Pancreatic Cancer: The Role of Cholecystokinin?

Axelson, Jan; Ihse, Ingemar; Håkanson, R.

doi:10.3109/00365529209028128

Cited by 16 publications

(8 citation statements)

References 80 publications

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“…Previous epidemiologic studies have suggested that pancreatic cancer risk may be elevated after cholecystectomy [8,58,59,60]. The presumed increased release of cholecystokinin, which has a trophic effect on pancreatic acinar cells [62,63], following cholecystectomy [61] may contribute to an increased risk of pancreatic cancer risk following gallbladder removal. Our findings do not support an important role for cholecystectomy in the carcinogenesis of pancreatic cancer, which is in line with the conclusions of most previous case-control studies on cholecystectomy.…”

Section: Discussionmentioning

confidence: 99%

Metabolic Syndrome Components and Risk Factors for Pancreatic Adenocarcinoma: A Case-Control Study in China

Chen

et al. 2012

Digestion

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Background: Metabolic syndrome is a complex collection of interrelated conditions. Recent data have shown that metabolic syndrome may play a role in several cancers. Pancreatic adenocarcinoma is the fourth most common cause of death from cancer in the United States and the fifth in Europe. Despite the increasing numbers of published studies, the etiology of pancreatic adenocarcinoma is incompletely defined. Therefore, this paper aims to evaluate the risk factors for pancreatic adenocarcinoma. Methods: This was a case-control study of pancreatic adenocarcinoma patients who were referred to the Peking Union Medical College Hospital. Controls were randomly selected from an existing database of healthy individuals at the Health Screening Center. Data on metabolic syndrome, pancreatic diseases, liver diseases, and a history of diabetes and history of hypertension were collected either by conducting a retrospective review of the patients’ records and health examination reports or by interview. Results: A history of smoking (OR = 2.981), diabetes (OR = 2.421), cholecystolithiasis (OR = 5.453), or chronic pancreatitis (OR = 28.264) as well as the levels of fasting blood glucose (OR = 4.241), total cholesterol (OR = 1.793), and apolipoprotein A (OR = 36.065) were significantly related to pancreatic adenocarcinoma. Conclusions: Cholelithiasis, chronic pancreatitis, and certain metabolic syndrome components are potential risk factors for the development of pancreatic adenocarcinoma.

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Section: Discussionmentioning

confidence: 99%

Metabolic Syndrome Components and Risk Factors for Pancreatic Adenocarcinoma: A Case-Control Study in China

Chen

et al. 2012

Digestion

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“…33 Cholecystokinin stimulates pancreatic growth and carcinogenesis, 15A2. 43 Elevation of plasma CCK directly by infusion or indirectly by treatment with protease inhibitors or by pancreaticobiliary diversion results in pancreatic hyperplasia and hypertrophy. These changes can be blocked by treatment with CCKA receptor-selective antagonists.…”

Section: Cholecystokinin: Structure and Functionmentioning

confidence: 99%

Brief Review Biology of Gut Cholecystokinin and Gastrin Receptors

Shulkes

Baldwin

1997

Clin Exp Pharma Physio

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1. The stomach hormone gastrin and the intestinal hormone cholecystokinin (CCK) share a common C-terminal pentapeptide sequence but have different biological roles. Gastrin is the major stimulant of gastric acid secretion and has a growth stimulatory effect on the secretory part of the stomach. The physiological roles of CCK are the stimulation of pancreatic secretion and the contraction of the gall-bladder. 2. Several classes of receptors have been defined for peptides of the gastrin/CCK family. The CCKA receptor on pancreatic acini has a greater affinity for sulfated CCK than for gastrin, while the gastrin/CCKB receptor in gastric mucosa and brain has similar affinities for both gastrin and CCK. Potent and selective antagonists have been developed for both receptor classes. 3. The structures of the CCKA and gastrin/CCKB receptors have been deduced from the nucleotide sequences of cloned cDNA. The receptors, which both belong to the family with seven transmembrane segments, control secretion via similar signalling mechanisms. Occupation of either receptor leads to activation of phospholipase C, with resultant increases in intracellular levels of inositol triphosphate and Ca2+. Mitogenic signalling pathways are also being defined. 4. Recent studies have questioned the previous assumption that gastrin precursors are inactive. Glycine-extended gastrin17 has been shown to stimulate mitogenesis in some cell lines and may also have an autocrine role in the growth of colonic cancers. The receptors involved, which are clearly distinct in binding properties from the CCKA and gastrin/CCKB receptors, have not yet been cloned. Specific antagonists for the novel receptors will be required to define their function in further detail.

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“…[10][11][12] Furthermore, elevated serum cholecystokinin is also thought to increase the risk of pancreatic and colon cancers. [13][14][15] A recent Norwegian study also revealed twofold increase in the overall cancer risk for patients with acute cholecystitis compared with patients with symptomatic gallstones. 16 This suggested that more pronounced inflammation is associated with a greater cancer risk.…”

mentioning

confidence: 93%

Risk of Cancer in Patients with Cholecystitis: A Nationwide Population-based Study

Lee

et al. 2015

The American Journal of Medicine

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Pancreatic Cancer: The Role of Cholecystokinin?

Cited by 16 publications

References 80 publications

Metabolic Syndrome Components and Risk Factors for Pancreatic Adenocarcinoma: A Case-Control Study in China

Metabolic Syndrome Components and Risk Factors for Pancreatic Adenocarcinoma: A Case-Control Study in China

Brief Review Biology of Gut Cholecystokinin and Gastrin Receptors

Risk of Cancer in Patients with Cholecystitis: A Nationwide Population-based Study

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