Our Research
Cancer development occurs through sequential genomic, epigenomic and cellular state alterations, which converge to transform normal cells into malignant clones. While these steps can differ based on the cell of origin, tissue identity and specific somatic alterations, the ultimate result is the same — unchecked proliferation/growth, abnormal signaling/response to signals and aberrant cell identity / function.
The Miles lab is interested in understanding this processive development of cancer using acute myeloid leukemia (AML) as a model disease. AML is thought to develop through sequential mutagenic events culminating in the aberrant expansion of mutant, immature cells in lieu of mature, fully functioning blood cells. The mutational landscape of AML is well known; however, critical questions remain unanswered that we hope to help answer including: