Ann-Kathrin Eisfeld, MD

Acute myeloid leukemia (AML) is an aggressive blood cancer, of which only ~25% of patients are currently cured despite modern therapies. It became clear over the past years that the cancer cells of leukemia patients respond differently to available treatments based on differences in the molecular underpinnings of the cells. We recently performed the thus far largest study that examined the outcomes of Black patients diagnosed with AML compared to White patients with similar characteristics. Notably, both in a population-based study and in the setting of clinical trials, Black patients fared worse with ~40% higher chances to die from their disease compared to White patients. Unexpectedly, the survival discrepancy was highest in the molecular “favorable” risk group of patients harboring gene mutations in a gene called NPM1, thereby suggesting differences in disease biology that affect treatment response, and specifically the ability of standard chemotherapy to eradicate the leukemic clone based on the constitutional contributors associated with a patient’s race. Our proposal is designed to further understand the underlying mechanisms for the survival discrepancy and treatment response specifically in the “favorable” risk group, based on the overarching hypothesis that race-associated genetic features cause differential molecular/pathologic responses to treatment in Black and White AML patients.