Abstract
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.
| Original language | English |
|---|---|
| Pages (from-to) | 4841-4851 |
| Number of pages | 11 |
| Journal | Blood |
| Volume | 111 |
| Issue number | 10 |
| DOIs | |
| State | Published - May 15 2008 |
| Externally published | Yes |
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ASJC Scopus subject areas
- Hematology
- Biochemistry
- Cell Biology
- Immunology
Cite this
Myelodysplastic syndromes. / Nimer, Stephen D.
In: Blood, Vol. 111, No. 10, 15.05.2008, p. 4841-4851.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Myelodysplastic syndromes
AU - Nimer, Stephen D
PY - 2008/5/15
Y1 - 2008/5/15
N2 - 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.
AB - 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.
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UR - http://www.scopus.com/inward/citedby.url?scp=46749151451&partnerID=8YFLogxK
U2 - 10.1182/blood-2007-08-078139
DO - 10.1182/blood-2007-08-078139
M3 - Article
C2 - 18467609
AN - SCOPUS:46749151451
VL - 111
SP - 4841
EP - 4851
JO - Blood
JF - Blood
SN - 0006-4971
IS - 10
ER -