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Journal ArticleDOI

MPL mutations in myeloproliferative disorders: analysis of the PT-1 cohort.

TLDR
It is demonstrated that MPL mutations outside exon 10 are uncommon in platelet cDNA and 4 different exon10 mutations in granulocyte DNA from a retrospective cohort of 200 patients with ET or IMF are identified.
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This article is published in Blood.The article was published on 2008-07-01. It has received 386 citations till now. The article focuses on the topics: Essential thrombocythemia & Polycythemia vera.

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Novel mutations and their functional and clinical relevance in myeloproliferative neoplasms: JAK2 , MPL , TET2 , ASXL1 , CBL , IDH and IKZF1

Ayalew Tefferi
- 29 Apr 2010 - 
TL;DR: The functional consequences of MPN-associated mutations including unregulated JAK-STAT signaling, epigenetic modulation of transcription and abnormal accumulation of oncoproteins are not clear as to whether and how these abnormalities contribute to disease initiation, clonal evolution or blastic transformation.
Journal ArticleDOI

JAK/STAT signaling in hematological malignancies

TL;DR: The nature and respective contribution of mutations dysregulating the JAK/STAT pathway in hematological malignancies are discussed and examples in which such mutations drive the disease, contribute to the phenotype, or provide a survival and proliferative advantage are presented.
Journal ArticleDOI

Genetic basis and molecular pathophysiology of classical myeloproliferative neoplasms

TL;DR: The genetic landscape of classical myeloproliferative neoplasm (MPN) is in large part elucidated and factors other than somatic mutations play an important role in disease initiation as well as disease progression such as germ line predisposition, inflammation, and aging.
Journal ArticleDOI

New mutations and pathogenesis of myeloproliferative neoplasms.

TL;DR: Loss-of-function mutations in 3 genes involved in epigenetic regulation, TET2, ASXL1, and EZH2, may be early events preceding JAK2V617F but may also occur late during disease progression, and IZF1 deletions or TP53 mutations are mainly found at transformation phases and are present at greater frequency in de novo acute myeloid leukemias.
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Myeloproliferative Neoplasms: Molecular Pathophysiology, Essential Clinical Understanding, and Treatment Strategies

TL;DR: Oncologists on pathogenesis, contemporary diagnosis, risk stratification, and treatment strategies in BCR-ABL1-negative myeloproliferative neoplasms, including polycythemia vera (PV), essential thrombocythemia (ET), and primary myelofibrosis (PMF).
References
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Journal ArticleDOI

A Gain-of-Function Mutation of JAK2 in Myeloproliferative Disorders

TL;DR: Genetic evidence and in vitro functional studies indicate that V617F gives hematopoietic precursors proliferative and survival advantages and a high proportion of patients with myeloproliferative disorders carry a dominant gain-of-function mutation of JAK2.
Journal ArticleDOI

Acquired mutation of the tyrosine kinase JAK2 in human myeloproliferative disorders.

TL;DR: A single acquired mutation of JAK2 was noted in more than half of patients with a myeloproliferative disorder and its presence in all erythropoietin-independent erythroid colonies demonstrates a link with growth factor hypersensitivity, a key biological feature of these disorders.
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A unique clonal JAK2 mutation leading to constitutive signalling causes polycythaemia vera

TL;DR: A clonal and recurrent mutation in the JH2 pseudo-kinase domain of the Janus kinase 2 (JAK2) gene in most (> 80%) polycythaemia vera patients leads to constitutive tyrosine phosphorylation activity that promotes cytokine hypersensitivity and induces erythrocytosis in a mouse model.
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