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• W792879081 abstract "AACR Centennial Conference: Translational Cancer Medicine-- Nov 4-8, 2007; SingaporeB72 Fms-like tyrosine kinase 3 (FLT3) receptor mutations - internal tandem duplication (ITD) of the juxta-membrane domain or point mutation of the activating loop domain - have been found in about 30% of adult AML and 15%-20% of pediatric AML. Presence of FLT3-ITD and FLT3-point mutation lead to constitutive activation of the FLT3 receptor tyrosine kinase and cause autonomous, ligand-independent proliferation of hematopoietic cells. High expression of FLT3 mRNA transcripts is found in most leukemia compared to normal bone marrow; it is especially raised in infant MLL leukaemia and hyperdiploid ALL independent of the FLT3 mutation status. Herein, we evaluated the clinical significance of FLT3-ITD, point mutations and FLT3 mRNA levels, and correlate with prognostic factors based on clinical or biological characteristics in pediatric ALL and AML, such as age, initial total white blood count, FAB classification and common cytogenetic subtypes. A total of 441 childhood acute leukemias (n[AML]=135, n[ALL]=306) were screened for FLT3-ITD and codon 835 mutation; 167 were analysed for FLT3 expression levels (n[AML]=95, n[ALL]=72). Point mutation within codon 835 was screened using PCR and restriction enzyme digest (EcoRV). Qualitative and quantitative analysis of FLT3-ITD were analysed using Genescan. We measured FLT3 mRNA transcript levels, normalized with ABL control gene, by quantitative real-time PCR. Statistical analysis was assessed using chi-square or fisher exact tests. Statistical significance was set at p < 0.05. Of the 135 children with AML, 14 (10.4%) harbored FLT3-ITD, and 8 (5.9%) harbored codon 835 variants. Three (21%) FLT3-ITD positive cases were PML-RARA, 2 (14%) had AML1-ETO and 1 (7%) showed 11q23 MLL rearrangement. Gene scan analysis showed 4/14 FLT3-ITD positive patients had a low allelic wildtype/ITD ratio of <0.5. High expression of ratio of FLT3 mRNA to ABL control gene of >1 were significantly associated with leukocytosis (TWC>50,000x109/L; p=0.01), and age (3 to 9 yrs > above 9years > below 3years; p=0.013). Among the 8 FAB classifications, FLT3 was significantly down regulated in AML-M7 FAB subtype (mean=0.8; median=0.02; range=0.001-4.4; p=0.022). In the ALL cohort, none of the 306 children harbored FLT3-ITD, and only 3 were positive for codon 835 mutation. High expression of FLT3/ABL ratio >1 were significantly associated with age (below 3years > 3 to 9 years > above 9years; p=0.03), and hyperdiploid cytogenetic subtype (DNA index ≥1.16, p<0.05). No other significant association was observed. Our results showed high frequency of FLT3 mutations of 15.6% (n=21/135) in childhood AML and low frequency of only 1% (n=3/306) in childhood ALL. Importantly, about 1/3 of the FLT-ITD positive patients showed more than 2-fold increase in mutant intensity as compared to wild type (i.e.WT/ITD ratio 0.05). We confirm that FLT3 expression is significantly upregulated in hyperdiploid (DNA index ≥ 1.16) subtype which have good prognosis." @default.
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• W792879081 date "2007-11-15" @default.
• W792879081 modified "2023-09-23" @default.
• W792879081 title "The frequency of FLT3-internal tandem duplication, point mutations and expression levels of FLT3 in childhood acute leukaemias" @default.
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