Peer-reviewed veterinary case report
Masitinib and imatinib reduce growth of dog mouth fibrosarcoma cells
By Milovancev, Milan et al.·Published in BMC veterinary research·2016·Department of Clinical Sciences, United States·View original on PubMed →
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Original publication title: Antiproliferative effects of masitinib and imatinib against canine oral fibrosarcoma in vitro.
- Species:
- dog
Plain-English summary
A study looked at two medications, masitinib and imatinib, to see if they could help treat oral fibrosarcoma, a common type of mouth tumor in dogs. The researchers found that both drugs were effective at reducing the growth of cancer cells in the lab, especially when combined with another chemotherapy drug called doxorubicin. They discovered that the cancer cells had specific targets that these medications could act on, which suggests that they might be useful in treating this type of tumor in dogs. Further research is needed, but these findings are promising for improving treatment options for dogs with oral fibrosarcoma.
People also search for: dog oral tumor treatment · masitinib for canine cancer · imatinib effectiveness in dogs
Abstract
BACKGROUND: Canine oral fibrosarcoma (COF) is one of the most common oral tumors in dogs and carries a guarded prognosis due to a lack of effective systemic therapeutic options. Mastinib and imatinib are two commonly used tyrosine kinase inhibitors (TKIs) in veterinary oncology but their potential efficacy against COF is uncharacterized. To begin investigating the rationale for use of these TKIs against COF, the present study tested for the presence TKI targets PDGFR-α, PDGFR-β, Kit, and VEGFR-2 and examined the in vitro effects on cell viability after TKI treatment alone or with doxorubicin. Immunohistochemistry for PDGFR-α, PDGFR-β, Kit, and VEGFR-2 was performed in 6 COF tumor biopsies. Presence of these same receptors within 2 COF cell lines was probed by reverse transcription-polymerase chain reaction and, for those with mRNA detected, confirmed via western blot. Effects on cell viability were assessed using an MTS assay after masitinib or imatinib treatment alone (0-100 μM), or in combination with doxorubicin (0-3000 nM doxorubicin). Anti-PDGFRB siRNA knockdown was performed and the effect on cell viability quantified. RESULTS: Expression of the TKI targets evaluated was similar between the 2 COF cell lines and the 6 COF tumor biopsies: PDGFR-α and PDGFR-β were detected in neoplastic cells from most COF tumor biopsies (5/6 and 6/6, respectively) and were present in both COF cell lines; KIT and KDR were not detected in any sample. Masitinib and imatinib IC50 values ranged from 7.9-33.4 μM, depending on the specific TKI and cell line tested. The addition of doxorubicin resulted in synergistic cytotoxicity with both TKIs. Anti-PDGFRB siRNA transfection reduced PDGFR-β protein expression by 77% and 67% and reduced cell viability by 24% (p < 0.0001) and 28% (0 = 0.0003) in the two cell lines, respectively. CONCLUSIONS: These results provide rationale for further investigation into the use of TKIs, possibly in combination with doxorubicin, as treatment options for COF.
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Search related cases →Original publication on PubMed: https://pubmed.ncbi.nlm.nih.gov/27259510/