Clonal hematopoiesis in familial polycythemia vera suggests the involvement of multiple mutational events in the early pathogenesis of the disease
Author:
Affiliation:
1. From the Department of Research, Experimental Hematology, Basel University Hospital, Basel, Switzerland; and the Departments of Molecular and Human Genetics, Medicine, and Ophthalmology, Baylor College of Medicine, Houston, TX.
Abstract
Publisher
American Society of Hematology
Subject
Cell Biology,Hematology,Immunology,Biochemistry
Link
http://ashpublications.org/blood/article-pdf/102/10/3793/1690792/h82203003793.pdf
Reference21 articles.
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2. Prchal JF, Axelrad AA. Bone-marrow responses in polycythemia vera [letter]. N Engl J Med.1974;290: 1382.
3. Sokol L, Luhovy M, Guan Y, Prchal JF, Semenza GL, Prchal JT. Primary familial polycythemia: a frameshift mutation in the erythropoietin receptor gene and increased sensitivity of erythroid progenitors to erythropoietin. Blood.1995;86: 15-22.
4. Liu E, Jelinek J, Pastore YD, Guan Y, Prchal JF, Prchal JT. Discrimination of polycythemias and thrombocytoses by novel, simple, accurate clonality assays and comparison with PRV-1 expression and BFU-E response to erythropoietin. Blood.2003;101: 3294-3301.
5. Shih LY, Lee CT. Identification of masked polycythemia vera from patients with idiopathic marked thrombocytosis by endogenous erythroid colony assay. Blood.1994;83: 744-748.
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