1. Dinçol G, Pekçelen Y, Atamer T, et al. Klinik Hematoloji. Nobel TıpKitabevleri; 2003;(1)238-253.
2. Yönal İ, Sargın DF. Esansiyel trombositemi: patogenez, teşhis ve tedaviningüncellenmesi. İst Tıp Fak Derg. 2014;77(1):14-20.
3. Levine RL, Pardanani A, Tefferi A, Gilliland DG. Role of JAK2 in thepathogenesis and therapy of miyeloproliferative disorders. Nat RevCancer. 2007;7(9):673-83.
4. Kralovics R ve ark. A gain of function mutation of JAK2 inmyeloproliferative disorders. N Engl J Med. 2005;(352):1779-1790.
5. Berlin NI. Diagnosis and classification of the polycythemias. SeminHematol. 1975;(12):339-351.
6. Ruben A. Primary myelofibrosis (PMF), post polycythemia veramyelofibrosis (post-PV MF), post essential thrombocythemiamyelofibrosis (post-ET MF), blast phase PMF (PMF-BP): Consensuson terminology by the international working group for myelofibrosisresearch and treatment (IWGMRT). Leukemia research. 2007;(31):737-740.
7. Lasho TL, Pardanani A, McClure RF, et al. Concurrent MPL515and JAK2V617F mutations in myelofibrosis: chronology of clonalemergence and changesin mutant allele burden over time. Br J Haematol.2006;(135):683-687.
8. Michiels JJ, Thiele J. Clinical and pathological criteria for the diagnosisof essential thrombocythemia, polycythemia vera, and idiopathicmyelofibrosis (agnogenic myeloid metaplasia). Int J Hematol.2002;(76):133-145.
9. Baxter EJ, Scott LM, Campbell PJ, et al. Cancer Genome Project. Acquiredmutation of the tyrosine kinase JAK2 in human myeloproliferativedisorders. Lancet. 2005;(365):1054-1061.
10. Hsu HC. Pathogenetic role of JAK2 V617F mutation in chronicmyeloproliferative disorders. J Chin Med Assoc. 2007;(70):89-93.
11. Kralovics R, Passamonti F, Buser AS, et al. A gain-of-function mutation ofJAK2 in myeloproliferative disorders. N Engl J Med. 2005;(17):1779-1790.
12. James C, Ugo V, Le Couédic JP, et al. A unique clonal JAK2 mutationleading to constitutive signalling causes polycythaemia vera. Nature.2005;434(7037):1144-1148.
13. Smith, MJ, Koch GL. Multiple zones in the sequence of Kalretikülin(CRP55, calregulin, HACBP), a major calcium binding ER/SR protein.EMBO Journal. 1989;(8):3581-3586
14. Waisman DM, Salimath BP. Isolation and characterization of CAB-63, anovel calcium-binding protein. J Biol Chem. 1985;(260):1652-1660.
15. Michalak M, Corbett EF. Kalretikülin: one protein, one gene, manyfunctions. Biochem J.1999;(344):281-292.
16. Tefferi A, Wassie EA, Guglielmelli P. et al. Type 1 versus Type 2calreticulin mutations in essential thrombocythemia: a collaborativestudy of 1027 patients. Am J Hematol. 2014;89(8);121-124.
17. Vannucchi AM, Antonioli E, Guglielmelli P, Pardanani A, TefferiA. Clinical correlates of JAK2 V617F presence or allele burdenin myeloproliferative neoplasms: a critical reappraisal. Leukemia.2008;22(7):1299-1307.
18. Vannucchi AM, Antonioli E, Guglielmelli P, et al. Prospectiveidentification of high-risk polycythemia vera patients based on JAK2V617F allele burden. Leukemia. 2007;21(9):1952-1959.
19. Panani AD. Janus kinase 2 mutations in Philadelphia negative chronicmyeloproliferative disorders: Clinical implications. Cancer Lett. 2009;284(1):7-14.
20. Wong RS, Cheng CK, Chan NP, et al. JAK2 V617F mutation is associatedwith increased risk of thrombosis in Chinese patients with essentialthrombocythaemia. Br J Haematol. 2008;141(6):902-904.
21. Demir AK, Atay MH, Kelkitli E, Kurt YT, Özatlı D, Turgut M. KronikMiyeloproliferatif Hastalıklarda JAK2V617F Mutasyon Sıklığı. ÇağdaşTıp Derg. 2013;3(2):101-107.
22. Tefferi A. Polycythemia vera and essential thrombocythemia: 2012update on diagnosis, risk stratification, and management. Am J Hematol.2012;87(3):285-293
23. Passamonti F, Rumi E, Arcaini L, et al. Prognostic factors for thrombosis,myelofibrosis, and leukemia in essential thrombocythemia: a study of 605patients. Haematologica. 2008;93(11):1645-1651.
24. Lundberg P, Nienhold R, Ambrosetti A, et al. Somatic mutations inKalretikülin can be found in pedigrees with familial predisposition tomyeloproliferative neoplasms. Blood. 2014;(123):2744-2745.
25. Rumi E, Pietra D, Pascutto C, et al. Clinical effect of driver mutations ofJAK2 , CALR, or MPL in primary myelofibrosis. Blood. 2014;(124):1062-1069.
26. Klampfl T, Gisslinger H, Harutyunyan AS, et al. Somatic mutationsof Kalretikülin in myeloproliferative neoplasms. N Engl J Med.2013;(369):2379-2390.
27. Nangalia, J, Massie C.E, Baxter EJ, et al. Somatic CALR mutations inmyeloproliferative neoplasms with nonmutated JAK2. N Engl J Med.2013;369(25):2391-2405.
28. Cabagnols X, Defour JP, Ugo V, et al. Differential association ofKalretikülin type 1 and type 2 mutations with myelofibrosis andessential thrombocytemia: relevance for disease evolution. Leukemia.2015;29(1):249-252.