JAK2V617F homozygosity arises commonly and recurrently in PV and ET, but PV is characterized by expansion of a dominant homozygous subclone. - Wikidata - wikimedia - TriplyDB

JAK2V617F homozygosity arises commonly and recurrently in PV and ET, but PV is characterized by expansion of a dominant homozygous subclone.

JAK2V617F homozygosity arises commonly and recurrently in PV and ET, but PV is characterized by expansion of a dominant homozygous subclone.

http://www.wikidata.org/entity/Q41545614

about

Somatic CALR mutations in myeloproliferative neoplasms with nonmutated JAK2 Polycythemia Vera: An Appraisal of the Biology and Management 10 Years After the Discovery of JAK2 V617F Myeloproliferative and thrombotic burden and treatment outcome of thrombocythemia and polycythemia patients Signal transduction in the chronic leukemias: implications for targeted therapies 2016 WHO Clinical Molecular and Pathological Criteria for Classification and Staging of Myeloproliferative Neoplasms (MPN) Caused by MPN Driver Mutations in the JAK2, MPL and CALR Genes in the Context of New 2016 WHO Classification: Prognostic and T JAK2V617F promotes replication fork stalling with disease-restricted impairment of the intra-S checkpoint response Clonal evolution revealed by whole genome sequencing in a case of primary myelofibrosis transformed to secondary acute myeloid leukemia Genetic variation at MECOM, TERT, JAK2 and HBS1L-MYB predisposes to myeloproliferative neoplasms.Clonal analyses reveal associations of JAK2V617F homozygosity with hematologic features, age and gender in polycythemia vera and essential thrombocythemia Acquired copy-neutral loss of heterozygosity of chromosome 1p as a molecular event associated with marrow fibrosis in MPL-mutated myeloproliferative neoplasms MicroRNAs in myeloproliferative neoplasms.Molecular determinants of pathogenesis and clinical phenotype in myeloproliferative neoplasms.JAK2 or CALR mutation status defines subtypes of essential thrombocythemia with substantially different clinical course and outcomes.Diagnosis, risk stratification, and response evaluation in classical myeloproliferative neoplasms.Inherited predisposition to myeloproliferative neoplasms Molecular classification of myeloproliferative neoplasms-pros and cons.What Do Molecular Tests Add to Prognostic Stratification in MF: Is It Time to Add These to Our Clinical Practice?Targeting glutamine metabolism in myeloproliferative neoplasms.BET protein inhibition shows efficacy against JAK2V617F-driven neoplasms.Myeloproliferative neoplasm stem cells.BLVRB redox mutation defines heme degradation in a metabolic pathway of enhanced thrombopoiesis in humans.Masked polycythaemia vera is genetically intermediate between JAK2V617F mutated essential thrombocythaemia and overt polycythaemia vera.JAK2V617F-mutant vascular niche contributes to JAK2V617F clonal expansion in myeloproliferative neoplasms.Nongenetic stochastic expansion of JAK2V617F-homozygous subclones in polycythemia vera?STAT1 activation in association with JAK2 exon 12 mutations.Myelofibrosis, JAK2 inhibitors and erythropoiesis.SOHO State-of-the-Art Update and Next Questions: MPN.Underlying mechanisms of the JAK2V617F mutation in the pathogenesis of myeloproliferative neoplasms.Apparent 'JAK2-negative' polycythaemia vera due to compound mutations in exon 14.A role for reactive oxygen species in JAK2 V617F myeloproliferative neoplasm progression.Mutations and long-term outcome of 217 young patients with essential thrombocythemia or early primary myelofibrosis.Use of the 46/1 haplotype to model JAK2(V617F) clonal architecture in PV patients: clonal evolution and impact of IFNα treatment.

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P2860

JAK2V617F homozygosity arises commonly and recurrently in PV and ET, but PV is characterized by expansion of a dominant homozygous subclone.

http://www.wikidata.org/entity/Q41545614

description

2012 nî lūn-bûn

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2012年の論文

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2012年論文

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2012年論文

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2012年論文

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2012年論文

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2012年論文

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2012年论文

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2012年论文

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2012年论文

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name

JAK2V617F homozygosity arises ...... dominant homozygous subclone.

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type

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JAK2V617F homozygosity arises ...... dominant homozygous subclone.

@en

prefLabel

JAK2V617F homozygosity arises ...... dominant homozygous subclone.

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BLOOD-2012-05-431791

P1433

P1476

JAK2V617F homozygosity arises ...... dominant homozygous subclone.

@en

P2093

Alessandro M Vannucchi

http://www.w3.org/2001/XMLSchema#string

Anna L Godfrey

http://www.w3.org/2001/XMLSchema#string

Anthony R Green

http://www.w3.org/2001/XMLSchema#string

Beatriz Bellosillo

http://www.w3.org/2001/XMLSchema#string

Carlos Besses

http://www.w3.org/2001/XMLSchema#string

Christina A Ortmann

http://www.w3.org/2001/XMLSchema#string

Claire N Harrison

http://www.w3.org/2001/XMLSchema#string

Edwin Chen

http://www.w3.org/2001/XMLSchema#string

Eric Lippert

http://www.w3.org/2001/XMLSchema#string

Fontanet Bijou

http://www.w3.org/2001/XMLSchema#string

P2860

JAK2 exon 12 mutations in polycythemia vera and idiopathic erythrocytosis

A unique clonal JAK2 mutation leading to constitutive signalling causes polycythaemia vera

Guideline for investigation and management of adults and children presenting with a thrombocytosis

Activating mutation in the tyrosine kinase JAK2 in polycythemia vera, essential thrombocythemia, and myeloid metaplasia with myelofibrosis

A gain-of-function mutation of JAK2 in myeloproliferative disorders

Acquired mutation of the tyrosine kinase JAK2 in human myeloproliferative disorders

Mutation in TET2 in myeloid cancers

JAK2V617F expression in murine hematopoietic cells leads to MPD mimicking human PV with secondary myelofibrosis.

Distinct clinical phenotypes associated with JAK2V617F reflect differential STAT1 signaling

X-inactivation-based clonality analysis and quantitative JAK2V617F assessment reveal a strong association between clonality and JAK2V617F in PV but not ET/MMM, and identifies a subset of JAK2V617F-negative ET and MMM patients with clonal hematopoies

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2704-2707

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scholarly article

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10.1182/BLOOD-2012-05-431791

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P433

13

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120

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Paola Guglielmelli

Konstanze Döhner

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2012-08-16T00:00:00Z

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230685166

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22898600

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3672970

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