نتایج جستجو برای: flt3 tyrosine kinase

تعداد نتایج: 262799  

2015
Alexa S. Green Thiago T. Maciel Marie-Anne Hospital Chae Yin Fetta Mazed Elizabeth C. Townsend Sylvain Pilorge Mireille Lambert Etienne Paubelle Arnaud Jacquel Florence Zylbersztejn Justine Decroocq Laury Poulain Pierre Sujobert Nathalie Jacque Kevin Adam Jason C. C. So Olivier Kosmider Patrick Auberger Olivier Hermine David M. Weinstock Catherine Lacombe Patrick Mayeux Gary J. Vanasse Anskar Y. Leung Ivan C. Moura Didier Bouscary Jerome Tamburini

Fms-like tyrosine kinase 3 internal tandem duplication (FLT3-ITD) is frequently detected in acute myeloid leukemia (AML) patients and is associated with a dismal long-term prognosis. FLT3 tyrosine kinase inhibitors provide short-term disease control, but relapse invariably occurs within months. Pim protein kinases are oncogenic FLT3-ITD targets expressed in AML cells. We show that increased Pim...

Journal: :Blood 2005
Thomas Kindler Frank Breitenbuecher Stefan Kasper Eli Estey Francis Giles Eric Feldman Gerhard Ehninger Gary Schiller Virginia Klimek Stephen D Nimer Alois Gratwohl Chuna Ram Choudhary Constan Mueller-Tidow Hubert Serve Harald Gschaidmeier Pamela S Cohen Christoph Huber Thomas Fischer

Fms-like tyrosine kinase 3 (FLT3) receptor mutations as internal tandem duplication (ITD) or within the kinase domain are detected in up to 35% of patients with acute myeloid leukemia (AML). N-benzoyl staurosporine (PKC412), a highly effective inhibitor of mutated FLT3 receptors, has significant antileukemic efficacy in patients with FLT3-mutated AML. Mutation screening of FLT3 exon 20 in AML p...

Journal: :Blood 2002
Karsten Spiekermann Ksenia Bagrintseva Claudia Schoch Torsten Haferlach Wolfgang Hiddemann Susanne Schnittger

Activating length mutations in the juxtamembrane (JM) domain of the FLT3 gene (FLT3-LM) and mutations in the catalytic domain (FLT3D835/836) of this receptor tyrosine kinase represent the most frequent genetic alterations in acute myeloid leukemia (AML). Here, we describe a 6-bp insertion in the activation loop of FLT3 between codons 840 and 841 of FLT3 (FLT3-840GS) in 2 unrelated patients with...

2002
Karsten Spiekermann Ksenia Bagrintseva Claudia Schoch Torsten Haferlach Wolfgang Hiddemann Susanne Schnittger

Activating length mutations in the juxtamembrane (JM) domain of the FLT3 gene (FLT3-LM) and mutations in the catalytic domain (FLT3D835/836) of this receptor tyrosine kinase represent the most frequent genetic alterations in acute myeloid leukemia (AML). Here, we describe a 6-bp insertion in the activation loop of FLT3 between codons 840 and 841 of FLT3 (FLT3-840GS) in 2 unrelated patients with...

2017
Bao Nguyen Allen B. Williams David J. Young Hayley Ma Li Li Mark Levis Patrick Brown Donald Small

Fms-like tyrosine kinase-3 (FLT3) is a receptor tyrosine kinase that normally functions in hematopoietic cell survival, proliferation and differentiation. Constitutively activating mutations of FLT3 map predominately to the juxtamembrane domain (internal tandem duplications; ITD) or the activation loop (AL) of the kinase domain and are detected in about 1/3 of de novo acute myeloid leukemia (AM...

2012
Yun Chen Yao Guo Jiayu Han Wanting Tina Ho Shibo Li Xueqi Fu Zhizhuang Joe Zhao

BACKGROUND Gain-of-function mutations of tyrosine kinase FLT3 are frequently found in acute myeloid leukemia (AML). This has made FLT3 an important marker for disease diagnosis and a highly attractive target for therapeutic drug development. This study is intended to generate a sensitive substrate for assays of the FLT3 enzymatic activity. METHODS We expressed in Escherichia coli cells a glut...

Journal: :Cancer research 2005
Obdulio Piloto Mark Levis David Huso Yiwen Li Hongli Li Mei-Nai Wang Rajiv Bassi Paul Balderes Dale L Ludwig Larry Witte Zhenping Zhu Daniel J Hicklin Donald Small

Aberrant FLT3 expression and/or mutation plays a significant role in leukemogenesis. This has prompted the development of selective small molecule tyrosine kinase inhibitors against FLT3. However, like most tyrosine kinase inhibitors, those against FLT3 are not completely specific and at the doses required to completely inhibit target, significant toxicities may occur. In addition, tyrosine kin...

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...

ژورنال: پیاورد سلامت 2013
اژدری, عبدالطیف, عباسی, سکینه, محمدی, شاهین,

Background and Aim: FLT3 gene is a member of class III receptor Tyrosine Kinase, which is expressed in most patients with acute myeloid leukemia (AML). Mutations of FLT3 such as Internal Tandem Duplication (ITD) and point mutation of the D835 are the most common genetic defects in myeloid leukemia. These two mutations in patients with MLA and their effect on survival rate were studied for the f...

Journal: :Blood 2012
De-Chen Lin Tong Yin Maya Koren-Michowitz Ling-Wen Ding Saskia Gueller Sigal Gery Takayuki Tabayashi Ulla Bergholz Julhash U Kazi Lars Rönnstrand Carol Stocking H Phillip Koeffler

Fms-like tyrosine kinase 3 (FLT3) is a receptor tyrosine kinase with important roles in hematopoietic progenitor cell survival and proliferation. It is mutated in approximately one-third of AML patients, mostly by internal tandem duplications (ITDs). Adaptor protein Lnk is a negative regulator of hematopoietic cytokine signaling. In the present study, we show that Lnk interacts physically with ...

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