Myelofibrosis pathophysiology
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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
Genes involved in the pathogenesis of myelofibrosis include JAK2, CALR, and MPL.[1]
Pathophysiology
- Bone marrow is replaced with collagen fibrosis due to cytokines, which are released from abnormal hematopoietic cells.
- Bone marrow is not able to make enough blood cells.
- Anemia, bleeding tendency, and infections may occur.
- Extramedullary hematopoiesis takes place, which causes hepatomegaly and splenomegaly.
- Secondary myelofibrosis may be caused by other blood malignancies, such as leukemia and lymphoma.
Genetics
Genes involved in the pathogenesis of myelofibrosis include JAK2, CALR, and MPL.[1][2][3]
References
- ↑ 1.0 1.1 Tefferi, A; Lasho, T L; Finke, C M; Knudson, R A; Ketterling, R; Hanson, C H; Maffioli, M; Caramazza, D; Passamonti, F; Pardanani, A (2014). "CALR vs JAK2 vs MPL-mutated or triple-negative myelofibrosis: clinical, cytogenetic and molecular comparisons". Leukemia. 28 (7): 1472–1477. doi:10.1038/leu.2014.3. ISSN 0887-6924.
- ↑ Baxter EJ, Scott LM, Campbell PJ; et al. (2005). "Acquired mutation of the tyrosine kinase JAK2 in human myeloproliferative disorders". Lancet. 365 (9464): 1054–61. doi:10.1016/S0140-6736(05)71142-9. PMID 15781101.
- ↑ Pikman Y, Lee BH, Mercher T; et al. (2006). "MPLW515L is a novel somatic activating mutation in myelofibrosis with myeloid metaplasia". PLoS Med. 3 (7): e270. doi:10.1371/journal.pmed.0030270. PMC 1502153. PMID 16834459. Unknown parameter
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