A Gain-of-Function Mutation ofJAK2in Myeloproliferative Disorders | Zendy

Róbert Královics | Zendy; Francesco Passamonti | Zendy; Andreas Buser | Zendy; Soon-Siong Teo | Zendy; Ralph Tiedt | Zendy; Jakob Passweg | Zendy; André Tichelli | Zendy; Mario Cazzola | Zendy; Radek C. Skoda | Zendy

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A Gain-of-Function Mutation ofJAK2in Myeloproliferative Disorders

Author(s) -

Róbert Královics,

Francesco Passamonti,

Andreas Buser,

Soon-Siong Teo,

Ralph Tiedt,

Jakob Passweg,

André Tichelli,

Mario Cazzola,

Radek C. Skoda

Publication year - 2005

Publication title -

new england journal of medicine

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 19.889

H-Index - 1030

eISSN - 1533-4406

pISSN - 0028-4793

DOI - 10.1056/nejmoa051113

Subject(s) - essential thrombocythemia , polycythemia vera , medicine , myelofibrosis , germline mutation , mutation , myeloproliferative disorders , cancer research , gastroenterology , biology , genetics , bone marrow , gene

Polycythemia vera, essential thrombocythemia, and idiopathic myelofibrosis are clonal myeloproliferative disorders arising from a multipotent progenitor. The loss of heterozygosity (LOH) on the short arm of chromosome 9 (9pLOH) in myeloproliferative disorders suggests that 9p harbors a mutation that contributes to the cause of clonal expansion of hematopoietic cells in these diseases.

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