Altered gene expression in myeloproliferative disorders correlates with activation of signaling by the V617F mutation of Jak2.
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Therapeutic approaches in myelofibrosis and myelodysplastic/myeloproliferative overlap syndromesMicroarray and Proteomic Analyses of Myeloproliferative Neoplasms with a Highlight on the mTOR Signaling PathwayJAK and MPL mutations in myeloid malignancies.Integrated genomic analysis illustrates the central role of JAK-STAT pathway activation in myeloproliferative neoplasm pathogenesis.Mechanistic insights into activation and SOCS3-mediated inhibition of myeloproliferative neoplasm-associated JAK2 mutants from biochemical and structural analysesAML1 is overexpressed in patients with myeloproliferative neoplasms and mediates JAK2V617F-independent overexpression of NF-E2Distinct clinical phenotypes associated with JAK2V617F reflect differential STAT1 signalingProteomic analysis reveals heat shock protein 70 has a key role in polycythemia Vera.Inflammation and thrombosis in essential thrombocythemia and polycythemia vera: different role of C-reactive protein and pentraxin 3.Interferon-alpha targets JAK2V617F-positive hematopoietic progenitor cells and acts through the p38 MAPK pathway.A novel model for IFN-γ-mediated autoinflammatory syndromes.Cell death induced by the Jak2 inhibitor, G6, correlates with cleavage of vimentin filaments.Deregulation of apoptosis-related genes is associated with PRV1 overexpression and JAK2 V617F allele burden in Essential Thrombocythemia and Myelofibrosis.JAK2 V617F: a single mutation in the myeloproliferative group of disordersProteomic approaches to dissect platelet function: Half the story.JAK Kinases in Health and Disease: An UpdateImpact of JAK2V617F Mutation Burden on Disease Phenotype in Chinese Patients with JAK2V617F-positive Polycythemia Vera (PV) and Essential thrombocythemia (ET)JAK2 Allele Burden in the Myeloproliferative Neoplasms: Effects on Phenotype, Prognosis and Change with Treatment.Development of new cancer therapeutic agents targeting mitosis.The chronic myeloproliferative disorders and mutation of JAK2: Dameshek's 54 year old speculation comes of age.A3669G polymorphism of glucocorticoid receptor is a susceptibility allele for primary myelofibrosis and contributes to phenotypic diversity and blast transformation.Histological and molecular classification of chronic myeloproliferative disorders in the age of JAK2: persistence of old questions despite new answers.Clinical correlates of JAK2V617F presence or allele burden in myeloproliferative neoplasms: a critical reappraisal.Genetic complexity of myeloproliferative neoplasms.NF-E2 overexpression delays erythroid maturation and increases erythrocyte production.Molecular drug targets in myeloproliferative neoplasms: mutant ABL1, JAK2, MPL, KIT, PDGFRA, PDGFRB and FGFR1.The JAK2V617 mutation induces constitutive activation and agonist hypersensitivity in basophils from patients with polycythemia veraPerspectives for the use of structural information and chemical genetics to develop inhibitors of Janus kinasesA structure-function perspective of Jak2 mutations and implications for alternate drug design strategies: the road not taken.Oncogenic Drivers in Myeloproliferative Neoplasms: From JAK2 to Calreticulin Mutations.How We Identify and Manage Patients with Inadequately Controlled Polycythemia Vera.The Association Between JAK2V617F Mutation and Bone Marrow Fibrosis at Diagnosis in Patients with Philadelphia-Negative Chronic Myeloproliferative Neoplasms.Inhibition of related JAK/STAT pathways with molecular targeted drugs shows strong synergy with ruxolitinib in chronic myeloproliferative neoplasm.Coexistence of lymphoproliferative and myeloproliferative neoplasms with simultaneous CALR and JAK2 V617F mutations.Targeted cancer exome sequencing reveals recurrent mutations in myeloproliferative neoplasms.Transcriptional profiling of polycythemia vera identifies gene expression patterns both dependent and independent from the action of JAK2V617F.SOCS-mediated downregulation of mutant Jak2 (V617F, T875N and K539L) counteracts cytokine-independent signaling.Analysis of genomic aberrations and gene expression profiling identifies novel lesions and pathways in myeloproliferative neoplasms.Mesenchymal stromal cells (MSC) from JAK2+ myeloproliferative neoplasms differ from normal MSC and contribute to the maintenance of neoplastic hematopoiesis.Transcriptional profiling of whole blood identifies a unique 5-gene signature for myelofibrosis and imminent myelofibrosis transformation.
P2860
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P2860
Altered gene expression in myeloproliferative disorders correlates with activation of signaling by the V617F mutation of Jak2.
description
2005 nî lūn-bûn
@nan
2005年の論文
@ja
2005年学术文章
@wuu
2005年学术文章
@zh
2005年学术文章
@zh-cn
2005年学术文章
@zh-hans
2005年学术文章
@zh-my
2005年学术文章
@zh-sg
2005年學術文章
@yue
2005年學術文章
@zh-hant
name
Altered gene expression in mye ...... by the V617F mutation of Jak2.
@en
Altered gene expression in mye ...... by the V617F mutation of Jak2.
@nl
type
label
Altered gene expression in mye ...... by the V617F mutation of Jak2.
@en
Altered gene expression in mye ...... by the V617F mutation of Jak2.
@nl
prefLabel
Altered gene expression in mye ...... by the V617F mutation of Jak2.
@en
Altered gene expression in mye ...... by the V617F mutation of Jak2.
@nl
P2093
P50
P1433
P1476
Altered gene expression in mye ...... by the V617F mutation of Jak2
@en
P2093
Andre Tichelli
Andreas S Buser
Mario Cazzola
Radek C Skoda
Ralph Tiedt
Soon-Siong Teo
P304
P356
10.1182/BLOOD-2005-05-1889
P407
P577
2005-08-04T00:00:00Z