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The effect of sulindac on colonic tumour formation in dimethylhydrazine-treated mice
M Moorghen1, P Ince, K J Finney
1Department of Pathology, University of Newcastle upon Tyne, Royal Victoria Infirmary, Newcastle upon Tyne, England.
Abstract:
Dimethylhydrazine has been used to produce colonic tumours in mice. If sulindac, a non-steroidal anti-inflammatory drug, is administered simultaneously fewer microadenomata and fewer macroscopic tumours are produced. Those which do appear are comparable in size to the ones in the mice which do not receive sulindac. Sulindac therefore appears to exert an anti-tumour influence at the stage between dysplasia and the formation of microadenomata.
Insights
Sulindac, a non-steroidal anti-inflammatory drug, reduces the formation of colon tumors and microadenomas in mice treated with dimethylhydrazine. This suggests sulindac has an anti-tumor effect during early stages of tumor development.
Area of Science:
- Oncology
- Pharmacology
Background:
- Dimethylhydrazine is a known carcinogen used to induce colonic tumors in research models.
- Non-steroidal anti-inflammatory drugs (NSAIDs) are being investigated for their potential chemopreventive properties.
Purpose of the Study:
- To investigate the effect of sulindac on dimethylhydrazine-induced colonic tumor formation in mice.
- To determine the stage at which sulindac exerts its anti-tumor influence.
Main Methods:
- Mice were administered dimethylhydrazine to induce colonic tumors.
- Simultaneously, some mice received sulindac treatment.
- Tumor incidence, number, and size were analyzed.
Main Results:
- Sulindac administration significantly reduced the number of microadenomas and macroscopic tumors.
- The size of the tumors that did develop was not significantly affected by sulindac.
- The drug appears to inhibit tumor development at a pre-adenoma stage.
Conclusions:
- Sulindac demonstrates a chemopreventive effect against dimethylhydrazine-induced colon carcinogenesis in mice.
- The anti-tumor activity of sulindac occurs between the stages of dysplasia and microadenoma formation.