Abstract |
Evaluation of: Barlow JL, Drynan LF, Hewett DR et al. A p53-dependent mechanism underlies macrocytic anemia in a mouse model of human 5q- syndrome. Nat. Med. 16(1), 59-66 (2010); and Starczynowski DT, Kuchenbauer F, Argiropoulos B et al. Identification of miR-145 and miR-146a as mediators of the 5q- syndrome phenotype. Nat. Med. 16(1), 49-58 (2009). Patients with 5q- syndrome are characterized by macrocytic anemia, normal to elevated platelet counts, and a propensity to develop acute myeloid leukemia. The 5q- syndrome is believed to be a clonal disorder of the hematopoietic precursors. Until recently, little was known regarding the molecular pathogenesis of this malignancy. Two recently published studies using genetic approaches have unraveled a small array of genes whose alteration recapitulates critical features of the 5q- syndrome including dysplasia, clonal dominance, and progression to acute myeloid leukemia.
|
Authors | Sean M Post, Alfonso Quintás-Cardama |
Journal | Expert review of anticancer therapy
(Expert Rev Anticancer Ther)
Vol. 10
Issue 5
Pg. 655-8
(May 2010)
ISSN: 1744-8328 [Electronic] England |
PMID | 20469997
(Publication Type: Journal Article, Review)
|
Topics |
- Anemia, Macrocytic
(diagnosis, etiology, genetics, pathology)
- Animals
- Chromosomes, Human, Pair 5
(genetics)
- Gene Deletion
- Genes, p53
(genetics)
- Humans
- Leukemia, Myeloid, Acute
(diagnosis, etiology, genetics, pathology)
- Myelodysplastic Syndromes
(diagnosis, etiology, genetics, pathology)
- Syndrome
|