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 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The only universally accepted risk factors for the development of pancreatic cancer are a positive family history or a history of smoking. Although the contribution of pancreatitis to pancreatic carcinogenesis has been debated for decades in the epidemiology literature, the actual mechanism is still unclear. With the rising epidemic of obesity, scientists have begun to focus on the contribution of chronic inflammatory state of morbidly obese patients in an effort to better understand the contribution of inflammation to the comorbidities of obesity. Notably, population studies are beginning to show that one of the most serious potential comorbidities of obesity is an increased lifetime risk of developing cancer. In this article, the current literature that exists supporting this Chronic Inflammatory Hypothesis as it pertains to obesity and pancreatic carcinogenesis is reviewed. To date, studies have focused on interleukin-6, a cytokine known to play a role in obesity, chronic pancreatitis and pancreatic cancer. The anti-inflammatory adipocytokine, adiponectin, has also shown promise as a key player in this mechanism and has recently been found to be more specific than standard tumor markers in differentiating pancreatic cancer from chronic pancreatitis. If the pathogenesis of pancreatic cancer is related to hormone levels associated with obesity, such as adipocytokines, and cytokines associated with chronic inflammation, this could potentially lead to the development of new pancreatic cancer tumor markers and ultimately new therapies and methods of prevention.
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PMID:Obesity, pancreatitis, and pancreatic cancer. 1856 97

A total of 138,503 women in the Women's Health Initiative in the United States were followed (for an average of 7.7 years) through 12 September 2005 to examine obesity, especially central obesity in relation to pancreatic cancer (n=251). Women in the highest quintile of waist-to-hip ratio had 70% (95% confidence interval 10-160%) excess risk of pancreatic cancer compared with women in the lowest quintile.
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PMID:Obesity and risk of pancreatic cancer among postmenopausal women: the Women's Health Initiative (United States). 1862 61

The prevalence of overweight (body mass index, BMI, between 25 and 30 kg/m2) and obesity (BMI of 30 kg/m2 or higher) is increasing rapidly worldwide, especially in developing countries and countries undergoing economic transition to a market economy. One consequence of obesity is an increased risk of developing type II diabetes. Overall, there is considerable evidence that overweight and obesity are associated with risk for some of the most common cancers. There is convincing evidence of a positive association between overweight/obesity and risk for adenocarcinoma of the oesophagus and the gastric cardia, colorectal cancer, postmenopausal breast cancer, endometrial cancer and kidney cancer (renal-cell). Premenopausal breast cancer seems to be inversely related to obesity. For all other cancer sites the evidence of an association between overweight/obesity and cancer is inadequate, although there are studies suggesting an increased risk of cancers of the liver, gallbladder, pancreas, thyroid gland and in lymphoid and haematopoietic tissue. Far less is known about the association between diabetes mellitus type I (also called insulin dependent diabetes mellitus or juvenile diabetes), type II diabetes (called non-insulin dependent diabetes mellitus or adult onset diabetes mellitus) and cancer risk. The most common type of diabetes mellitus, type II, seems to be associated with liver and pancreas cancer and probably with colorectal cancer. Some studies suggest an association with endometrial and postmenopausal breast cancer. Studies reporting on the association between type I diabetes mellitus, which is relatively rare in most populations and cancer risk are scanty, but suggest a possible association with endometrial cancer. Overweight and obesity, as well as type II diabetes mellitus are largely preventable through changes in lifestyle. The fundamental causes of the obesity epidemic-and consequently the diabetes type II epidemic-are societal, resulting from an environment that promotes sedentary lifestyles and over-consumption of energy. The health consequences and economic costs of the overweight, obesity and type II diabetes epidemics are enormous. Avoiding overweight and obesity, as well as preventing type II diabetes mellitus, is an important purpose to prevent cancer and other diseases. Prevention of obesity and type II diabetes should begin early in life and be based on the life-long health eating and physical activity patterns. Substantial public investments in preventing overweight, obesity and type II diabetes mellitus are both appropriate and necessary in order to have a major impact on their adverse health effects including cancer.
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PMID:Obesity and diabetes epidemics: cancer repercussions. 1863 86

Early diagnosis and curative resection are significant predictors of survival in patients with pancreatic cancer. We hypothesize that cholecystectomy within 12 months of pancreatic cancer affects 1-year survival. The Surveillance Epidemiology and End Result (SEER) database linked to Medicare data was used to identify patients diagnosed with pancreatic cancer who underwent cholecystectomy 1 to 12 months prior to cancer diagnosis. The SEER database identified 32,569 patients from 1995 to 2002; 415 (1.3%) underwent cholecystectomy prior to cancer diagnosis. Patients who underwent cholecystectomy had a higher proportion of diabetes (40.2% vs 20.5%; P < 0.01), obesity (8.9% vs 3.1%; P < 0.01), jaundice (17.3% vs 0.7%; P < 0.01), cholelithiasis (70.4% vs 4.2%; P < 0.01), choledocholithiasis (0.7% vs 0.0%; P < 0.01), weight loss (17.3% vs 4.7%; P < 0.01), abdominal pain (79.5% vs 22.5%), steatorrhea (0.7% vs 0.0%; P < 0.01), and cholecystitis (32.3% vs 1.7% ; P < 0.0001). After controlling for tumor stage, patient demographics, and symptoms, survival at 1 year was significantly lower in patients undergoing cholecystectomy (OR, 0.75; 95% CI, 0.58-0.97). Recent cholecystectomy is associated with decreased 1-year survival among patients with pancreatic cancer. For patients older than 65 years of age, further evaluation prior to cholecystectomy may be necessary to exclude pancreatic cancer, especially patients with jaundice, weight loss, and steatorrhea.
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PMID:Does cholecystectomy prior to the diagnosis of pancreatic cancer affect outcome? 1864 77

Obesity is associated with diverse health risks, but the role of body weight (BMI) as a risk factor for all and site-specific cancers remains controversial and risks for cancer associated with obesity have not been well-characterized in Asians. Body weight and risk for cancer were examined in a 14-year prospective cohort study of 1,213,829 Koreans aged 30-95 years insured by the National Health Insurance Corporation who had a biennial medical evaluation in 1992-1995. Incidence rates for all cancers and site-specific cancers were examined in relation to BMI. Age- and smoking-status adjusted hazard ratios (HR) with 95% confidence intervals (CI) were examined using the Cox proportional hazards model. For both sexes, the average baseline BMI was 23.2 kg/m(2), and the association of risk for all-cancers with BMI was positive. Obese men (BMI >or= 30 kg/m(2)) were at increased risk for developing the following cancers: stomach (1.31, 1.05-1.64), colon (1.42, 1.02-1.98), liver (1.63, 1.27-2.10) and gallbladder (1.65, 1.11-2.44). Obese women (BMI >or= 30 kg/m(2)) were at increased risk for developing liver cancer (1.39, 1.00-1.94), pancreatic cancer (1.80, 1.14-2.86) and breast cancer among women aged >or=50 years old (1.38, 1.00-1.90). The HRs were comparable in never and ever smokers for all cancers and all specific sites except for lung cancer. For all cancers common to both sexes, the association was significantly weaker (p < 0.01) in females. Our study provides further confirmation of the excess cancer risk associated with obesity. Rising obesity in Asian populations raises concern that increasing numbers of avoidable cancer cases will occur among Asians.
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PMID:Body mass index and cancer risk in Korean men and women. 1865 71

Morbid obesity is a recognized risk factor for gastrointestinal cancer. Little is known about pancreatic cancer developing after gastric bypass surgery or about surgery for this type of tumor following bariatric surgery. This report describes a case of pancreatic head cancer identified 3 months after laparoscopic sleeve gastrectomy for morbid obesity. During routine follow-up, mild abdominal pain and elevated pancreatic enzymes prompted computed tomography, which revealed mild edematous pancreatitis. Hyperbilirubinemia developed, and magnetic resonance imaging showed a pancreatic head tumor. CA19-9 was elevated. After a pylorus-preserving pancreatic head resection, the postoperative course was uneventful. The patient received adjuvant chemotherapy. Unfortunately, at the time of writing (9 months postoperatively), a local recurrence and hepatic metastases were diagnosed. Patients treated with bariatric surgery who develop new symptoms or report constant mild symptoms should be evaluated using endoscopy and radiomorphological imaging. Interdisciplinary obesity treatment can then offer significant benefits for the patient, particularly in the case of pancreatic cancer, which is still difficult to diagnose. In addition, there is a need for epidemiological studies of patients who undergo bariatric surgery and subsequently develop cancer.
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PMID:Morbid obesity and subsequent pancreatic cancer: pylorus-preserving pancreatoduodenectomy after laparoscopic sleeve gastrectomy. 1881 48

Obesity and insulin resistance have been implicated in the etiology of pancreatic cancer (PC). Whether adiponectin and/or leptin, two adipocyte-secreted hormones important in metabolic regulation, are associated with PC pathogenesis and whether adiponectin receptors are expressed in PC remains unknown. In a hospital-based case-control study, we studied 81 cases with incident, histologically confirmed PC and 81 controls matched on gender and age between 2000 and 2007 to investigate the role of adiponectin and leptin adjusting for risk factors linked to PC. In a separate study, we also studied for the first time whether adiponectin receptors 1 and 2 are expressed in PC by studying 16 PC tumor tissue samples which were analyzed using immunohistochemistry. When subjects were divided into control-defined quartiles of adiponectin and leptin, lower leptin but higher adiponectin levels were associated with PC (p = 0.001 and p = 0.05 respectively) before and after controlling for age, gender, BMI, smoking status, alcohol consumption, history of diabetes, and family history of pancreatic cancer. Of the PC tumor tissue samples analyzed, 87.5% had positive or strong positive expression of AdipoR1 and 93.7% had positive or strong positive expression of AdipoR2. Further prospective studies are needed to determine whether the elevated adiponectin and low leptin levels reported in this study reflect compensatory changes during PC progression and thus can be used as markers for PC or whether they are causally implicated in PC.
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PMID:Pancreatic cancer expresses adiponectin receptors and is associated with hypoleptinemia and hyperadiponectinemia: a case-control study. 1905 Oct 43

Obesity is associated with increased risk for developing pancreatic cancer, and it is suggested that insulin resistance provides the missing link. Here we demonstrate that under the context of genetic susceptibility, a high fat diet (HFD) predisposes mice with oncogenic K-ras activation to accelerated pancreatic intraepithelial neoplasm (PanIN) development. Tumor promotion is closely associated with increased inflammation and abrogation of TNFR1 signaling significantly blocks this process underlining a central role for TNFalpha in obesity-mediated enhancement of PanIN lesions. Interestingly, however, despite increased TNFalpha levels, mice remain insulin sensitive. We show that, while aggravating tumor promotion, a HFD exerts dramatic changes in energy metabolism through enhancement of pancreatic exocrine insufficiency, metabolic rates, and expression of genes involved in mitochondrial fatty acid (FA) beta-oxidation that collectively contribute to improved glucose tolerance in these mice. While on one hand these findings provide significant evidence that obesity is linked to tumor promotion in the pancreas, on the other it suggests alterations in inflammatory responses and bioenergetic pathways as the potential underlying cause.
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PMID:Inflammation and mitochondrial fatty acid beta-oxidation link obesity to early tumor promotion. 1920 10

The genes TSC1 and TSC2, encoding hamartin and tuberin, respectively, have been shown to be involved in the development of the autosomal dominantly inherited tumor syndrome tuberous sclerosis (TSC). However, inactivation of these genes has also been demonstrated to be associated with sporadic bladder cancer, ovarian and gall bladder carcinoma, non-small-cell carcinoma of the lung, breast cancer, pancreatic cancer, astrocytoma, xanthoastrocytoma, ependymomas, oral squamous cell carcinoma and endometrial cancer. The hamartin/tuberin protein complex plays a central role in the regulation of the mammalian target of rapamycin (mTOR) signalling network. A wide variety of components of the mTOR cascade have been demonstrated to be involved in many different human cancers. Mutations in several mTOR pathway component genes are known to cause specific monogenic human genetic diseases and this signalling cascade has been shown to be of relevance for Alzheimer's disease, type 2 diabetes, obesity and hypertrophy. Consequently, e.g. clinical trials for the treatment with rapamycin, a negative regulator of mTOR, of hamartomas in TSC have already been initiated. Now the first evidence is provided for an involvement of the TSC genes in acute leukemia.
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PMID:New insights into the role of the tuberous sclerosis genes in leukemia. 1925 Jun 71

Since the prognosis of pancreatic cancer is poor in spite of surgical and drug therapy, the focus should be on the prevention and early detection of the disease. In Europe, smoking accounts for up to 30% of pancreatic cancers, and heavy drinking increases the risk of chronic pancreatitis and pancreatic cancer. Diabetes can be a risk factor for pancreatic cancer and constitute its initial symptom. Obesity and low physical activity are linked to the risk of pancreatic cancer. An increased risk of pancreatic cancer is also associated with a hereditary inflammation, cystic fibrosis, and with part of cystic tumors of the pancreas.
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PMID:[Pancreatic cancer linked to life style and genome]. 1943 81


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