Clonal Architecture of Secondary Acute Myeloid Leukemia

Whole-genome sequencing of samples from seven subjects with secondary acute myeloid leukemia identified somatic mutations. These data, together with genotype analysis of the antecedent myelodysplastic syndromes (MDS), revealed the clonal evolution of MDS and secondary AML. The myelodysplastic syndro...

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Vydáno v:The New England journal of medicine Ročník 366; číslo 12; s. 1090 - 1098
Hlavní autoři: Walter, Matthew J, Shen, Dong, Ding, Li, Shao, Jin, Koboldt, Daniel C, Chen, Ken, Larson, David E, McLellan, Michael D, Dooling, David, Abbott, Rachel, Fulton, Robert, Magrini, Vincent, Schmidt, Heather, Kalicki-Veizer, Joelle, O'Laughlin, Michelle, Fan, Xian, Grillot, Marcus, Witowski, Sarah, Heath, Sharon, Frater, John L, Eades, William, Tomasson, Michael, Westervelt, Peter, DiPersio, John F, Link, Daniel C, Mardis, Elaine R, Ley, Timothy J, Wilson, Richard K, Graubert, Timothy A
Médium: Journal Article
Jazyk:angličtina
Vydáno: Waltham, MA Massachusetts Medical Society 22.03.2012
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ISSN:0028-4793, 1533-4406, 1533-4406
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Shrnutí:Whole-genome sequencing of samples from seven subjects with secondary acute myeloid leukemia identified somatic mutations. These data, together with genotype analysis of the antecedent myelodysplastic syndromes (MDS), revealed the clonal evolution of MDS and secondary AML. The myelodysplastic syndromes, a heterogeneous group of diseases characterized by ineffective hematopoiesis, are the most common cause of acquired bone marrow failure in adults. 1 Secondary acute myeloid leukemia (AML) develops in approximately one third of persons with myelodysplastic syndromes. 2 Clinical discrimination between the myelodysplastic syndromes and secondary AML currently rests predominantly on cytomorphologic analysis, since patients with myelodysplastic syndromes have dysplastic hematopoiesis and a myeloblast count of less than 20%, whereas those with a myeloblast count of 20% or more have AML. Although considerable overlap exists between the spectrum of cytogenetic and molecular lesions seen in the two disorders, there . . .
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Drs. Walter, Shen, and Ding contributed equally to this article
ISSN:0028-4793
1533-4406
1533-4406
DOI:10.1056/NEJMoa1106968