Myeloproliferative neoplasm historical perspective: Difference between revisions
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__NOTOC__ | __NOTOC__ | ||
{{Myeloproliferative disease}} | {{Myeloproliferative disease}} | ||
{{CMG}} | {{CMG}}{{AE}} {{MJK}} | ||
==Overview== | |||
Myeloproliferative disease was first discovered by [[William Dameshek]], a hematologist, in 1951.<ref>{{cite journal |author = Dameshek W | title = Some speculations on the myeloproliferative syndromes. | journal = Blood | volume = 6 | issue = 4 | pages = 372-5 | year = 1951 | id = PMID 14820991}}</ref> | |||
==Historical Perspective== | ==Historical Perspective== | ||
The concept of myeloproliferative disease was first proposed in 1951 by the eminent hematologist [[William Dameshek]].<ref>{{cite journal |author = Dameshek W | title = Some speculations on the myeloproliferative syndromes. | journal = Blood | volume = 6 | issue = 4 | pages = 372-5 | year = 1951 | id = PMID 14820991}}</ref> In 2005, the discovery of the JAK2 V617F mutation provided some evidence to suggest a common pathogenesis for the Philadelphia Chromosome negative MPDs.<ref>{{cite journal | author = Baxter EJ, Scott LM, Campbell PJ, et al. | title = Acquired mutation of the tyrosine kinase JAK2 in human myeloproliferative disorders. | journal = Lancet | volume = 365 | pages = 1054-1061 | year = 2005 | id = PMID 15781101}}</ref><ref>{{cite journal | author = James C, Ugo V, Le Couedic JP, et al. | title = A unique clonal JAK2 mutation leading to constitutive signalling causes polycythaemia vera. | journal = Nature | volume = 434 | issue = 7037 | pages = 1144–1148 | year = 2005 | id =PMID 15793561}}</ref><ref>{{cite journal | author = Levine RL, Wadleigh M, Cools J, et al. | title = Activating mutation in the tyrosine kinase JAK2 in polycythemia vera, essential thrombocythemia, and myeloid metaplasia with myelofibrosis | journal = Cancer Cell | volume = 7 |issue = 4 | pages = 387–397 | year = 2005 | id = PMID 15837627}}</ref><ref>{{cite journal | author = Kralovics R, Passamonti F, Buser AS, et al. | title = A gain-of-function mutation of JAK2 in myeloproliferative disorders | journal = N Engl J Med | volume = 352 | issue = 17 | pages = 1779–1790 | year = 2005 | id = PMID 15858187}}</ref><ref>{{cite journal | author = Campbell PJ, Scott LM, Buck G, et al. | title = Definition of subtypes of essential thrombocythaemia and relation to polycythaemia vera based on JAK2 V617F mutation status: a prospective study | journal = Lancet | volume = 366 | issue = 9501 | pages = 1945–1953 | year = 2005 | id = PMID 16325696}}</ref> | The concept of myeloproliferative disease was first proposed in 1951 by the eminent hematologist [[William Dameshek]].<ref>{{cite journal |author = Dameshek W | title = Some speculations on the myeloproliferative syndromes. | journal = Blood | volume = 6 | issue = 4 | pages = 372-5 | year = 1951 | id = PMID 14820991}}</ref> In 2005, the discovery of the JAK2 V617F mutation provided some evidence to suggest a common pathogenesis for the Philadelphia Chromosome negative MPDs.<ref>{{cite journal | author = Baxter EJ, Scott LM, Campbell PJ, et al. | title = Acquired mutation of the tyrosine kinase JAK2 in human myeloproliferative disorders. | journal = Lancet | volume = 365 | pages = 1054-1061 | year = 2005 | id = PMID 15781101}}</ref><ref>{{cite journal | author = James C, Ugo V, Le Couedic JP, et al. | title = A unique clonal JAK2 mutation leading to constitutive signalling causes polycythaemia vera. | journal = Nature | volume = 434 | issue = 7037 | pages = 1144–1148 | year = 2005 | id =PMID 15793561}}</ref><ref>{{cite journal | author = Levine RL, Wadleigh M, Cools J, et al. | title = Activating mutation in the tyrosine kinase JAK2 in polycythemia vera, essential thrombocythemia, and myeloid metaplasia with myelofibrosis | journal = Cancer Cell | volume = 7 |issue = 4 | pages = 387–397 | year = 2005 | id = PMID 15837627}}</ref><ref>{{cite journal | author = Kralovics R, Passamonti F, Buser AS, et al. | title = A gain-of-function mutation of JAK2 in myeloproliferative disorders | journal = N Engl J Med | volume = 352 | issue = 17 | pages = 1779–1790 | year = 2005 | id = PMID 15858187}}</ref><ref>{{cite journal | author = Campbell PJ, Scott LM, Buck G, et al. | title = Definition of subtypes of essential thrombocythaemia and relation to polycythaemia vera based on JAK2 V617F mutation status: a prospective study | journal = Lancet | volume = 366 | issue = 9501 | pages = 1945–1953 | year = 2005 | id = PMID 16325696}}</ref> | ||
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Mohamad Alkateb, MBBCh [2]
Overview
Myeloproliferative disease was first discovered by William Dameshek, a hematologist, in 1951.[1]
Historical Perspective
The concept of myeloproliferative disease was first proposed in 1951 by the eminent hematologist William Dameshek.[2] In 2005, the discovery of the JAK2 V617F mutation provided some evidence to suggest a common pathogenesis for the Philadelphia Chromosome negative MPDs.[3][4][5][6][7]
References
- ↑ Dameshek W (1951). "Some speculations on the myeloproliferative syndromes". Blood. 6 (4): 372–5. PMID 14820991.
- ↑ Dameshek W (1951). "Some speculations on the myeloproliferative syndromes". Blood. 6 (4): 372–5. PMID 14820991.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.