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Masayuki Towatari

Researcher at Nagoya University

Publications -  43
Citations -  3538

Masayuki Towatari is an academic researcher from Nagoya University. The author has contributed to research in topics: Leukemia & Myeloid leukemia. The author has an hindex of 27, co-authored 43 publications receiving 3440 citations.

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Tandem-duplicated Flt3 constitutively activates STAT5 and MAP kinase and introduces autonomous cell growth in IL-3-dependent cell lines.

TL;DR: In this paper, the internal tandem duplication of the human Flt3 gene in approximately 20% of acute myeloid leukemia (AML) cases was identified, and the wild-type and the mutant FLt3 genes were transfected into two IL-3-dependent cell lines, 32D and BA/F3 cells.
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Internal tandem duplication of the FLT3 gene is a novel modality of elongation mutation which causes constitutive activation of the product.

TL;DR: Findings suggest that the elongation of the JM domain rather than increase of tyrosine residues causes gain-of-function of FLT3, and ITD is a novel modality of somatic mutation which activates its product.
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Up-regulation of costimulatory/adhesion molecules by histone deacetylase inhibitors in acute myeloid leukemia cells.

TL;DR: Results suggest that the immunotherapeutic use of HDACIs may become a novel tool for treatment of AML.
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Combination of intensive chemotherapy and imatinib can rapidly induce high-quality complete remission for a majority of patients with newly diagnosed BCR-ABL-positive acute lymphoblastic leukemia.

TL;DR: Although the number of patients is small and the observation period is too short, the combination therapy is very promising and produces high-quality CR for most newly diagnosed patients with BCR-ABL-positive ALL, and provides the patients with a better chance to receive an allogeneic HSC transplant.
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Histone deacetylase inhibitors are the potent inducer/enhancer of differentiation in acute myeloid leukemia: a new approach to anti-leukemia therapy.

TL;DR: HDRIs are the potent inducer or enhancer of differentiation in acute myeloid leukemia and regulate transcription in an ordered manner.