Sorafenib (Nexavar®) induces molecular remission and regression of extramedullary disease in a patient with FLT3-ITD+

The fins-related tyrosine kinase 3 internal tandem duplication (FLT3-ITD) can he found in about one quarter of patients with acute myeloid leukemia (AML) [Small D. FLT3 mutations: biology and treatment. Hematology Am Soc Hematology. Educ. Program 2006; 178-84 [Review]]. Patients who carry this Mutation have a high risk of relapse even after allogeneic stern cell transplantation [Sheikhha MH. A, van A, Tobal K. Liu Yin JA. Prognostic significance of FLT3 ITD and D835 mutations in AML patients. Hematol J 2003;4;41-6: Meshinchi S. Arceci RJ, sanders JE, Smith FO. Woods WB. Radich JP, et al. Role of allogeneic stern cell transplantation in FLT3/ITD-positive AML. Blood 2006;108(1):400-1]. Recent reports show that Sorafenib. a multikinase inhibitor has significant activity against FLT3-ITD+ blasts in vitro [Auclair D, Miller D. Yatsula V. Pickett W, Carter C. Chang Y, et al. Antitumor activity of sorafenib in FLT3-driven leukemic cells. Leukemia 2007 21(3):439-45]. We here report the first Clinical case of Molecular remission induced by Sorafenib in a patient with FLT3-ITD+ AML and extramedullary disease after allogenic stern cell transplantation. (C) 2008 Elsevier Ltd. All rights reserved.