نتایج جستجو برای: jak2 v617f

تعداد نتایج: 4704  

2014
Toshikage Nagao Tetsuya Kurosu Yoshihiro Umezawa Ayako Nogami Gaku Oshikawa Shuji Tohda Masahide Yamamoto Osamu Miura

The gain of function mutation JAK2-V617F is very frequently found in myeloproliferative neoplasms (MPNs) and is strongly implicated in pathogenesis of these and other hematological malignancies. Here we report establishment of a new leukemia cell line, PVTL-1, homozygous for JAK2-V617F from a 73-year-old female patient with acute myeloid leukemia (AML) transformed from MPN. PVTL-1 is positive f...

Journal: :The New England journal of medicine 2007
Linda M Scott Wei Tong Ross L Levine Mike A Scott Philip A Beer Michael R Stratton P Andrew Futreal Wendy N Erber Mary Frances McMullin Claire N Harrison Alan J Warren D Gary Gilliland Harvey F Lodish Anthony R Green

BACKGROUND The V617F mutation, which causes the substitution of phenylalanine for valine at position 617 of the Janus kinase (JAK) 2 gene (JAK2), is often present in patients with polycythemia vera, essential thrombocythemia, and idiopathic myelofibrosis. However, the molecular basis of these myeloproliferative disorders in patients without the V617F mutation is unclear. METHODS We searched f...

Journal: :Blood 2008
Sai Li Robert Kralovics Gennaro De Libero Alexandre Theocharides Heinz Gisslinger Radek C Skoda

We studied the lineage distribution of JAK2 mutations in peripheral blood of 8 polycythemia vera (PV) patients with exon 12 mutations and in 21 PV patients with JAK2-V617F. Using a quantitative allele discrimination assay, we detected exon 12 mutations in purified granulocytes, monocytes, and platelets of 8 patients studied, but lymphoid cells showed variable involvement and the mutation was ab...

Journal: :Medicina 2011
Ana Lisa Basquiera Aldo H Tabares Néstor Soria Miriam Salguero Ricardo Ryser Juan José García

We aimed to study patients with splanchnic vein thrombosis (SVT) and cerebral vein thrombosis (CVT) searching for JAK2 mutations. We evaluated 14 patients (median age: 41.5 years) with portal vein thrombosis (PVT) = 7; mesenteric vein thrombosis (MVT) = 3; and CVT = 4. JAK2 V617F was assessed by allele specific PCR of peripheral blood DNA. In addition, DNA was sequenced for other JAK2 mutations...

Journal: :Molecular cancer therapeutics 2010
Fabienne Baffert Catherine H Régnier Alain De Pover Carole Pissot-Soldermann Gisele A Tavares Francesca Blasco Josef Brueggen Patrick Chène Peter Drueckes Dirk Erdmann Pascal Furet Marc Gerspacher Marc Lang David Ledieu Lynda Nolan Stephan Ruetz Joerg Trappe Eric Vangrevelinghe Markus Wartmann Lorenza Wyder Francesco Hofmann Thomas Radimerski

The recent discovery of an acquired activating point mutation in JAK2, substituting valine at amino acid position 617 for phenylalanine, has greatly improved our understanding of the molecular mechanism underlying chronic myeloproliferative neoplasms. Strikingly, the JAK2(V617F) mutation is found in nearly all patients suffering from polycythemia vera and in roughly every second patient sufferi...

Journal: :Blood 2006
Peter J Campbell E Joanna Baxter Philip A Beer Linda M Scott Anthony J Bench Brian J P Huntly Wendy N Erber Rajko Kusec Thomas Stauffer Larsen Stéphane Giraudier Marie-Caroline Le Bousse-Kerdilès Martin Griesshammer John T Reilly Betty Y Cheung Claire N Harrison Anthony R Green

The identification of an acquired mutation of JAK2 in patients with myeloproliferative disorders has raised questions about the relationship between mutation-positive and mutation-negative subtypes, timing of the JAK2 mutation, and molecular mechanisms of disease progression. Here we demonstrate that patients with V617F(-) essential thrombocythemia do not commonly progress to become V617F(+). C...

Journal: :The Journal of biological chemistry 2008
Alexandra Dusa Judith Staerk Joanne Elliott Christian Pecquet Hélène A Poirel James A Johnston Stefan N Constantinescu

Explaining the uniqueness of the acquired somatic JAK2 V617F mutation, which is present in more than 95% of polycythemia vera patients, has been a challenge. The V617F mutation in the pseudokinase domain of JAK2 renders the unmutated kinase domain constitutively active. We have performed random mutagenesis at position 617 of JAK2 and tested each of the 20 possible amino acids for ability to ind...

Journal: :Molecular cancer therapeutics 2008
Jacqueline Sayyah Andrew Magis David A Ostrov Robert W Allan Raul C Braylan Peter P Sayeski

Jak2 tyrosine kinase is essential for animal development and hyperkinetic Jak2 function has been linked to a host of human diseases. Control of this pathway using Jak2-specific inhibitors would therefore potentially serve as a useful research tool and/or therapeutic agent. Here, we used a high-throughput program called DOCK to predict the ability of 20,000 small molecules to interact with a str...

Journal: :Experimental hematology 2015
Anthony D Pomicter Anna M Eiring Anna V Senina Matthew S Zabriskie James E Marvin Josef T Prchal Thomas O'Hare Michael W Deininger

Activation of Janus kinase 2 (JAK2), frequently as a result of the JAK2(V617F) mutation, is a characteristic feature of the classical myeloproliferative neoplasms (MPNs) polycythemia vera, essential thrombocythemia, and myelofibrosis, and it is thought to be responsible for the constitutional symptoms associated with these diseases. BMS-911543 is a JAK2-selective inhibitor that induces apoptosi...

2015
Sang Hyuk Park Shine Young Kim Sun Min Lee Jongyoun Yi In-Suk Kim Hyung Hoi Kim Chulhun Ludgerus Chang Eun Yup Lee Moo-Kon Song Ho-Jin Shin Joo Seop Chung

We evaluated the incidence, clinical characteristics, and prognostic impact of calreticulin (CALR) mutations in essential thrombocythemia (ET) and primary myelofibrosis (PMF) patients. In all, 48 ET and 14 PMF patients were enrolled, and the presence of CALR mutations was analyzed by direct sequencing. Patients were classified into three subgroups according to Janus kinase 2 (JAK2) V617F and CA...

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