A Novel Molecular Mechanism of Primary Resistance to FLT 3-Kinase Inhibitors in Acute Myeloid Leukemia
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Kristina Masson | L. Rönnstrand | S. Kasper | B. Markova | F. Breitenbuecher | C. Huber | T. Fischer | T. Kindler | F. Böhmer | B. Carius | T. Stauder | Birgit Carius
[1] T. Haferlach,et al. Identification of a novel type of ITD mutations located in nonjuxtamembrane domains of the FLT3 tyrosine kinase receptor. , 2009, Blood.
[2] M. Caligiuri,et al. Mcl-1 Is a Relevant Therapeutic Target in Acute and Chronic Lymphoid Malignancies: Down-Regulation Enhances Rituximab-Mediated Apoptosis and Complement-Dependent Cytotoxicity , 2007, Clinical Cancer Research.
[3] N. Barbarroja,et al. Inhibition of Flt3‐activating mutations does not prevent constitutive activation of ERK/Akt/STAT pathways in some AML cells: a possible cause for the limited effectiveness of monotherapy with small‐molecule inhibitors , 2007, Hematological oncology.
[4] Kyu-Tae Kim,et al. Prolonged exposure to FLT3 inhibitors leads to resistance via activation of parallel signaling pathways. , 2006, Blood.
[5] P. Roller,et al. Structure-based design of potent Grb2-SH2 domain antagonists not relying on phosphotyrosine mimics. , 2006, Biochemical and biophysical research communications.
[6] D. Gilliland,et al. Roles of tyrosine 589 and 591 in STAT5 activation and transformation mediated by FLT3-ITD. , 2006, Blood.
[7] D. Green,et al. Glycogen synthase kinase-3 regulates mitochondrial outer membrane permeabilization and apoptosis by destabilization of MCL-1. , 2006, Molecular cell.
[8] Megan L. Peach,et al. Discovery of a novel nonphosphorylated pentapeptide motif displaying high affinity for Grb2-SH2 domain by the utilization of 3'-substituted tyrosine derivatives. , 2006, Journal of medicinal chemistry.
[9] Richard Clark,et al. A phase 2 trial of the FLT3 inhibitor lestaurtinib (CEP701) as first-line treatment for older patients with acute myeloid leukemia not considered fit for intensive chemotherapy. , 2004, Blood.
[10] R. Stone,et al. Clinical resistance to the kinase inhibitor PKC412 in acute myeloid leukemia by mutation of Asn-676 in the FLT3 tyrosine kinase domain. , 2006, Blood.
[11] S. Jayaraman. Flow cytometric determination of mitochondrial membrane potential changes during apoptosis of T lymphocytic and pancreatic beta cell lines: comparison of tetramethylrhodamineethylester (TMRE), chloromethyl-X-rosamine (H2-CMX-Ros) and MitoTracker Red 580 (MTR580). , 2005, Journal of immunological methods.
[12] F. Bussolino,et al. Direct recruitment of CRK and GRB2 to VEGFR-3 induces proliferation, migration, and survival of endothelial cells through the activation of ERK, AKT, and JNK pathways. , 2005, Blood.
[13] G. Gores,et al. Interleukin-6 contributes to Mcl-1 up-regulation and TRAIL resistance via an Akt-signaling pathway in cholangiocarcinoma cells. , 2005, Gastroenterology.
[14] Randy Allred,et al. A phase 1 study of SU11248 in the treatment of patients with refractory or resistant acute myeloid leukemia (AML) or not amenable to conventional therapy for the disease. , 2005, Blood.
[15] E. Estey,et al. Identification of a novel activating mutation (Y842C) within the activation loop of FLT3 in patients with acute myeloid leukemia (AML). , 2005, Blood.
[16] E. Estey,et al. Patients with acute myeloid leukemia and an activating mutation in FLT3 respond to a small-molecule FLT3 tyrosine kinase inhibitor, PKC412 , 2004 .
[17] Doriano Fabbro,et al. Prediction of Resistance to Small Molecule FLT3 Inhibitors , 2004, Cancer Research.
[18] H. Pehamberger,et al. Mcl-1 Is a Novel Therapeutic Target for Human Sarcoma , 2004, Clinical Cancer Research.
[19] A. Marx,et al. Efficacy and safety of imatinib in adult patients with c-kit-positive acute myeloid leukemia. , 2004, Blood.
[20] H. Kantarjian,et al. Single-agent CEP-701, a novel FLT3 inhibitor, shows biologic and clinical activity in patients with relapsed or refractory acute myeloid leukemia. , 2004, Blood.
[21] Axel Benner,et al. Prognostic significance of activating FLT3 mutations in younger adults (16 to 60 years) with acute myeloid leukemia and normal cytogenetics: a study of the AML Study Group Ulm. , 2002, Blood.
[22] G. Mcmahon,et al. SU5416 and SU5614 inhibit kinase activity of wild-type and mutant FLT3 receptor tyrosine kinase. , 2002, Blood.
[23] Martin Dugas,et al. Analysis of FLT3 length mutations in 1003 patients with acute myeloid leukemia: correlation to cytogenetics, FAB subtype, and prognosis in the AMLCG study and usefulness as a marker for the detection of minimal residual disease. , 2002 .
[24] G. Ehninger,et al. Analysis of Flt3-activating Mutations in 979 Patients with Acute Myelogenous Leukemia: Association with Fab Subtypes and Identification of Subgroups with Poor Prognosis , 2022 .
[25] Doriano Fabbro,et al. Inhibition of mutant FLT3 receptors in leukemia cells by the small molecule tyrosine kinase inhibitor PKC412. , 2002, Cancer cell.
[26] B. Smith,et al. A FLT3-targeted tyrosine kinase inhibitor is cytotoxic to leukemia cells in vitro and in vivo. , 2002, Blood.
[27] M. Yaffe. Phosphotyrosine-binding domains in signal transduction , 2002, Nature Reviews Molecular Cell Biology.
[28] P. N. Rao,et al. Clinical Resistance to STI-571 Cancer Therapy Caused by BCR-ABL Gene Mutation or Amplification , 2001, Science.
[29] H. Broxmeyer,et al. Flt3 signaling involves tyrosyl‐phosphorylation of SHP‐2 and SHIP and their association with Grb2 and Shc in Baf3/Flt3 cells , 1999, Journal of leukocyte biology.
[30] D. Allen,et al. The X-linked lymphoproliferative-disease gene product SAP regulates signals induced through the co-receptor SLAM , 1998, Nature.
[31] F. Hobbs,et al. Identification of a Novel Inhibitor of Mitogen-activated Protein Kinase Kinase* , 1998, The Journal of Biological Chemistry.
[32] John Calvin Reed,et al. Elevated expression of the apoptotic regulator Mcl-1 at the time of leukemic relapse. , 1998, Blood.
[33] John Calvin Reed,et al. Immunohistochemical analysis of bcl-2, bax, bcl-X, and mcl-1 expression in prostate cancers. , 1996, The American journal of pathology.
[34] J. Darnell,et al. Maximal activation of transcription by statl and stat3 requires both tyrosine and serine phosphorylation , 1995, Cell.
[35] R. Craig,et al. MCL1, a gene expressed in programmed myeloid cell differentiation, has sequence similarity to BCL2. , 1993, Proceedings of the National Academy of Sciences of the United States of America.