FLT3 mutations in canine acute lymphocytic leukemia |
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| Authors: | Steven E Suter George W Small Eric L Seiser Rachael Thomas Matthew Breen Kristy L Richards |
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| Affiliation: | (1) Department of Clinical Sciences, College of Veterinary Medicine, North Carolina State University, Raleigh, NC, USA;(2) Center for Comparative Medicine and Translational Research, North Carolina State University, Raleigh, NC, USA;(3) Lineberger Comprehensive Cancer Center, Chapel Hill, NC, USA;(4) Department of Molecular Biomedical Sciences, College of Veterinary Medicine, North Carolina State University, Raleigh, NC, USA;(5) Division of Hematology/Oncology, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA |
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| Abstract: | Background FMS-like tyrosine kinase 3 (FLT3) is a commonly mutated protein in a variety of human acute leukemias. Mutations leading to constitutively active FLT3, including internal tandem duplications of the juxtamembrane domain (ITD), result in continuous cellular proliferation, resistance to apoptotic cell death, and a poorer prognosis. A better understanding of the molecular consequences of FLT3 activation would allow improved therapeutic strategies in these patients. Canine lymphoproliferative diseases, including lymphoma and acute leukemias, share evolutionarily conserved chromosomal aberrations and exhibit conserved mutations within key oncogenes when compared to their human counterparts. A small percentage of canine acute lymphocytic leukemias (ALL) also exhibit FLT3 ITD mutations. |
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