Annals of Hematology, 21 July 2010, Vol.90(4), pp.473-475
Dear Editor, We report on two patients with acute myeloid leukemia (AML) initially presenting in 2007. Both patients were tested positive for the FLT3-ITD mutation and were therefore treated with the FLT3 tyrosine kinase inhibitor sorafenib (400 mg/day) after progress of AML following several protocols of conventional chemotherapy. Both patients responded with a significant reduction of peripheral blast counts after 10 to 17 days leading to hematological response for 12 and 14 weeks, respectively. At the time of relapse, molecular analysis investigating mutations of both tyrosine kinase domains by sequencing of each individual FLT3-ITD cDNA did not demonstrate any additional mutations. We therefore suggest that the secondary resistance to sorafenib is mediated by other mechanisms than the acquisition of secondary mutations of FLT3 in these patients. FLT3-ITD mutations represent the second most frequent molecular aberration in AML leading to a constitutive activity of the class III receptor tyrosine kinase FLT3. FLT3-ITD mutations can be found in 25–30% of all AML patients and are associated with a reduced disease-free survival and overall survival [1–3].
Medicine ; Medicine
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