Personalized medicine for AML?
Almost a decade ago, Gillil and proposed a model of leukemogenesis for acute myeloid leukemia (AML). In this model, AML results from activating mutations in genes that confer increased proliferation and survival capabilities (class I mutations) acting in concert with chromosomal abnormalities or gene mutations that block differentiation and subsequent apoptosis (class II mutations). In this issue of Blood, Bach as and colleagues present data that clearly demonstrate mutational shifts in class I/II genes that occur between diagnosis and relapse in children with AML. The authors suggest that these findings may allow for personalized treatment.
Cincinnati Children's Hospital Medical Center, OH, USA.
Franklin O
FO
Smith