Acute Myeloid Leukemia is one of the most common and deadly hematopoietic malignancies in older adults, with its incidence increasing with age. Why do older patients with AML have such a poor prognosis over their younger counterparts? To answer this question, we are using AML as a prototype to explore the relationship of aging and malignant transformation, and how aging may be changing the biology of the hematopoietic diseases in older adults.
We are exploring these ideas by comparing the molecular biology of AML in younger and older patients through two methods. First, we are examining known molecular pathways involved in its biology such as the FLT3/RAS/ERK pathway. Second, we are developing novel statistical approaches to model gene associations in AML and normal hematopoietic progenitor cells using microarrays and next generation sequencing.
We then compare how these relationships break down in the malignant state. Both approaches will provide a better understanding of how individual gene pathways and their functional properties may be responsible for the development of the disease and clinical outcomes. Along with these studies, we are also investigating the importance of separating individual malignant cell populations to further strengthen clinical significance.