As an assistant professor in the Department of Leukemia at MD Anderson Cancer Center, one of my primary research interests is in drug development in myeloid leukemias and conduct translational research that is aimed at understanding the mechanisms of sensitivity or resistance to such approaches. Through my prior training and as faculty at MD Anderson, I have had the opportunity to be actively involved in several phase I and phase II clinical trials and have also published about such trials, as well as present such data at important meetings like the American Society of Hematology (ASH), American Society of Clinical Oncology (ASCO), European Hematology Association (EHA) annual meetings. My primary focus of research has been in high-risk acute myeloid leukemia (AML) though I have worked on other subtypes of AML and conducted clinical research in other types of leukemia. I reported the phase I clinical trial of milademetan, a novel MDM2 inhibitor, in combination with venetoclax and low dose cytarabine in patients with relapsed/refractory (R/R) AML, and this work has been published in Blood Cancer Journal. I have also published in Clinical Cancer Research the phase I trial evaluating a novel bromodomain and extra terminal (BET) inhibitor, PLX 51107, in patients with R/R high-risk AML and myelodysplastic syndrome (MDS). I have published in Blood, a large retrospective study showing improved outcomes of patients with AML and splicing factor gene mutations when they are treated with venetoclax containing regimens. I reported at the ASH 2022 annual meeting the data on a novel combination of CPX-351 and gemtuzumab ozogamicin in patients with R/R AML or HR-MDS and showed early promising results. I have also been actively involved in the phase II clinical trial of magrolimab in combination with azacitidine and venetoclax in patients with AML, with a particular focus on patients with high-risk AML harboring TP53 aberrations.  With respect to core-binding factor AML (CBF-AML) I have reported one of the first data on the use of decitabine maintenance in patients with CBF-AML having inadequate response to intensive fludarabine based chemotherapy. Additionally, I have also reported on the impact of kinase mutations in CBF-AML and their effect on the cadence of molecular responses in these patients.

My ongoing work includes understanding the impact of additional myeloid mutations in patients with CBF-AML, the effect of aberrations in cohesin complex in patients with AML in the frontline and salvage settings. Additionally, my ongoing work also includes dissecting the outcomes of patients with AML and HR-MDS with TP53 aberrations, developing a clinical trial protocol for patients with TP53^Y220C mutation in myeloid malignancies amongst others. I am also interested in health equity and understanding the challenges of leukemia care in low-middle income countries.