Pancreatic carcinogenesis - enhancement by cholecystokinin in the hamster-nitrosamine model
1985

Cholecystokinin and Pancreatic Cancer in Hamsters

Sample size: 100 publication Evidence: moderate

Author Information

Author(s): A.G. Howatson, D.C. Carter

Primary Institution: University Department of Surgery, Royal Infirmary, Glasgow, Scotland, UK

Hypothesis

Does cholecystokinin enhance pancreatic carcinogenesis in the hamster-nitrosamine model?

Conclusion

Cholecystokinin acts as a co-carcinogen, reducing the latency period and increasing the induction rate of pancreatic tumors.

Supporting Evidence

  • Exogenous cholecystokinin increased pancreatic wet weight significantly.
  • CCK treatment resulted in earlier and more frequent ductal lesions in hamsters.
  • Histological assessments showed a significant increase in duct carcinoma-in-situ in CCK treated groups.

Takeaway

This study found that a hormone called cholecystokinin can make hamsters more likely to get pancreatic cancer when they are exposed to certain chemicals.

Methodology

The study involved administering cholecystokinin and a carcinogen to groups of hamsters and assessing pancreatic changes over time.

Limitations

Some animals died from unrelated infections, which may have affected the results.

Participant Demographics

10-week-old male Syrian hamsters

Statistical Information

P-Value

p<0.02

Statistical Significance

p<0.001

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