Acute leukemia in infants (less than one year of age) is characterized by rearrangements of the Mixed Lineage Leukemia (MLL) gene (MLL-R) and a very poor survival. MLL-R leukemia can also be found in children above one year of age; these typically have a better survival. Thus, new therapeutic approaches are needed to improve the cure rates for these patients, in particular for infant ALL.
My research efforts focus on defining the landscape of epigenetic and genetic lesions that underlie pediatric MLL-R leukemia at diagnosis and at relapse. We use high-resolution genomic methods to identify aberrant genes and signaling pathways, in combination with murine models, to unravel their impact on tumor behavior. These studies will enhance our understanding of the differences between infant and non-infant MLL-R leukemia, and the nature of alterations that drive its development, and will increase our understanding about the genetic basis of relapse. In addition, we are interested in defining how distinct tumor clones cooperate to drive the growth of MLL-R leukemia, and the mechanisms behind clonal cooperation using murine models and in vitro assays to determine its biological significance. Our studies will advance our understanding of leukemogenesis, and may influence how leukemia is diagnosed, classified and treated in the future, and will help identify targets for novel treatment modalities.