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Query: UMLS:C0030305 (pancreatitis)
 16,014 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A highly specific pancreatitis primarily affecting the intralobular and intrainsular ductules has been demonstrated in Syrian golden hamsters bearing homologous, non-syngeneic, transplantable pancreatic adenocarcinomas induced by N-nitrosobis(2-oxopropyl)amine (BOP). The ductulitis provides further evidence that induced pancreatic neoplasms originate from ductules.
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PMID:Pancreatic ductulitis in Syrian golden hamsters bearing homologous transplantable pancreatic adenocarcinomas. 68 4

Changes of amylase activity and isozymic pattern in the serum, urine, ascites, pancreas and parotid gland of hamsters during pancreatic carcinogenesis induced by N-nitrosobis (2-oxopropyl) amine (BOP) were examined. During the early stage of pancreatic carcinogenesis, amylase activity in the urine was greatly increased and the pancreatic type of isozyme increased in the serum and urine, but in the terminal stage, the activity decreased and the isozymic pattern reverted to normal. These alterations of amylase could be due to focal pancreatitis around dysplastic ductules and small carcinoma lesions causing leakage of pancreatic juice. This phenomenon may be of value in diagnosis of the early stage of pancreatic cancer.
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PMID:Changes of amylase during experimental pancreatic carcinogenesis in hamsters. 617 74

The effect of acute and recurrent pancreatitis was investigated in pancreatic cancer induction by N-nitrosobis(2-oxopropyl)amine (BOP) in Syrian golden hamsters. For the correlation of the cellular alteration with carcinogenesis, BOP (20 mg/kg body wt) was injected once sc into hamsters at day 3 (group 2), week 1 (group 3), and week 8 (group 4), corresponding to cellular degeneration, regeneration, and healing, respectively. Additional groups received BOP 30 minutes before common duct ligation for 48 hours (group 1) or before repeated induction of pancreatitis at 4 weekly intervals for 4 weeks (group 5). Group 6 was a pancreatitis control. Two groups of hamsters received BOP only, at the age of 8 weeks (group 7, which served as a BOP control for groups 1-3 and 5) or at the age of 16 weeks (group 8, the control for group 4). Hamsters were killed 46 weeks after BOP injection (with the exception of group 1 animals, which were killed 52 wk after BOP) to guarantee the same postcarcinogen exposure time in each group. The results showed that BOP, when given during cellular degeneration (group 2) and healing (group 4), induced significantly fewer carcinomas than in the control groups, whereas the tumor pattern was not affected when BOP was given before pancreatitis induction (group 1) or at the time of cellular regeneration (group 3). Recurrent pancreatitis (group 5), however, resulted in carcinomas significantly larger in number and size than those in control group 8. A significantly higher incidence of carcinomas occurred in group 8 controls (treated with BOP at the age of 16 wk) compared to the incidence in group 7 controls (treated with BOP at the age of 8 wk).
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PMID:Modification of pancreatic carcinogenesis in the hamster model. IX. Effect of pancreatitis. 657 34

Chronic inflammation is known to be a risk for many cancers, including pancreatic cancer. Heavy alcohol drinking and cigarette smoking are major causes of pancreatitis, and epidemiological studies have shown that smoking and chronic pancreatitis are risk factors for pancreatic cancer. Meanwhile, inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) are elevated in pancreatitis and pancreatic cancer tissues in humans and in animal models. Selective inhibitors of iNOS and COX-2 suppress pancreatic cancer development in a chemical carcinogenesis model of hamsters treated with N-nitrosobis(2-oxopropyl)amine (BOP). In addition, hyperlipidemia, obesity, and type II diabetes are also suggested to be associated with chronic inflammation in the pancreas and involved in pancreatic cancer development. We have shown that a high-fat diet increased pancreatic cancer development in BOP-treated hamsters, along with aggravation of hyperlipidemia, severe fatty infiltration, and increased expression of adipokines and inflammatory factors in the pancreas. Of note, fatty pancreas has been observed in obese and/or diabetic cases in humans. Preventive effects of anti-hyperlipidemic/anti-diabetic agents on pancreatic cancer have also been shown in humans and animals. Taking this evidence into consideration, modulation of inflammatory factors by anti-inflammatory agents will provide useful data for prevention of pancreatic cancer.
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PMID:Involvement of inflammatory factors in pancreatic carcinogenesis and preventive effects of anti-inflammatory agents. 2295 27