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注意：仅列出部分参考文献，下载原文获取全部文献信息。Loss of the wild-type allele contributes to myeloid expansion and disease aggressiveness in FLT3/ITD knockin mice
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The Flt3 receptor tyrosine kinase collaborates with NUP98-HOX fusions in acute myeloid leukemia
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Lineage specification and plasticity in CD19- early B cell precursors
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Block of C/EBPα function by phosphorylation in acute myeloid leukemia with FLT3 activating mutations
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Internal tandem duplications of the FLT3 gene are present in leukemia stem cells
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HOXA genes are included in genetic and biologic networks defining human acute T-cell leukemia (TALL)
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FLT3-ITD and tyrosine kinase domain mutants induce 2 distinct phenotypes in a murine bone marrow transplantation model
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Dimerization of MLL fusion proteins and FLT3 activation synergize to induce multiple-lineage leukemogenesis
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HOXB6 overexpression in munine bone marrow immortalizes a myelomonocytic precursor in vitro and causes hematopoietic stem cell expansion and acute myeloid leukemia in vivo
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Internal tandem duplication mutation of FLT3 blocks myeloid differentiation through suppression of C/EBPα expression
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Acquisition of FLT3 or N-ras mutations is frequently associated with progression of myelodysplastic syndrome to acute myeloid leukemia
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Expression of HOX genes in acute leukemia cell lines with and without MLL translocations
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Differential and common leukemogenic potentials of multiple NUP98-Hox fusion proteins alone or with Meis1
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The role of NUP98 gene fusions in hematologic malignancy
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Expression pattern of HOXB6 homeobox gene in myelomonocytic differentiation and acute myeloid leukemia
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HOXB4-induced expansion of adult hematopoietic stem cells ex vivo
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