نتایج جستجو برای: jak2v617f mutation

تعداد نتایج: 291772  

2016
Daria Sollazzo Dorian Forte Nicola Polverelli Marco Romano Margherita Perricone Lara Rossi Emanuela Ottaviani Simona Luatti Giovanni Martinelli Nicola Vianelli Michele Cavo Francesca Palandri Lucia Catani

Along with molecular abnormalities (mutations in JAK2, Calreticulin (CALR) and MPL genes), chronic inflammation is the major hallmark of Myelofibrosis (MF). Here, we investigated the in vitro effects of crucial factors of the inflammatory microenvironment (Interleukin (IL)-1β, Tumor Necrosis Factor (TNF)-α, Tissue Inhibitor of Metalloproteinases (TIMP)-1 and ATP) on the functional behaviour of ...

2012
Christoph Walz Wesam Ahmed Katherine Lazarides Monica Betancur Nihal Patel Lothar Hennighausen Virginia M. Zaleskas Richard A. Van Etten

STAT5 proteins are constitutively activated in malignant cells from many patients with leukemia, including the myeloproliferative neoplasms (MPNs) chronic myeloid leukemia (CML) and polycythemia vera (PV), but whether STAT5 is essential for the pathogenesis of these diseases is not known. In the present study, we used mice with a conditional null mutation in the Stat5a/b gene locus to determine...

2011
K L Rice X Lin K Wolniak B L Ebert W Berkofsky-Fessler M Buzzai Y Sun C Xi P Elkin R Levine T Golub D G Gilliland J D Crispino J D Licht W Zhang

Polycythemia vera (PV), essential thrombocythemia and primary myelofibrosis, are myeloproliferative neoplasms (MPNs) with distinct clinical features and are associated with the JAK2V617F mutation. To identify genomic anomalies involved in the pathogenesis of these disorders, we profiled 87 MPN patients using Affymetrix 250K single-nucleotide polymorphism (SNP) arrays. Aberrations affecting chr9...

Journal: :American Society of Clinical Oncology educational book. American Society of Clinical Oncology. Meeting 2013
Clodagh Keohane Ruben Mesa Claire Harrison

In 2005, the description of the JAK2V617F mutation for the first time provided a molecular key to enable more rapid diagnosis and target for novel therapeutics in the myeloproliferative neoplasms. In 2007, the first-in-class agent INC18424, ruxolitinib, JAKafi, or JAKAVI was first tested in patients with intermediate-risk 2 or high-risk myelofibrosis regardless of whether they possessed the JAK...

2012
Lasse Kjær Maj Westman Caroline Hasselbalch Riley Estrid Høgdall Ole Weis Bjerrum Hans Hasselbalch

Mutations in the Janus kinase 2 (JAK2) gene have become an important identifier for the Philadelphia-chromosome negative chronic myeloproliferative neoplasms. In contrast to the JAK2V617F mutation, the large number of JAK2 exon 12 mutations has challenged the development of quantitative assays. We present a highly sensitive real-time quantitative PCR assay for determination of the mutant allele...

Journal: :Blood 2016
Xénia Cabagnols Fabrizia Favale Florence Pasquier Kahia Messaoudi Jean Philippe Defour Jean Christophe Ianotto Christophe Marzac Jean Pierre Le Couédic Nathalie Droin Ilyas Chachoua Remi Favier M'boyba Khadija Diop Valérie Ugo Nicole Casadevall Najet Debili Hana Raslova Christine Bellanné-Chantelot Stefan N Constantinescu Olivier Bluteau Isabelle Plo William Vainchenker

Mutations in signaling molecules of the cytokine receptor axis play a central role in myeloproliferative neoplasm (MPN) pathogenesis. Polycythemia vera is mainly related to JAK2 mutations, whereas a wider mutational spectrum is detected in essential thrombocythemia (ET) with mutations in JAK2, the thrombopoietin (TPO) receptor (MPL), and the calreticulin (CALR) genes. Here, we studied the mutat...

Journal: :Hematology. American Society of Hematology. Education Program 2007
Alessandro M Vannucchi Tiziano Barbui

The aim of this review is to discuss current diagnostic approaches to, and classification of, patients presenting with thrombocytosis, in light of novel information derived from the discovery of specific molecular abnormalities in chronic myeloproliferative disorders (CMPD), which represent the most common cause of primary thrombocytosis. The JAK2V617F and the MPLW515L/K mutations have been fou...

Journal: :Blood 2009
Andrew D Wood Edwin Chen Ian J Donaldson Shilpa Hattangadi Karly A Burke Mark A Dawson Diego Miranda-Saavedra Harvey F Lodish Anthony R Green Berthold Göttgens

The discovery of JAK2V617F as an acquired mutation in the majority of patients with myeloproliferative disorders (MPDs) and the key role of the JAK2-STAT5 signaling cascade in normal hematopoiesis has focused attention on the downstream transcriptional targets of STAT5. Despite evidence of its vital role in normal erythropoiesis and its ability to recapitulate many of the features of myeloid ma...

2012
Fiorina Giona Luciana Teofili Maria Luisa Moleti Maurizio Martini Giovanna Palumbo Angela Amendola Maria Gabriella Mazzucconi Anna Maria Testi Patrizia Pignoloni Sonia Maria Orlando Sara Capodimonti Mauro Nanni Giuseppe Leone Luigi Maria Larocca Robin Foà

Sixty-four patients < 20 years of age, investigated for a suspicion of Philadelphianegative myeloproliferative disease (MPD), were retrospectively evaluated to characterize the different forms and to examine the treatments used and longterm outcome. JAK2 mutations, endogenous erythroid colony growth, and clonality were investigated in 51 children. Mutations of thrombopoietin, the thrombopoietin...

Journal: :Haematologica 2013
Sabine Jeromin Torsten Haferlach Vera Grossmann Tamara Alpermann Andreas Kowarsch Claudia Haferlach Wolfgang Kern Susanne Schnittger

Mutations of spliceosome genes were shown to occur frequently in different entities. Remarkably, mutations in SF3B1 (splicing factor 3b, subunit 1) were associated with the morphological feature of ring sideroblasts and were also found in refractory anemia with ring sideroblasts and marked thrombocytosis (RARS-T). This malignancy has been assigned as a provisional entity in the chapter “Myelody...

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