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Molecular bases of myelodysplastic syndromes: Lessons from animal models
Author(s) -
Komeno Yukiko,
Kitaura Jiro,
Kitamura Toshio
Publication year - 2009
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.21739
Subject(s) - cytopenia , myelodysplastic syndromes , dysplasia , haematopoiesis , myeloid leukemia , biology , myeloid , leukemia , cancer research , runx1 , myeloproliferative disorders , bone marrow , stem cell , genetics , immunology
Myelodysplastic syndrome (MDS) is a clonal disorder of hematopietic stem cells characterized by ineffective hematopoiesis, peripheral blood cytopenia, morphologic dysplasia, and susceptibility to acute myeloid leukemia. Several mechanisms have been suggested as causes of MDS: unbalanced chromosomal abnormalities reflecting a gain or loss of chromosomal material, point mutations of transcription factors, and inactivation of p53. However, appropriate animal models that mimic MDS have long been lacking. We recently reported a novel murine model of MDS that recapitulates trilineage dysplasia and transformation to AML. In this review, we summarize the animal models of MDS and discuss the molecular bases of MDS as well as those of leukemia and myeloproliferative disorders (MPD). J. Cell. Physiol. 219: 529–534, 2009. © 2009 Wiley‐Liss, Inc.