Reversal of Acquired Drug Resistance in FLT 3 - mutated Acute Myeloid Leukemia Cells via 1 Distinct Drug Combination Strategies
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چکیده
5 Author Affiliations: Section of Molecular Hematology and Therapy, Department of Leukemia 6 and Department of Stem Cell Transplantation and Cellular Therapy, The University of Texas M. 7 D. Anderson Cancer Center, Houston, Texas, USA; and AROG Pharmaceuticals LLC, Dallas, 8 Texas, USA. 9 Note: Supplementary data for this article are available at Clinical Cancer Research Online 10 (http://clincancerres.aacrjournals.org/). 11 W. Zhang and C. Gao contributed equally to this study. 12 Corresponding Author: Dr. Michael Andreeff, The University of Texas M. D. Anderson Cancer 13 Center, 1515 Holcombe Blvd., Unit 448, Houston, TX 77030, U.S.A.; Phone: 713-792-7261; Fax: 14 713-563-7355; E-mail: [email protected]. 15 Running title: Combination strategies targeting sorafenib-resistant AML. 16 Manuscript word count (excluding references): 4906. 17 Manuscript tables: 0. 18 Manuscript figures: 6. 19
منابع مشابه
Reversal of acquired drug resistance in FLT3-mutated acute myeloid leukemia cells via distinct drug combination strategies.
PURPOSE FMS-like tyrosine kinase-3 (FLT3) internal tandem duplication (FLT3-ITD) mutations are common in patients with acute myeloid leukemia (AML). These patients regularly develop resistance to FLT3 inhibitors suggesting that targeted combination drug strategies are needed to enhance AML therapy efficacy. EXPERIMENTAL DESIGN Acquired point mutations of FLT3-ITD gene were screened using cDNA...
متن کاملCancer Therapy: Preclinical Reversal ofAcquiredDrugResistance inFLT3-MutatedAcute Myeloid Leukemia Cells via Distinct Drug Combination Strategies
Purpose: FMS-like tyrosine kinase-3 (FLT3) internal tandem duplication (FLT3-ITD) mutations are common in patients with acute myeloid leukemia (AML). These patients regularly develop resistance to FLT3 inhibitors suggesting that targeted combination drug strategies are needed to enhance AML therapy
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Introduction: Leukemia is a heterogeneous malignant disease in which progression at the level of CD34+ cells has a major impact in drug resistance and relapse. The multi-drug resistance gene product, P-glycoprotein is an inhibitor of apoptosis proteins (IAPs), such as Survivin that are expressed simultaneously with several putative drug resistance parameters in CD34+ leukemia cells. In fact, IA...
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تاریخ انتشار 2013