The roles of FLT3 in hematopoiesis and leukemia.

By D. Gilliland, J. Griffin. Blood, 2002

1,621 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/0c53b09c48827b28bca1ff05d5f61dc5191a48b1

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In Hematology

Citations in the corpus

Mutations in nucleophosmin (NPM1) in acute myeloid leukemia (AML): association with other gene abnormalities and previously established gene expression signatures and their favorable prognostic significance. (2005, background): “The unfavorable-risk category was defined by the presence of 5/del(5q), 7del(7q), t(6;9), t(9;22), 3q26 abnormality, or complex karyotype (more than 3 abnormalities).”
SU5416, a small molecule tyrosine kinase receptor inhibitor, has biologic activity in patients with refractory acute myeloid leukemia or myelodysplastic syndromes. (2003, neutral): “Characteristic N = 22 Median (range) Age 66 (22-80) WBC (x109/L) 2.”
Prognostically useful gene-expression profiles in acute myeloid leukemia. (2004, neutral): “(%)* t(15;17) t(8;21) inv(16)/t(16;16) +8 +11 +21 ¡5 ¡5(q) ¡7 ¡7(q) 3q t(6;9) t(9;22) t(11q23) Complex karyotype (>3 chromosomal abnormalities) Other abnormal karyotypes Normal karyotype Not determined 18 (6) 22 (8) 19 (7) 26 (9) 7 (2) 2 (1) 3 (1) 1 (<1) 13 (5) 7 (2) 6 (2) 4 (1) 2 (1) 19 (7) 11 (4) ”
Tet2 loss leads to increased hematopoietic stem cell self-renewal and myeloid transformation (2011, neutral): “complementation groups: one class that includes mutations that activate oncogenic signaling pathways, and a second class of mutations that perturbs myeloid differentiation (Gilliland and Griffin, 2002).”
Acute Myeloid Leukemia: Epidemiology and Etiology (2006, neutral): “, molecular targeting of both, FLT-3 and fusion proteins) [58].”
Patients with acute myeloid leukemia and an activating mutation in FLT3 respond to a small-molecule FLT3 tyrosine kinase inhibitor, PKC412. (2005, neutral): “Median platelet count, 1000/ L (range) 30 (1-619)”
The impact of FLT3 internal tandem duplication mutant level, number, size, and interaction with NPM1 mutations in a large cohort of young adult patients with acute myeloid leukemia. (2008, background): “that normally stabilizes the kinase in its inactive conformation and protects the ATP binding pocket.(33,34) An increasing length of additional sequence may therefore influence the ability of this interaction to either partially form or be completely abolished, and could lead to progressively increa”
Origins of chromosome translocations in childhood leukaemia (2003, background): “cgi?l=2322"> FLT3 -kinase mutations do seem to provide complementary genetic event”