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Likewise, Zwaan et al used GO (up to three doses) to treat 15 children with relapsed/refractory CD33+ AML, on a compassionate-use basis [ 23, 24].
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A recent study examining children with AML enrolled on a Children's Cancer Group clinical trial found that age >16 years, non-white ethnicity, and underweight status were all significantly associated with infection-related mortality (Sung et al, 2007).
We have focused our interest on the possible role of FLT3 ITD, a common oncogenic lesion in AML, on PTP expression.
AML, on the other hand, is more often found in older individuals with a mean age of diagnosis of 70 years and 1 case per 100,000 adults [ 5, 7– 10].
Though these cells had short-term repopulating potential, they were for the most part incapable of inducing AML on their own but could readily be converted into AML-inducing cells when complemented with MEIS1 or other genes [26].
Further experimental studies will have to examine the consequences of reduced BRCA1 gene expression in AML on DNA repair and genomic stability.
Clearly, if FLT3 small molecule inhibitors were to have an impact on AML treatment, a better understanding of how FLT3 signaling contributes to the disease, and how FLT3 drugs work at the cellular level, would be necessary.
Different categories of AML can depend on a particular mutation event that creates a block in differentiation and the stage within the myeloid lineage when the event occurs.
Leukemic cells were obtained from peripheral blood or bone marrow samples in 29 AML patients, separated on a gradient of density (Ficoll).
Dr. Wilson focused his talk on AML, a relatively common form of cancer with a particularly low survival rate.
This review discusses current knowledge of AML antigens and immune responses to AML with a particular focus on the role of T cells and natural killer cells.
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