EDITORIAL
Roads Diverge — A Robert Frost View of Leukemia Development
This article has no abstract; the first 100 words appear below.
Genomic studies have increased our understanding of the genetic basis for human cancers, including myeloid leukemias. In the past 5 years, our knowledge of the effect of key driver mutations has expanded and molecular genetic testing has become a mainstay of acute myeloid leukemia (AML) diagnosis and risk stratification and a guide for postremission therapy.1 However, our understanding of the ways in which various combinations of mutations can cooperate to induce the development of leukemia remains incomplete. In this issue of the Journal, Papaemmanuil and colleagues2 provide practice-changing insights that redefine molecular classification of AML and elucidate a deeper understanding . . .
Disclosure forms provided by the authors are available with the full text of this article at NEJM.org.
SOURCE INFORMATION
From the Human Oncology and Pathogenesis Program, Leukemia Service, Department of Medicine, Memorial Sloan Kettering Cancer Center, New York.
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