for pancreatic cancer are not well-established. Over the past 2 decades, epidemiological studies on pancreatic cancer have been plagued with methodological issues associated with studying a highly fatal disease, and inconsistent findings have hindered our understanding of the etiology of pancreatic cancer. Although familial pancreatic cancer is well-documented, the genes responsible for this condition have not been identified and are unlikely to explain more than 5-10% of all pancreatic cancer cases. Chronic pancreatitis and diabetes mellitus are medical conditions that have been consistently related to pancreatic cancer. Data from numerous studies suggest that these conditions are likely to be causally related to pancreatic cancer, rather than being consequences of the cancer. Recent cohort studies, which are less prone to biases than case-control studies, suggest that obesity increases the risk of pancreatic cancer. Other studies support the hypothesis that glucose intolerance and hyperinsulinemia are important in the development of pancreatic cancer. Other potential risk factors include physical inactivity, aspirin use, occupational exposure to certain pesticides, and dietary factors such as carbohydrate or sugar intake.
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PMID:Epidemiology of pancreatic cancer. 1523 85

Risk of development of some gastrointestinal tract cancers (colorectal cancer, pancreas cancer and liver cancer) is higher in type II diabetics. Another important risk factor is obesity (for gall bladder cancer in women and in men also for stomach and esophageal cancer). Pathogenetic factors have been explored especially in colorectal cancer (diet, hyperinsulinaemia, metabolic receptors activation, absence of physical activity). Our Czech study also proved up to 4 times increased risk of colorectal cancer in diabetics and, in accordance with literature, probable influence of persistent diabetes on tumour development. Type II diabetes mellitus should be considered as a risk factor especially for colorectal cancer, liver cancer, and pancreas cancer. In type I diabetics no risk of gastrointestinal tract cancers was proved.
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PMID:[Gastrointestinal tract cancer and diabetes mellitus]. 1530 38

The objective of this study was to determine the site-specific cancer incidence of hypertensive patients and examine the effect of blood pressure-related variables on the risk of cancers with elevated incidence among the hypertensive patients. A record linkage study of Hypertension Register of the North Karelia Project and the Finnish Cancer Registry was conducted. The mean follow-up time was 16 years. A total of 20 529 hypertensive patients were studied. Main outcome measures were standardised incidence ratios and hazard ratios. The overall cancer incidence was close to that of the general population for both men and women. The incidence rate for the kidney cancer was significantly increased in hypertensive patients (standardised incidence ratio 1.34, 95% confidence interval (CI) 1.11-1.60), as well as incidence rates for cancers of pancreas (1.26, 1.02-1.54), and endometrium (1.22, 1.01-1.44) in hypertensive women. The incidence of lung cancer was significantly decreased (0.86, 0.77-0.95). The incidence of liver cancer was elevated with borderline significance (1.36, 0.99-1.82). In Cox regression models, the use of antihypertensive drugs at baseline was a significant predictor of kidney (hazard ratio for use of antihypertensive drugs 1.89, 95% CI 0.96-3.75) and pancreatic cancer (1.78, 0.99-3.22) in women but not in men. The incidence of endometrial cancer or liver cancer was not related to blood pressure levels or the use of antihypertensive drugs. In women, obesity was a significant predictor of cancers of the endometrium, kidney and liver. In conclusion, increased occurrence of some cancer types among hypertensive patients seem to be partly explained by obesity and the use of antihypertensive drugs.
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PMID:Cancer pattern among hypertensive patients in North Karelia, Finland. 1570 72

In the United States, acute pancreatitis, chronic pancreatitis, and pancreatic cancer are the most common pancreatic disorders requiring diagnosis and treatment. Pancreatic cancer is responsible for nearly 30,000 annual deaths and is the second most common cause of death from any type of gastrointestinal disease. Gallstone disease, which is strongly associated with obesity, and excessive consumption of alcohol are the major risk factors for benign pancreatic disease, whereas smoking is the most important factor known to cause pancreatic cancer. Therefore, to reduce the overall burden of pancreatic disease, we should focus on the control of three lifestyle factors: smoking, drinking, and obesity.
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PMID:The epidemiology and impact of pancreatic diseases in the United States. 1580 95

The incidence of hepatocellular carcinoma is increasing, but the temporal changes of risk factors remain unclear. A significant proportion of hepatocellular carcinoma (7-30%) develops in cryptogenic cirrhosis, and may represent the most worrisome complication of non-alcoholic steatohepatitis. Non-alcoholic steatohepatitis is tightly related to insulin resistance and several features of the metabolic syndrome, i.e obesity, type 2 diabetes and dyslipidaemia. Nearly two-thirds of adults in the United States and an increasing percentage of the population worldwide are overweight or obese. Diabetes prevalence is increasing as well. The rising prevalence of risk factors associated with non-alcoholic steatohepatitis can partially account for the increasing incidence of cryptogenic cirrhosis and subsequent hepatocellular carcinoma. Moreover, recent evidence demonstrates that both obesity and diabetes are per se associated with an increased cancer risk. Large prospective studies show a significant association with obesity for several cancers, including cancers of the colon, female breast, endometrium, kidney, oesophagus and liver (hepatocellular carcinoma). Type 2 diabetes is also related with increased risks of colon, endometrial, kidney, pancreatic cancer and hepatocellular carcinoma. In western countries, the insulin resistance syndrome is emerging as a risk factor for a wide variety of cancers, including hepatocellular carcinoma.
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PMID:Review article: steatosis, the metabolic syndrome and cancer. 1622 71

We investigated the relation of overweight and obesity with cancer in a population-based cohort of more than 145 000 Austrian adults over an average of 9.9 years. Incident cancers (n=6241) were identified through the state cancer registry. Using Cox proportional-hazards models adjusted for smoking and occupation, increases in relative body weight in men were associated with colon cancer (hazard rate (HR) ratio 2.48; 95% confidence interval (CI): 1.15, 5.39 for body mass index (BMI) > or =35 kg m(-2)) and pancreatic cancer (HR 2.34, 95% CI: 1.17, 4.66 for BMI>30 kg m(-2)) compared to participants with normal weight (BMI 18.5-24.9 kg m(-2)). In women, there was a weak positive association between increasing BMI and all cancers combined, and strong associations with non-Hodgkin's lymphomas (HR 2.86, 95% CI: 1.49, 5.49 for BMI> or =30 kg m(-2)) and cancers of the uterine corpus (HR 3.93, 95% CI: 2.35, 6.56 for BMI> or =35 kg m(-2)). Incidence of breast cancer was positively associated with high BMI only after age 65 years. These findings provide further evidence that overweight is associated with the incidence of several types of cancer.
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PMID:Obesity and incidence of cancer: a large cohort study of over 145,000 adults in Austria. 1623 22

We examined the associations of body mass index (BMI), waist circumference, a history of diabetes, and cigarette smoking with risk of pancreatic cancer among 37,147 women and 45,906 men followed up during 560,666 person-years in the Swedish Mammography Cohort and the Cohort of Swedish Men; 136 incident cases of pancreatic cancer were diagnosed. The multivariate rate ratio (RR) of pancreatic cancer for obese women and men (BMI > or =30 kg/m(2)) was 1.81 (95% CI: 1.04-3.15) compared to those with a BMI of 20-25 kg/m(2). For a difference of 20 cm (about two standard deviations) in waist circumference, the multivariate RRs were 1.32 (95% CI: 0.73-2.37) among women and 1.74 (95% CI: 1.00-3.01) among men. Pancreatic cancer risk was associated with history of diabetes (multivariate RR: 1.88; 95% CI: 1.09-3.26) and cigarette smoking (multivariate RR for current compared with never smokers: 3.06; 95% CI: 1.99-4.72). Current smokers of > or =40 pack-years had a five-fold elevated risk compared with never smokers. Risk among past smokers approached the RR for never smokers within 5-10 years following smoking cessation. Findings from this prospective study support positive relationships of overall obesity, abdominal adiposity, diabetes and smoking with risk of pancreatic cancer.
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PMID:Overall obesity, abdominal adiposity, diabetes and cigarette smoking in relation to the risk of pancreatic cancer in two Swedish population-based cohorts. 1628

Although only 32,000 new cases of adenocarcinoma of the pancreas occur in the United States each year, it is the fourth leading cause of cancer deaths in this country. The overall five-year survival rate is 4 percent, and localized, resectable disease has only a 17 percent survival rate. Risk factors include smoking, certain familial cancer syndromes, and familial chronic pancreatitis. The link between risk of pancreatic cancer and other factors (e.g., diabetes, obesity) is less clear. Most patients present with obstructive jaundice caused by compression of the bile duct in the head of the pancreas. Epigastric or back pain, vague abdominal symptoms, and weight loss also are characteristic of pancreatic cancer. More than one half of cases have distant metastasis at diagnosis. Computed tomography is the most useful diagnostic and staging tool. Ultrasonography, magnetic resonance imaging, and endoscopic retrograde cholangiopancreatography may provide additional information. The majority of tumors are not surgically resectable because of metastasis and invasion of the major vessels posterior to the pancreas. Resectable tumors are treated with the Whipple procedure or the pylorus-preserving Whipple procedure. Adjuvant fluorouracil-based chemotherapy may prolong survival. For nonresectable tumors, chemotherapy with gemcitabine prolongs survival. Other agents are being studied. Radiation combined with chemotherapy has slowed progression in locally advanced cancers. Throughout the illness and during end-of-life care, patients need comprehensive symptom control.
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PMID:Pancreatic cancer: diagnosis and management. 1647 97

Adenocarcinoma of the exocrine pancreas is the fourth leading cause of cancer-related death in men and women in the U.S. Cytokines and other proinflammatory mediators have been implicated in inflammatory pancreatic diseases including pancreatitis and cancer. We analyzed cytokine gene polymorphisms as risk factors for pancreatic cancer using questionnaire data obtained by in-person interviews and germ line DNA collected in a population-based case-control study of pancreatic cancer (532 cases and 1,701 controls) conducted in the San Francisco Bay Area. We used mass spectrometry and gel-based methods to genotype 308 cases and 964 population-based controls. Odds ratios (OR) and 95% confidence intervals (CI) were estimated using logistic regression analysis and included adjustment for age, sex, and smoking. We assessed potential interactions between these polymorphisms, proinflammatory conditions (e.g., pancreatitis, ulcer, and obesity), and smoking as risk factors for pancreatic cancer. There was no overall association between pancreatic cancer risk and tumor necrosis factor-alpha (TNF-A -308G/A), regulated upon activation, normally T cell-expressed, and presumably secreted (RANTES -403G/A), and CC chemokine receptor 5 (CCR5-Delta32) polymorphisms. There was a nearly 7-fold increased relative risk estimate for pancreatic cancer in individuals with a history of pancreatitis (adjusted OR, 6.9; 95% CI, 3.4-14.1). Among patients with pancreatic cancer, pancreatitis was significantly associated with TNF-A -308 GA + AA (OR, 3.1; 95% CI, 1.3-7.4) and with RANTES -403 GA + AA (OR, 2.3; 95% CI, 1.0-5.4). There was evidence for a possible interaction between current active smoking and CCR5-32del. Our results lend support for the hypothesis that proinflammatory gene polymorphisms, in combination with proinflammatory conditions, may influence the development of pancreatic cancer.
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PMID:Inflammation, genetic polymorphisms in proinflammatory genes TNF-A, RANTES, and CCR5, and risk of pancreatic adenocarcinoma. 1661 15

Case of pancreatic cancer have increased in number, and the number of deaths from that disease has reached 20,000 in recent years in Japan. Only a few patients with pancreatic cancer can be cured. However, the prognosis in small pancreatic cancer such as TS1 less than 2 cm is relatively good if radical surgical resection is performed. Therefore early diagnosis of pancreatic cancer is important to improve the dismal prognosis. Although clinical symptoms are not reliable for the diagnosis of pancreatic cancer, 30% of TS1 patients have abdominal or back pain. Recent epidemiologic studies have shown that familial history of pancreatic cancer, chronic pancreatitis, diabetes, obesity, and smoking are possible high-risk factors for pancreatic cancer. Serum pancreatic enzyme and tumor markers in terms of CA19-9 and CEA are measured first. Ultrasonography (US) should be performed as soon as possible. Not only tumors but also slightly dilated main pancreatic ducts and/or small simple cysts that may represent indirect changes due to pancreatic cancer can be detected with US. Enhanced computed tomography, magnetic resonance cholangiopancreatography and endoscopic US are also useful. Endoscopic retrograde cholangiopancreatography yields more detailed images of branch ducts, and the cytology of pancreatic juice can be determined following examination. Unfortunately, position-emission tomography is not a reliable method for the diagnosis of small tumors in the pancreas. Finally, TNM staging of pancreatic cancer is performed based on the results of these imaging examinations.
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PMID:[Early diagnosis and staging of pancreatic cancer]. 1687 7


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