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Revision as of 22:46, 29 October 2013

Myeloproliferative Neoplasm Microchapters

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Differentiating myeloproliferative neoplasm from other Diseases

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Pathophysiology

All MPDs arise from precursors of the "myeloid" lineage in the bone marrow.

Genetics

In 2005, the discovery of the JAK2 V617F mutation provided some evidence to suggest a common pathogenesis for the Philadelphia Chromosome negative MPDs.[1][2][3][4][5]

References

  1. Baxter EJ, Scott LM, Campbell PJ; et al. (2005). "Acquired mutation of the tyrosine kinase JAK2 in human myeloproliferative disorders". Lancet. 365: 1054–1061. PMID 15781101.
  2. James C, Ugo V, Le Couedic JP; et al. (2005). "A unique clonal JAK2 mutation leading to constitutive signalling causes polycythaemia vera". Nature. 434 (7037): 1144–1148. PMID 15793561.
  3. Levine RL, Wadleigh M, Cools J; et al. (2005). "Activating mutation in the tyrosine kinase JAK2 in polycythemia vera, essential thrombocythemia, and myeloid metaplasia with myelofibrosis". Cancer Cell. 7 (4): 387–397. PMID 15837627.
  4. Kralovics R, Passamonti F, Buser AS; et al. (2005). "A gain-of-function mutation of JAK2 in myeloproliferative disorders". N Engl J Med. 352 (17): 1779–1790. PMID 15858187.
  5. Campbell PJ, Scott LM, Buck G; et al. (2005). "Definition of subtypes of essential thrombocythaemia and relation to polycythaemia vera based on JAK2 V617F mutation status: a prospective study". Lancet. 366 (9501): 1945–1953. PMID 16325696.

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