Ami B. Patel, MD

• Chronic Myelomonocytic Leukemia

Dr. Ami Patel is an Assistant Professor of Medicine within the Division of Hematology and Hematologic Malignancies at the Huntsman Cancer Institute/University of Utah. She is a hematologist and physician-scientist with an NIH-funded independent translational research program investigating the biology of myeloid malignancies, specifically myeloid leukemogenesis as it relates to the intersection of inflammation, aging and oncogenic kinase signaling. Her clinical practice encompasses the diagnosis and treatment of myelodysplastic/myeloproliferative (MDS/MPN) overlap disorders, myeloproliferative neoplasms (MPNs), and acute myeloid leukemia (AML). Dr. Patel's research focuses on understanding cell signaling in myeloid leukemias and the molecular mechanisms governing drug resistance to targeted agents in these diseases. Her laboratory-based research complements her clinical practice by informing novel treatment strategies for implementation in early-phase clinical trials - with the goal of rapidly translating relevant preclinical findings and improving outcomes for leukemia patients. Dr. Patel's laboratory has specific expertise in studying resistance mechanisms to kinase inhibitors that act upon oncogenic kinases such as MEK1/2, BCR-ABL1, JAK2 and FLT3-ITD. Previously, she found that resistance to the FLT3 inhibitor quizartinib is mediated through soluble factors secreted by bone marrow stromal cells in AML (Patel et al, Leukemia, 2020). Dr. Patel has led the effort to functionally characterize a novel JAK2 insertion-deletion mutant associated with resistance to JAK2 inhibition and clinical features of both polycythemia and hypereosinophilia (Patel et al, Blood, 2019). She is the principal investigator on an investigator-initiated trial (NCT04409639) of the MEK inhibitor cobimetinib in RAS/MAPK-activated chronic myelomonocytic leukemia (CMML) that will help define the efficacy of RAS/MAPK inhibition in this disease and elucidate mechanisms of resistance to oncogenic RAS/MAPK signaling in myeloid leukemias.