Binding of FLT3L to its cognate tyrosine kinase receptor, FLT3, activates STAT3 and STAT5 (1, 3).
FLT3L结合到与它同源的酪氨酸激酶的受体FLT3结合激活STAT3和STAT 5 (1,3)。
Secondary FLT3-TKD mutations are associated with treatment failure with tyrosine kinase inhibitors.
继发性FLT3 - TKD突变与酪氨酸激酶抑制剂治疗失败有关。
We investigated the effects and mechanisms of Flt3 signaling and 4-1bbl reverse signaling to monocytes.
同时还探讨了4 - 1bbl逆向信号对单核细胞的作用及可能的机理。
BACKGROUND: Fms-like tyrosine kinase-3 (FLT3) gene is one of the receptors for growth factors in early hematogenesis.
背景：Flt3基因是近年来发现的早期造血生长因子受体基因。
Using genomic PCR and sequencing, FLT3/ITD mutation with or without chromosome translocation were examined in AML patients.
采用PCR联合序列检测伴有或不伴有染色体易位的急性髓性白血病患者FLT3基因突变情况。
Complete response rates were similar for children with either mutation and children with wild-type FLT3, the authors report.
作者报道，有突变患儿和野生型FLT3患儿的完全有效率是相似的。
FLT3 Internal tandem duplication (ITD) and tyrosine kinase domain (TKD) mutations are seen in 30% of AML patients (PTS) and are associated with poor survival.
30%的急性髓系白血病(aml)患者发生FLT3内部串联重复(itd)和酪氨酸激酶域(TKD)突变，而且生存预后较差。
This study was to explore the clinical significance of FLT3 internal tandem duplication (FLT3/ITD) in acute myeloid leukemia (AML) with chromosome abnormality.
本研究旨在探讨伴有染色体异常急性髓系白血病患者FLT3跨膜区内部串联重复突变检测的临床意义。
Conclusions Genotypes defined by the mutational status of NPM1, FLT3, CEBPA, and MLL are associated with the outcome of treatment for patients with cytogenetically normal AML.
结论：由npm 1,FLT3,CEBPA，和MLL基因的突变状态所界定的基因型与细胞遗传学正常的急性髓细胞白血病患者的临床治疗结局之间存在相关性。
Conclusions Genotypes defined by the mutational status of NPM1, FLT3, CEBPA, and MLL are associated with the outcome of treatment for patients with cytogenetically normal AML.
结论：由npm 1,FLT3,CEBPA，和MLL基因的突变状态所界定的基因型与细胞遗传学正常的急性髓细胞白血病患者的临床治疗结局之间存在相关性。
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