Closing in on the pathogenesis of the 5q- syndrome.
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.
Post
Sean M
SM
University of Texas MD Anderson Cancer Center, 1515 Holcombe Boulevard, Unit 1010, Houston, TX 77030, USA. spost@mdanderson.org
Quintás-Cardama
Alfonso
A
D000748:Anemia, Macrocytic / Q000175:diagnosis / Q000209:etiology* / Q000235:genetics* / Q000473:pathology; D000818:Animals; D002895:Chromosomes, Human, Pair 5 / Q000235:genetics*; D017353:Gene Deletion; D016158:Genes, p53 / Q000235:genetics; D006801:Humans; D015470:Leukemia, Myeloid, Acute / Q000175:diagnosis / Q000209:etiology* / Q000235:genetics* / Q000473:pathology; D009190:Myelodysplastic Syndromes / Q000175:diagnosis / Q000209:etiology / Q000235:genetics / Q000473:pathology; D013577:Syndrome