Western blot analysis of B-lymphoma moloney murine insertion region (BMI-1) and vascular endothelial growth factor (VEGF) when utilizing imiquimod and/ or bevacizumab treatment on DMBA induced hamster buccal pouch carcinoma

Purpose of this research was to study how immunotherapy and bevacizumabaffected cancer stem cell(s) (CSC(s)) in induced hamsters buccal pouch (HBP) carcinoma.Material and methods: 50 hamsters were split into 5 groups. Animals in GI were left untreatedfor 19 weeks (ws), the right pouches of those belongs to (GII- GV) were painted with 7,12-dimethylbenz (a) anthracene (DMBA), 3times a week for 14 ws, then, the following was done: GIIwas left with no additional treatment for other 5 ws, whereas GIII was painted with imiquimodonce daily for other 4 ws, Those in GIV were injected intraperitoneally (IP) with bevacizumab(10mg/kg / once daily for a week), and those in GV were painted with imiquimod similar to GIIIin addition to IP injection with bevacizumab similar to GIV. Gross observations and tumor volumewere recorded for each group. After slaughtering the animals, all right pouches were divided intotwo pieces, one of which was prepared for hematoxylin and eosin (H&E) stain. The other piecewas used for western blot analysis for identification of CSCs using BMI-1stem cell marker andVEGF) antibody. Results: Western blot examination of BMI-1 and VEGF antibodies indicated asignificantly significant (p-value < 0.001) discrepancy between GV and the subsequent; GIII andGIV. In comparison, BMI-1 showed a non-significant variation (p-value < 0.125) between GIIIand GIV, but VEGF showed a very substantial difference (p-value < 0.001). Conclusion:Combination of imiquimod-bevacizumab has an inhibitory effect on carcinoma cell and CSCs inHBP SCC