نتایج جستجو برای: jak2 v617f

تعداد نتایج: 4704  

Journal: :Blood 2011
Luciana Teofili Maurizio Martini Maria Grazia Iachininoto Sara Capodimonti Eugenia Rosa Nuzzolo Lorenza Torti Tonia Cenci Luigi Maria Larocca Giuseppe Leone

In this study we investigated whether neoplastic transformation occurring in Philadelphia (Ph)-negative myeloproliferative neoplasms (MPNs) could involve also the endothelial cell compartment. We evaluated the level of endothelial colony-forming cells (E-CFCs) in 42 patients (15 with polycythemia vera, 12 with essential thrombocythemia, and 15 with primary myelofibrosis). All patients had 1 mol...

2015
João Agostinho Machado-Neto Paula de Melo Campos Patricia Favaro Mariana Lazarini Adriana da Silva Santos Duarte Irene Lorand-Metze Fernando Ferreira Costa Sara Teresinha Olalla Saad Fabiola Traina

The JAK/STAT pathway is constitutively activated in myeloproliferative neoplasms and can be inhibited by ruxolitinib, a selective JAK1/2 inhibitor. The JAK2(V617F) mutation leads to constitutive STAT3 phosphorylation and potentially leads to inhibition of Stathmin 1 activity via STAT3. In support of this hypothesis, we found that, in HEL JAK2(V617F) cells, ruxolitinib treatment decreased STAT3 ...

2006
William Vainchenker

JAK2, an acquired mutation of JAK2, is present in a majority of patients with polycythemia vera and to a lesser extent among patients with the other myeloproliferative disorders. We analyzed the effect of JAK2 on the expression of polycythemia rubra vera 1(PRV-1), using an in vitro model. Compared to wild-type JAK2, the presence of JAK2 increased both PRV-1 protein and mRNA levels in murine mye...

Journal: :Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology 2009
Hajnalka Andrikovics Nora Meggyesi Aniko Szilvasi Julia Tamaska Gabriella Halm Sandor Lueff Sarolta Nahajevszky Miklos Egyed Judit Varkonyi Gabor Mikala Andrea Sipos Laszlo Kalasz Tamas Masszi Attila Tordai

Iron metabolism has been implicated in carcinogenesis and several studies assessed the potential role of genetic variants of proteins involved in iron metabolism (HFE C282Y, TFR S142G) in different malignancies. Few reports addressed this issue with relation to chronic myeloproliferative disorders (CMPD). The aims of our study were (a) to examine the potential associations of CMPD development w...

2009
Jan-Rung Mo Anjili Mathur Minilik Angagaw Shuxia Zhao Yuxun Wang Diana Gargano Alessandra DiBacco Eric S. Bachman

Splenic enlargement (splenomegaly) develops in numerous disease states, although a specific pathogenic role for the spleen has rarely been described. In polycythemia vera (PV), an activating mutation in Janus kinase 2 (JAK2(V617)) induces splenomegaly and an increase in hematocrit. Splenectomy is sparingly performed in patients with PV, however, due to surgical complications. Thus, the role of ...

2016
Goro Sashida Changshan Wang Takahisa Tomioka Motohiko Oshima Kazumasa Aoyama Akinori Kanai Makiko Mochizuki-Kashio Hironori Harada Kazuya Shimoda Atsushi Iwama

EZH2 is a component of polycomb repressive complex 2 (PRC2) and functions as an H3K27 methyltransferase. Loss-of-function mutations in EZH2 are associated with poorer outcomes in patients with myeloproliferative neoplasms (MPNs), particularly those with primary myelofibrosis (MF [PMF]). To determine how EZH2 insufficiency is involved in the pathogenesis of PMF, we generated mice compound for an...

2015
SHU-PENG ZHANG HUI LI REN-SHENG LAI

The Janus kinase (JAK)2 gene, which is located on chromosome 9p24, is involved in the signaling transduction pathways of the hematopoietic and immune system. Mutations in the JAK2 gene have served as disease markers for myeloproliferative neoplasms (MPNs). The aim of the present study was to investigate the occurrence of the JAK2 gene mutation in 140 clinical samples, and to evaluate its clinic...

Journal: :Blood 2013
Dominick Amato Chen Wang

The Janus kinase 2 (JAK2) V617F mutation is known to provide a growth and survival advantage to the affected clones of hematopoetic cells. It may result in clinical phenotypes of polycythemia vera, essential thrombocythemia, and primary myelofibrosis. Although constitutive JAK2 activation is largely responsible for developing myeloproliferative neoplasms (MPNs), an exaggeration of hematopoiesis...

2013
Joseph Saliba Sofiane Hamidi Gaëlle Lenglet Thierry Langlois Jingkui Yin Xénia Cabagnols Lise Secardin Céline Legrand Anne Galy Paule Opolon Baya Benyahia Eric Solary Olivier A. Bernard Longyun Chen Najet Debili Hana Raslova Françoise Norol William Vainchenker Isabelle Plo Antonio Di Stefano

JAK2(V617F) is the predominant mutation in myeloproliferative neoplasms (MPN). Modeling MPN in a human context might be helpful for the screening of molecules targeting JAK2 and its intracellular signaling. We describe here the derivation of induced pluripotent stem (iPS) cell lines from 2 polycythemia vera patients carrying a heterozygous and a homozygous mutated JAK2(V617F), respectively. In ...

Journal: :Hepatology 2006
Massimo Primignani Giovanni Barosi Gaetano Bergamaschi Umberto Gianelli Federica Fabris Raffaella Reati Alessandra Dell'Era Paolo Bucciarelli Pier Mannuccio Mannucci

The diagnosis of an underlying chronic myeloproliferative disorder (CMPD) is often problematic in patients with primary extrahepatic portal vein obstruction (EHPVO) or Budd-Chiari syndrome (BCS); indeed, conventional clinical and hematological parameters usually yield insufficient information. To assess the diagnostic contribution of the gain-of-function mutation V617F of the JAK2 gene, 93 pati...

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