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Abstract
Canine acanthomatous ameloblastomas (CAA), analogs of human ameloblastoma, are oral tumors of odontogenic origin for which the genetic drivers have remained undefined. By whole-exome sequencing, we have now discovered recurrent HRAS and BRAF activating mutations, respectively, in 63% and 8% of CAA. Notably, cell lines derived from CAA with HRAS mutation exhibit marked sensitivity to MAP kinase (MAPK) pathway inhibitors, which constrain cell proliferation and drive ameloblast differentiation. Our findings newly identify a large-animal spontaneous cancer model to study the progression and treatment of RAS-driven cancer. More broadly, our study highlights the translational potential of canine cancer genome sequencing to benefit both humans and their companion animals.
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Details
1 Stanford University School of Medicine, Department of Pathology, Stanford, USA (GRID:grid.168010.e) (ISNI:0000000419368956)
2 UC Davis School of Veterinary Medicine, Department of Pathology, Microbiology & Immunology, Davis, USA (GRID:grid.27860.3b) (ISNI:0000 0004 1936 9684)
3 UC Davis School of Veterinary Medicine, Department of Surgical & Radiological Sciences, Davis, USA (GRID:grid.27860.3b) (ISNI:0000 0004 1936 9684)