Closing in on the pathogenesis of the 5q- syndrome.

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