Journal ArticleDOI
A constitutively active SPTBN1-FLT3 fusion in atypical chronic myeloid leukemia is sensitive to tyrosine kinase inhibitors and immunotherapy.
Francis H. Grand,Sameena Iqbal,Lingyan Zhang,Nigel H. Russell,Andrew Chase,Nicholas C.P. Cross +5 more
TLDR
Although FLT3 abnormalities are uncommon in aCML, SPTBN1-FLT3 is a novel constitutively active tyrosine kinase that appears to responsive to both targeted signal transduction therapy and immunotherapy.About:
This article is published in Experimental Hematology.The article was published on 2007-11-01. It has received 49 citations till now. The article focuses on the topics: Fms-Like Tyrosine Kinase 3 & Fusion gene.read more
Citations
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Journal ArticleDOI
Frequent CBL mutations associated with 11q acquired uniparental disomy in myeloproliferative neoplasms.
Francis H. Grand,Claire Hidalgo-Curtis,Thomas Ernst,Katerina Zoi,Christine Zoi,Carolann McGuire,Sebastian Kreil,Amy V. Jones,Joannah Score,Georgia Metzgeroth,David Oscier,Andrew J. Hall,Christian Brandts,Hubert Serve,Andreas Reiter,Andrew Chase,Nicholas C.P. Cross +16 more
TL;DR: It is concluded that acquired, transforming CBL mutations are a novel and widespread pathogenetic abnormality in morphologically related, clinically aggressive MPNs.
Journal ArticleDOI
Myeloid neoplasms with eosinophilia
Andreas Reiter,Jason Gotlib +1 more
TL;DR: Myeloid mutation panels have identified somatic variants in patients with a provisional diagnosis of hypereosinophilia of undetermined significance, reclassifying some of these cases as eos inophilia-associated neoplasms.
Journal ArticleDOI
ETV6 fusion genes in hematological malignancies: a review.
Etienne De Braekeleer,Nathalie Douet-Guilbert,Frédéric Morel,Marie-Josée Le Bris,Audrey Basinko,Marc De Braekeleer +5 more
TL;DR: Five potential mechanisms of ETV6-mediated leukemogenesis have been identified: constitutive activation of the kinase activity of the partner protein, modification of the original functions of a transcription factor, loss of function of the fusion gene, and activation of a proto-oncogene in the vicinity of a chromosomal translocation.
Journal ArticleDOI
ABL1 fusion genes in hematological malignancies: a review.
Etienne De Braekeleer,Nathalie Douet-Guilbert,David W. Rowe,Nick Bown,Frédéric Morel,Christian Berthou,Claude Férec,Marc De Braekeleer +7 more
TL;DR: Screening for A BL1 chimeric genes could be performed in patients with ALL, more particularly in those with T‐cell ALL because ABL1 modulates T‐ cell development and plays a role in cytoskeletal remodeling processes in T cells.
Journal ArticleDOI
FMS-like Tyrosine Kinase 3/FLT3: From Basic Science to Clinical Implications
Julhash U. Kazi,Lars Rönnstrand +1 more
TL;DR: Current knowledge regarding structural and functional aspects of FLT3 signaling, both under normal and pathological conditions, are provided, and challenges for the future regarding the use of targeted inhibition of these pathways for the treatment of patients are discussed.
References
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Journal ArticleDOI
A comprehensive genetic map of the human genome based on 5,264 microsatellites
Colette Dib,Sabine Fauré,Cécile Fizames,Delphine Samson,N. Drouot,Alain Vignal,P Millasseau,S Marc,Jamilé Hazan,Eric Seboun,Mark Lathrop,Gabor Gyapay,Jean Morissette,Jean Morissette,Jean Weissenbach +14 more
TL;DR: The last version of the Généthon human linkage map is reported, which consists of 5,264 short tandem repeat polymorphisms with a mean heterozygosity of 70%.
Journal ArticleDOI
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
TL;DR: Analysis of the mutation of D835 of FLT3, which corresponds to D816 of c-KIT, in a large series of human hematologic malignancies demonstrates that the FLT 3 gene is the target most frequently mutated to become constitutively active in AML.
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
Inhibition of mutant FLT3 receptors in leukemia cells by the small molecule tyrosine kinase inhibitor PKC412.
Ellen Weisberg,Christina L. Boulton,Louise M Kelly,Paul W. Manley,Doriano Fabbro,Thomas Meyer,D. Gary Gilliland,D. Gary Gilliland,James D. Griffin,James D. Griffin +9 more
TL;DR: KPC412 is a potent inhibitor of mutant FLT3 and is a candidate for testing as an antileukemia agent in AML patients with mutantFLT3 receptors.
Journal ArticleDOI
Studies of FLT3 mutations in paired presentation and relapse samples from patients with acute myeloid leukemia: implications for the role of FLT3 mutations in leukemogenesis, minimal residual disease detection, and possible therapy with FLT3 inhibitors
Panagiotis D. Kottaridis,Rosemary E. Gale,Rosemary E. Gale,Stephen E. Langabeer,Stephen E. Langabeer,Marion E. Frew,Marion E. Frew,David T. Bowen,David T. Bowen,David C. Linch,David C. Linch +10 more
TL;DR: The results indicate that FLT3 mutations are secondary events in leukemogenesis, are unstable, and thus should be used cautiously for the detection of minimal residual disease.