نتایج جستجو برای: jak2v617f

تعداد نتایج: 776  

2012
Wanke Zhao Yanhong Du Wanting Tina Ho Xueqi Fu Zhizhuang Joe Zhao

UNLABELLED BACKGROUND JAK2V617F, a gain-of-function mutant form of tyrosine kinase JAK2, is found in the majority of patients with Ph- myeloproliferative neoplasms (MPNs), a group of chronic hematological diseases that often lead to acute leukemia. The current study is intended to find other gene mutations that collaborate with JAK2V617F to cause leukemic transformation. METHODS Total RNA ...

Journal: :Blood 2015
Takuro Kameda Kotaro Shide Takumi Yamaji Ayako Kamiunten Masaaki Sekine Yasuhiro Taniguchi Tomonori Hidaka Yoko Kubuki Haruko Shimoda Kousuke Marutsuka Goro Sashida Kazumasa Aoyama Makoto Yoshimitsu Taku Harada Hiroo Abe Tadashi Miike Hisayoshi Iwakiri Yoshihiro Tahara Mitsue Sueta Shojiro Yamamoto Satoru Hasuike Kenji Nagata Atsushi Iwama Akira Kitanaka Kazuya Shimoda

Acquired mutations of JAK2 and TET2 are frequent in myeloproliferative neoplasms (MPNs). We examined the individual and cooperative effects of these mutations on MPN development. Recipients of JAK2V617F cells developed primary myelofibrosis-like features; the addition of loss of TET2 worsened this JAK2V617F-induced disease, causing prolonged leukocytosis, splenomegaly, extramedullary hematopoie...

2015
Ipek Yonal-Hindilerden Aynur Daglar-Aday Basak Akadam-Teker Ceylan Yilmaz Meliha Nalcaci Akif Selim Yavuz Deniz Sargin

BACKGROUND Studies regarding the impact of JAK2V617F allele burden on phenotypic properties and clinical course in Philadelphia-negative myeloproliferative neoplasms (Ph-negative MPNs) have reported variable results. We aimed to analyze the association of mutated JAK2V617F allele burden with laboratory characteristics and clinical phenotype in Turkish patients (107 essential thrombocythemia (ET...

2013
L Ma J R Clayton R A Walgren B Zhao R J Evans M C Smith K M Heinz-Taheny E L Kreklau L Bloem C Pitou W Shen J M Strelow C Halstead M E Rempala S Parthasarathy J R Gillig L J Heinz H Pei Y Wang L F Stancato M S Dowless P W Iversen T P Burkholder

Owing to the prevalence of the JAK2V617F mutation in myeloproliferative neoplasms (MPNs), its constitutive activity, and ability to recapitulate the MPN phenotype in mouse models, JAK2V617F kinase is an attractive therapeutic target. We report the discovery and initial characterization of the orally bioavailable imidazopyridazine, LY2784544, a potent, selective and ATP-competitive inhibitor of ...

Journal: :Blood 2012
Hajime Akada Saeko Akada Ajeet Gajra Alicia Bair Stephen Graziano Robert E Hutchison Golam Mohi

The discovery of the JAK2V617F mutation in most patients with Ph-negative myeloproliferative neoplasms has led to the development of JAK2 kinase inhibitors. However, JAK2 inhibitor therapy has shown limited efficacy and dose-limiting hematopoietic toxicities in clinical trials. In the present study, we describe the effects of vorinostat, a small-molecule inhibitor of histone deacetylase, agains...

Journal: :Blood 2012
Jasper H Smalberg Lidia R Arends Dominique C Valla Jean-Jacques Kiladjian Harry L A Janssen Frank W G Leebeek

Myeloproliferative neoplasms (MPNs) are the most common cause of Budd-Chiari syndrome (BCS) and nonmalignant, noncirrhotic portal vein thrombosis (PVT). In this meta-analysis, we determined the prevalence of MPNs and their subtypes as well as JAK2V617F and its diagnostic role in these uncommon disorders. MEDLINE and EMBASE databases were searched. Prevalence of MPNs, JAK2V617F, and MPN subtypes...

Journal: :Blood 2010
Sivahari P Gorantla Tobias N Dechow Rebekka Grundler Anna Lena Illert Christian Meyer Zum Büschenfelde Marcus Kremer Christian Peschel Justus Duyster

The oncogenic JAK2V617F mutation is found in myeloproliferative neoplasms (MPNs) and is believed to be critical for leukemogenesis. Here we show that JAK2V617F requires an intact SH2 domain for constitutive activation of downstream signaling pathways. In addition, there is a strict requirement of cytokine receptor expression for the activation of this oncogene. Further analysis showed that the ...

Journal: :Proceedings of the National Academy of Sciences of the United States of America 2005
Xiaohui Lu Ross Levine Wei Tong Gerlinde Wernig Yana Pikman Sara Zarnegar D Gary Gilliland Harvey Lodish

A recurrent somatic activating mutation in the nonreceptor tyrosine kinase JAK2 (JAK2V617F) occurs in the majority of patients with the myeloproliferative disorders polycythemia vera, essential thrombocythemia, myelofibrosis with myeloid metaplasia, and, less commonly, chronic myelomonocytic leukemia. We do not understand the basis for the specificity of the JAK2V617F mutation in clonal disorde...

Journal: :Blood 2012
Dongqing Yan Robert E Hutchison Golam Mohi

The JAK2V617F mutation has been identified in most cases of Ph-negative myeloproliferative neoplasms (MPNs) including polycythemia vera (PV), essential thrombocythemia (ET), and primary myelofibrosis (PMF). Expression of JAK2V617F results in constitutive activation of multiple signaling molecules/pathways. However, the key signaling downstream of JAK2V617F required for transformation and induct...

2016
İpek Yönal Aynur Dağlar-Aday Başak Akadam-Teker Ceylan Yılmaz Meliha Nalçacı Akif Selim Yavuz Fatma Deniz Sargın

OBJECTIVE The JAK2V617F mutation is present in the majority of patients with essential thrombocythemia (ET) and primary myelofibrosis (PMF). The impact of this mutation on disease phenotype in ET and PMF is still a matter of discussion. This study aims to determine whether there are differences in clinical presentation and disease outcome between ET and PMF patients with and without the JAK2V61...

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