Flt3 mutations from patients with acute myeloid leukemia induce transformation of 32D cells mediated by the Ras and STAT5 pathways.

By M. Mizuki, R. Fenski, H. Halfter, I. Matsumura, R. Schmidt, C. Müller, W. Grüning, K. Kratz-Albers, S. Serve, C. Steur and 5 more. Blood, 2000

642 citations recorded by the source corpus.

Subfields: Hematology, Oncology

View Paper: https://www.semanticscholar.org/paper/f6b0d3e18cb04bf00f57abe699fd12c0ece47055

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In Hematology

1. M. Heinrich

In Oncology

1. William E. Evans
2. D. Teachey
3. S. Maude
4. S. Grupp

Citations in the corpus

• Analysis of FLT3 length mutations in 1003 patients with acute myeloid leukemia: correlation to cytogenetics, FAB subtype, and prognosis in the AMLCG study and usefulness as a marker for the detection of minimal residual disease. (2002, neutral): “2 In most study groups, the good risk group is defined by t(15;17), t(8;21), and inv(16)/t(16;16); the intermediate group is defined by normal karyotypes and other chromosomal aberrations; and the poor risk group is defined by complex karyotypes, 5/5q , 7/7q , 3q aberrations, and 11q23 translocation”
• SU5416, a small molecule tyrosine kinase receptor inhibitor, has biologic activity in patients with refractory acute myeloid leukemia or myelodysplastic syndromes. (2003, neutral): “% Peripheral blood blasts (range) 14 (1-75)”
• SU11248 is a novel FLT3 tyrosine kinase inhibitor with potent activity in vitro and in vivo. (2003, background): “To address if the apparent difference in sensitivity of FLT3-WT and FLT3-ITD to SU11248 could be attributed to use of these non-isogenic cell lines, a 32D myeloid cell line engineered to express FLT3-WT or FLT3-ITD (5) was tested.”
• The role of FLT3 in haematopoietic malignancies (2003, background): “In vitro transduction studies have shown that FLT3 ITDs promote ligand-independent dimerization, auto-phosphorylation and constitutive activation of the recepto”
• Genetic alterations activating kinase and cytokine receptor signaling in high-risk acute lymphoblastic leukemia (2012, background): “Similar to PDGFRB and JAK2 rearrangements, FLT3 mutations facilitate leukemic transformation by inducing constitutive kinase activation and signaling through the Ras and JAK/STAT5 pathways (Mizuki et al., 2000).”
• 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, neutral): “Adverse 139 130 (93) 4 (3) 5 (4) 0 — 88 84 (95) 4 (5) —”
• Analysis of FLT3-activating mutations in 979 patients with acute myelogenous leukemia: association with FAB subtypes and identification of subgroups with poor prognosis. (2002, neutral): “CD34 cells (%) 30 (0-98) 20‡ (0-96) 22 (0-91) 10 (3-73)”