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Activating mutation of D835 within the activation loop of FLT3 in human hematologic malignancies
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The article was published on 2002-01-01 and is currently open access. It has received 376 citations till now.read more
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Journal ArticleDOI
Mutations and Treatment Outcome in Cytogenetically Normal Acute Myeloid Leukemia
Richard F. Schlenk,Konstanze Döhner,Jürgen Krauter,Stefan Fröhling,Andrea Corbacioglu,Lars Bullinger,Marianne Habdank,Daniela Späth,Michael Morgan,Axel Benner,Brigitte Schlegelberger,Gerhard Heil,Arnold Ganser,Hartmut Döhner +13 more
TL;DR: Genotypes defined by the mutational status of NPM1, FLT3, CEBPA, MLL, and MLL are associated with the outcome of treatment for patients with cytogenetically normal AML.
Journal ArticleDOI
Tyrosine kinases as targets for cancer therapy.
TL;DR: A comprehensive review discusses the molecular and clinical aspects of tyrosine kinases, enzymes that catalyze the transfer of phosphate from ATP to tyrosin residues in polypeptides.
Journal ArticleDOI
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.
Stefan Fröhling,Richard F. Schlenk,Jochen Breitruck,Axel Benner,Sylvia Kreitmeier,Karen Tobis,Hartmut Döhner,K Döhner +7 more
TL;DR: In this article, pre-treatment samples from 224 patients with acute myeloid leukemia (AML) and normal cytogenetics were analyzed for FLT3 internal tandem duplications (ITDs) and Asp835 mutations.
Journal ArticleDOI
Single-agent CEP-701, a novel FLT3 inhibitor, shows biologic and clinical activity in patients with relapsed or refractory acute myeloid leukemia
B. Douglas Smith,Mark J. Levis,Mark J. Levis,Miloslav Beran,Miloslav Beran,Francis J. Giles,Francis J. Giles,Hagop M Kantarjian,Hagop M Kantarjian,Karin D. Berg,Karin D. Berg,Kathleen M. Murphy,Kathleen M. Murphy,Tianna Dauses,Tianna Dauses,Jeffrey Allebach,Jeffrey Allebach,Donald Small,Donald Small +18 more
TL;DR: Results show that FLT3 inhibition is associated with clinical activity in AML patients harboringFLT3-activating mutations and indicate that CEP-701 holds promise as a novel, molecularly targeted therapy for this disease.
Journal ArticleDOI
FLT3 internal tandem duplication mutations associated with human acute myeloid leukemias induce myeloproliferative disease in a murine bone marrow transplant model.
Louise M Kelly,Qing Liu,Jeffrey L. Kutok,Ifor R. Williams,Christina L. Boulton,D. Gary Gilliland +5 more
TL;DR: It is demonstrated that FLT3-ITD mutant proteins are sufficient to induce a myeloproliferative disorder, but are insufficient to recapitulate the AML phenotype observed in humans.
References
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Journal ArticleDOI
Analysis of FLT3-activating mutations in 979 patients with acute myelogenous leukemia: association with FAB subtypes and identification of subgroups with poor prognosis
Christian Thiede,Christine Steudel,Brigitte Mohr,Markus Schaich,Ulrike Schäkel,Uwe Platzbecker,Martin Wermke,Martin Bornhäuser,Markus Ritter,Andreas Neubauer,Gerhard Ehninger,Thomas Illmer +11 more
TL;DR: In this paper, the authors analyzed the prevalence and the potential prognostic impact of FLT3 mutations in 979 acute myelogenous leukemia (AML) patients and found that a high mutant/wt ratio in ITD-positive patients appears to have a major impact on the prognostic relevance.
Journal ArticleDOI
Mutations and Treatment Outcome in Cytogenetically Normal Acute Myeloid Leukemia
Richard F. Schlenk,Konstanze Döhner,Jürgen Krauter,Stefan Fröhling,Andrea Corbacioglu,Lars Bullinger,Marianne Habdank,Daniela Späth,Michael Morgan,Axel Benner,Brigitte Schlegelberger,Gerhard Heil,Arnold Ganser,Hartmut Döhner +13 more
TL;DR: Genotypes defined by the mutational status of NPM1, FLT3, CEBPA, MLL, and MLL are associated with the outcome of treatment for patients with cytogenetically normal AML.
Journal ArticleDOI
Tyrosine kinases as targets for cancer therapy.
TL;DR: A comprehensive review discusses the molecular and clinical aspects of tyrosine kinases, enzymes that catalyze the transfer of phosphate from ATP to tyrosin residues in polypeptides.
Journal ArticleDOI
The role of FLT3 in haematopoietic malignancies
TL;DR: Exploring the mechanism by which mutations in the FLT3 gene cause uncontrolled proliferation might lead to a better understanding of how cells become cancerous and provide insights for the development of new drugs.
Journal ArticleDOI
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.
Stefan Fröhling,Richard F. Schlenk,Jochen Breitruck,Axel Benner,Sylvia Kreitmeier,Karen Tobis,Hartmut Döhner,K Döhner +7 more
TL;DR: In this article, pre-treatment samples from 224 patients with acute myeloid leukemia (AML) and normal cytogenetics were analyzed for FLT3 internal tandem duplications (ITDs) and Asp835 mutations.
Related Papers (5)
Activating mutation of D835 within the activation loop of FLT3 in human hematologic malignancies.
Yukiya Yamamoto,Hitoshi Kiyoi,Yasuyuki Nakano,Ritsuro Suzuki,Yoshihisa Kodera,Shuichi Miyawaki,Norio Asou,Kazutaka Kuriyama,Fumiharu Yagasaki,Chihiro Shimazaki,Hideki Akiyama,Kenji Saito,Miki Nishimura,Toshiko Motoji,Katsuji Shinagawa,Akihiro Takeshita,Hidehiko Saito,Ryuzo Ueda,Ryuzo Ohno,Tomoki Naoe +19 more