نتایج جستجو برای: پروتئین انسانی flt3

تعداد نتایج: 58749  

Journal: :Cancer research 2014
Hayley S Ma Bao Nguyen Amy S Duffield Li Li Allison Galanis Allen B Williams Patrick A Brown Mark J Levis Daniel J Leahy Donald Small

There have been a number of clinical trials testing the efficacy of FMS-like tyrosine kinase-3 (FLT3) tyrosine kinase inhibitors (TKI) in patients with acute myeloid leukemia (AML) harboring a constitutively activating mutation in FLT3. However, there has been limited efficacy, most often because of inadequate achievement of FLT3 inhibition through a variety of mechanisms. In a previous study, ...

2012
Samuel J. Taylor Samantha A. Dagger Christine B. F. Thien Matthew E. Wikstrom Wallace Y. Langdon

High levels of expression of wild-type Flt3 characterize many hematopoietic proliferative diseases and neoplasms, providing a potential therapeutic target. Using the c-Cbl RING finger mutant mouse as a model of a myeloproliferative disease (MPD) driven by wild-type Flt3, in the present study, we show that treatment with the Flt3 kinase inhibitor AC220 blocks MPD development by targeting Flt3 mu...

2014
Alexander A Warkentin Michael S Lopez Elisabeth A Lasater Kimberly Lin Bai-Liang He Anskar YH Leung Catherine C Smith Neil P Shah Kevan M Shokat

Activating mutations in FLT3 confer poor prognosis for individuals with acute myeloid leukemia (AML). Clinically active investigational FLT3 inhibitors can achieve complete remissions but their utility has been hampered by acquired resistance and myelosuppression attributed to a 'synthetic lethal toxicity' arising from simultaneous inhibition of FLT3 and KIT. We report a novel chemical strategy...

2008
Carola Reindl Ruth Kern Konstantin Petropoulos Vegi M. Naidu Christian Buske Wolfgang Hiddemann Karsten Spiekermann

Purpose: Mutations in the receptor tyrosine kinase FLT3 are found in up to 30% of acute myelogenous leukemia patients and are associated with an inferior prognosis. In this study, we characterized critical tyrosine residues responsible for the transforming potential of active FLT3-receptor mutants and ligand-dependent activation of FLT3-WT. Experimental Design: We performed a detailed structure...

Journal: :Journal of immunology 2012
Tewfik Miloud Nathalie Fiegler Janine Suffner Günter J Hämmerling Natalio Garbi

Bone marrow-derived dendritic cell (DC) precursors seed peripheral organs, where they encounter diverse cellular environments during their final differentiation into DCs. Flt3 ligand (Flt3-L) is critical for instructing DC generation throughout different organs. However, it remains unknown which cells produce Flt3-L and, importantly, which cellular source drives DC development in such a variety...

Journal: :Blood 2006
Jennifer L Rocnik Rachel Okabe Jin-Chen Yu Benjamin H Lee Neill Giese David P Schenkein D Gary Gilliland

Acquired mutations in the FLT3 receptor tyrosine kinase are common in acute myeloid leukemia and result in constitutive activation. The most frequent mechanism of activation is disruption of the juxtamembrane autoregulatory domain by internal tandem duplications (ITDs). FLT3-ITDs confer factor-independent growth to hematopoietic cells and induce a myeloproliferative syndrome in murine bone marr...

Journal: :The Journal of Experimental Medicine 2005
Stephen L. Nutt Donald Metcalf Angela D'Amico Matthew Polli Li Wu

PU.1 is an Ets family transcription factor that is essential for fetal liver hematopoiesis. We have generated a PU.1(gfp) reporter strain that allowed us to examine the expression of PU.1 in all hematopoietic cell lineages and their early progenitors. Within the bone marrow progenitor compartment, PU.1 is highly expressed in the hematopoietic stem cell, the common lymphoid progenitor, and a pro...

2004
B. Douglas Smith Mark Levis Miloslav Beran Francis Giles Hagop Kantarjian Karin Berg Kathleen M. Murphy Tianna Dauses Jeffrey Allebach

Activating mutations of FMS-like tyrosine kinase 3 (FLT3) are present in approximately 30% of patients with de novo acute myeloid leukemia (AML) and are associated with lower cure rates from standard chemotherapy-based treatment. Targeting the mutation by inhibiting the tyrosine kinase activity of FLT3 is cytotoxic to cell lines and primary AML cells harboring FLT3 mutations. Successful FLT3 in...

Journal: :Blood 2014
Allison Galanis Hayley Ma Trivikram Rajkhowa Abhijit Ramachandran Donald Small Jorge Cortes Mark Levis

Mutations of the type III receptor tyrosine kinase FLT3 occur in approximately 30% of acute myeloid leukemia patients and lead to constitutive activation. This has made FLT3-activating mutations an attractive drug target because they are probable driver mutations of this disease. As more potent FLT3 inhibitors are developed, a predictable development of resistance-conferring point mutations, co...

Journal: :The Journal of Experimental Medicine 2003
Holger Karsunky Miriam Merad Antonio Cozzio Irving L. Weissman Markus G. Manz

Stimulation of Flt3 receptor tyrosine kinase through its cognate ligand expands early hematopoietic progenitor and dendritic cells (DCs) in humans and mice. The exact developmental stages at which hematopoietic progenitors express Flt3, are responsive to its ligand, and subsequently develop to DCs, are not known. Here we show that common lymphoid and common myeloid progenitors, as well as stead...

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