نتایج جستجو برای: ژن flt3

تعداد نتایج: 19081  

2014
Chuanjiang Yu Rama Krishna Kancha Justus Duyster

FLT3 is the most frequently mutated kinase in acute myeloid leukemia (AML). Internal tandem duplications (ITDs) in the juxta-membrane region constitute the majority of activating FLT3 mutations. Several FLT3 kinase inhibitors were developed and tested in the clinic with significant success. However, recent studies have reported the development of secondary drug resistance in patients treated wi...

Journal: :Blood 2008
Ellen Weisberg Johannes Roesel Guido Bold Pascal Furet Jingrui Jiang Jan Cools Renee D Wright Erik Nelson Rosemary Barrett Arghya Ray Daisy Moreno Elizabeth Hall-Meyers Richard Stone Ilene Galinsky Edward Fox Gary Gilliland John F Daley Suzan Lazo-Kallanian Andrew L Kung James D Griffin

An attractive target for therapeutic intervention is constitutively activated, mutant FLT3, which is expressed in a subpopulation of patients with acute myelocyic leukemia (AML) and is generally a poor prognostic indicator in patients under the age of 65 years. PKC412 is one of several mutant FLT3 inhibitors that is undergoing clinical testing, and which is currently in late-stage clinical tria...

Journal: :Blood 2005
Patrick Brown Mark Levis Sheila Shurtleff Dario Campana James Downing Donald Small

FMS-like tyrosine kinase 3 (FLT3) is almost universally expressed in B-precursor childhood acute lymphoblastic leukemia (ALL). Cases of ALL with MLL gene rearrangements and those with high hyperdiploidy (> 50 chromosomes) express the highest levels of FLT3, and activating mutations of FLT3 occur in 18% of MLL-rearranged and 28% of hyperdiploid ALL cases. We determined the antileukemic activity ...

2014
Ghaleb Elyamany Mohammad Awad Kamal Fadalla Mohamed Albalawi Mohammad Al Shahrani Abdulaziz Al Abdulaaly

The Fms-like tyrosine kinase-3 (FLT3) is a receptor tyrosine kinase that plays a key role in cell survival, proliferation, and differentiation of hematopoietic stem cells. Mutations of FLT3 were first described in 1997 and account for the most frequent molecular mutations in acute myeloid leukemia (AML). AML patients with FLT3 internal tandem duplication (ITD) mutations have poor cure rates the...

Journal: :Blood 2012
Sarah Greenblatt Li Li Christopher Slape Bao Nguyen Rachel Novak Amy Duffield David Huso Stephen Desiderio Michael J Borowitz Peter Aplan Donald Small

Constitutive activation of FLT3 by internal tandem duplication (ITD) is one of the most common molecular alterations in acute myeloid leukemia (AML). FLT3/ITD mutations have also been observed in myelodysplastic syndrome patients both before and during progression to AML. Previous work has shown that insertion of an FLT3/ITD mutation into the murine Flt3 gene induces a myeloproliferative neopla...

Journal: :Blood 2007
Lisheng Wang Jie Wang Bradley W Blaser Anne-Marie Duchemin Donna F Kusewitt Tom Liu Michael A Caligiuri Roger Briesewitz

Entry into the cell cycle is mediated by cyclin-dependent kinase 4/6 (CDK4/6) activation, followed by CDK2 activation. We found that pharmacologic inhibition of the Flt3 internal tandem duplication (ITD), a mutated receptor tyrosine kinase commonly found in patients with acute myelogenous leukemia (AML), led to the down-regulation of cyclin D2 and D3 followed by retinoblastoma protein (pRb) dep...

Journal: :Molecular cancer therapeutics 2014
Warren Fiskus Sunil Sharma Jun Qi Bhavin Shah Santhana G T Devaraj Christopher Leveque Bryce P Portier Swaminathan Iyer James E Bradner Kapil N Bhalla

Recently, treatment with bromodomain and extraterminal protein antagonist (BA) such as JQ1 has been shown to inhibit growth and induce apoptosis of human acute myelogenous leukemia (AML) cells, including those expressing FLT3-ITD. Here, we demonstrate that cotreatment with JQ1 and the FLT3 tyrosine kinase inhibitor (TKI) ponatinib or AC220 synergistically induce apoptosis of cultured and primar...

Journal: :Clinical cancer research : an official journal of the American Association for Cancer Research 2003
Anne-Marie O'Farrell James M Foran Walter Fiedler Hubert Serve Ron L Paquette Maureen A Cooper Helene A Yuen Sharianne G Louie Heidi Kim Susan Nicholas Michael C Heinrich Wolfgang E Berdel Carlo Bello Mark Jacobs Paul Scigalla William C Manning Stephen Kelsey Julie M Cherrington

PURPOSE Obtaining direct and rapid proof of molecular activity in early clinical trials is critical for optimal clinical development of novel targeted therapies. SU11248 is an oral multitargeted kinase inhibitor with selectivity for fms-related tyrosine kinase 3/Flk2 (FLT3), platelet-derived growth factor receptor alpha/beta, vascular endothelial growth factor receptor 1/2, and KIT receptor tyr...

2010
Yeo-Kyeoung Kim Hee-Nam Kim Se Ryeon Lee Jae-Sook Ahn Deok-Hwan Yang Je-Jung Lee Il-Kwon Lee Myung-Geun Shin Hyeoung-Joon Kim

BACKGROUND Nucleophosmin (NPM1) gene and fms-like tyrosine kinase 3 gene-internal tandem duplication (FLT3-ITD) mutations are the most frequent mutations in patients with cytogenetically normal (CN)-AML. We analyzed the prognostic impact of these mutations and their interactions in adults with CN-AML. METHODS NPM1 mutation (NPM1mut) and FLT3-ITD mutation (FLT3-ITD+) were analyzed by GeneScan ...

Journal: :Blood 2005
Rosemary E Gale Robert Hills Arnold R Pizzey Panagiotis D Kottaridis David Swirsky Amanda F Gilkes Elizabeth Nugent Kenneth I Mills Keith Wheatley Ellen Solomon Alan K Burnett David C Linch David Grimwade

The prognostic significance of FLT3 mutations in acute promyelocytic leukemia (APL) is not firmly established and is of particular interest given the opportunities for targeted therapies using FLT3 inhibitors. We studied 203 patients with PML-RARA-positive APL; 43% of the patients had an FLT3 mutation (65 internal tandem duplications [ITDs], 19 D835/I836, 4 ITD+D835/I836). Both mutations were a...

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