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Blood, 15 May 2008, Vol. 111, No. 10, pp. 4841-4851. This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Nimer, S. D. Search for Related Content PubMed PubMed Citation Articles by Nimer, S. D. Related Collections Hematopoiesis and Stem Cells Neoplasia Free Research Articles ASH 50th Anniversary Reviews Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  ASH 50TH ANNIVERSARY REVIEW Myelodysplastic syndromes Stephen D. Nimer1 1 Division of Hematologic Oncology and Sloan-Kettering Institute, Memorial Sloan-Kettering Cancer Center, New York, NY There has been a remarkable explosion of knowledge into the molecular defects that underlie the acute and chronic leukemias, leading to the introduction of targeted therapies that can block key cellular events essential for the viability of the leukemic cell. Our understanding of the pathogenesis of the myelodysplastic syndromes (MDSs) has lagged behind, at least in part, because they represent a more heterogeneous group of disorders. The significant immunologic abnormalities described in this disease, coupled with the admixture of MDS stem or progenitor cells within the myriad types of dysplastic and normal cells in the bone marrow and peripheral blood, have made it difficult to molecularly characterize and model MDS. The recent availability of several, effective (ie, FDA-approved) therapies for MDS and newly described mouse models that mimic aspects of the human disease provide an opportune moment to try to leverage this new knowledge into a better understanding of and better therapies for MDS. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: M. L. Chen, T. D. Logan, M. L. Hochberg, S. G. Shelat, X. Yu, G. E. Wilding, W. Tan, G. C. Kujoth, T. A. Prolla, M. A. Selak, et al. Erythroid dysplasia, megaloblastic anemia, and impaired lymphopoiesis arising from mitochondrial dysfunction Blood, November 5, 2009; 114(19): 4045 - 4053. [Abstract] [Full Text] [PDF] O. Kosmider, V. Gelsi-Boyer, M. Cheok, S. Grabar, V. Della-Valle, F. Picard, F. Viguie, B. Quesnel, O. Beyne-Rauzy, E. Solary, et al. TET2 mutation is an independent favorable prognostic factor in myelodysplastic syndromes (MDSs) Blood, October 8, 2009; 114(15): 3285 - 3291. [Abstract] [Full Text] [PDF] T. A. Konrad, A. Karger, H. Hackl, I. Schwarzinger, I. Herbacek, and R. Wieser Inducible expression of EVI1 in human myeloid cells causes phenotypes consistent with its role in myelodysplastic syndromes J. Leukoc. Biol., October 1, 2009; 86(4): 813 - 822. [Abstract] [Full Text] [PDF] N. Goardon, E. Nikolousis, A. Sternberg, W.-K. Chu, C. Craddock, P. Richardson, R. Benson, M. Drayson, G. Standen, P. Vyas, et al. Reduced CD38 expression on CD34+ cells as a diagnostic test in myelodysplastic syndromes Haematologica, August 1, 2009; 94(8): 1160 - 1163. [Abstract] [Full Text] [PDF] K. I. Mills, A. Kohlmann, P. M. Williams, L. Wieczorek, W.-m. Liu, R. Li, W. Wei, D. T. Bowen, H. Loeffler, J. M. Hernandez, et al. Microarray-based classifiers and prognosis models identify subgroups with distinct clinical outcomes and high risk of AML transformation of myelodysplastic syndrome Blood, July 30, 2009; 114(5): 1063 - 1072. [Abstract] [Full Text] [PDF] W. R. Sperr, F. Wimazal, M. Kundi, C. Baumgartner, T. Nosslinger, A. Makrai, R. Stauder, O. Krieger, M. Pfeilstocker, and P. Valent Comorbidity as prognostic variable in MDS: comparative evaluation of the HCT-CI and CCI in a core dataset of 419 patients of the Austrian MDS Study Group Ann. Onc., July 15, 2009; (2009) mdp258v1. [Abstract] [Full Text] [PDF] R. M. Stone How I treat patients with myelodysplastic syndromes Blood, June 18, 2009; 113(25): 6296 - 6303. [Full Text] [PDF] F. Delhommeau, S. Dupont, V. D. Valle, C. James, S. Trannoy, A. Masse, O. Kosmider, J.-P. Le Couedic, F. Robert, A. Alberdi, et al. Mutation in TET2 in Myeloid Cancers N. Engl. J. Med., May 28, 2009; 360(22): 2289 - 2301. [Abstract] [Full Text] [PDF] L. Ades, S. Boehrer, T. Prebet, O. Beyne-Rauzy, L. Legros, C. Ravoet, F. Dreyfus, A. Stamatoullas, M. Pierre Chaury, J. Delaunay, et al. Efficacy and safety of lenalidomide in intermediate-2 or high-risk myelodysplastic syndromes with 5q deletion: results of a phase 2 study Blood, April 23, 2009; 113(17): 3947 - 3952. [Abstract] [Full Text] [PDF] M. Y. Follo, C. Finelli, C. Clissa, S. Mongiorgi, C. Bosi, G. Martinelli, M. Baccarani, L. Manzoli, A. M. Martelli, and L. Cocco Phosphoinositide-Phospholipase C {beta}1 Mono-Allelic Deletion Is Associated With Myelodysplastic Syndromes Evolution Into Acute Myeloid Leukemia J. Clin. Oncol., February 10, 2009; 27(5): 782 - 790. [Abstract] [Full Text] [PDF] N. S. Young Paroxysmal nocturnal hemoglobinuria and myelodysplastic sydromes: clonal expansion of PIG-A-mutant hematopoietic cells in bone marrow failure Haematologica, January 1, 2009; 94(1): 3 - 7. [Full Text] [PDF] C. N. Abboud Unlocking the dysplasia puzzle Blood, October 15, 2008; 112(8): 3005 - 3006. 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