References

1. Dameshek W: Some speculations on the myeloproliferative syndromes. Blood 6:372-375, 1951.

2. Vardiman JW, Harris NL, Brunning RD: The World Health Organization (WHO) classification of the myeloid neoplasms. Blood 100(7):2292-2302, 2002.

3. Baxter EJ, Scott LM, Campbell PJ, et al.: Acquired mutation of the tyrosine kinase JAK2 in human myeloproliferative disorders. Lancet 365(9464):1054-1061, 2005.

4. James C, Ugo V, Le Couedic JP, et al.: A unique clonal JAK2 mutation leading to constitutive signalling causes polycythaemia vera. Nature 434(7038):1144-1148, 2005.

5. Kralovics R, Passamonti F, Buser AS, et al.: A gain-of-function mutation of JAK2 in myeloproliferative disorders. N Engl J Med 352(17):1779-1790, 2005.

6. Levine RL, Wadleigh M, Cools J, et al.: Activating mutation in the tyrosine kinase JAK2 in polycythemia vera, essential thrombocythemia, and myeloid metaplasia with myelofibrosis. Cancer Cell 7(4):387-397, 2005.

7. Zhao R, Xing S, Li Z, et al.: Identification of an acquired JAK2 mutation in Polycythemia vera. J Biol Chem 286(24):22788-22792, 2005.

features resemble CML, but an increase in monocytes is the feature which suggests atypical rather than typical CML. In common with CMML, karyotypic abnormalities are frequent in atypical CML, occurring in 30-80%,78 +8 being the most frequent. Interestingly, a fusion gene between PDGFRß and H4 has been reported in at least one patient.79

0 0

Post a comment