I am an Associate Director, Translational Medicine Lead at AstraZeneca specializing in hematologic malignancies, building and leading end-to-end biomarker strategy across diagnostics and oncology drug development. Currently I direct biomarker programs at AstraZeneca Hematology R&D, serving as the functional lead at the intersection of translational biology, clinical development, computational/genomic data, and precision medicine. My track record translating preclinical mechanistic and genomic insights into regulatory-grade clinical biomarker evidence that drives dose selection, patient stratification, and go/no-go decisions — from first-in-human through registrational submissions. Deep companion diagnostic (CDx) expertise, including a role in an FDA-approved, commercially launched CDx. Skilled at leading cross-functional and external teams (CROs, CDx partners, regulatory bodies, and computational scientists) and communicating complex translational strategy to stakeholders at all levels, including health authorities.

I did my PhD work in the University of New Mexico’s Biomedical Sciences Graduate Program under the mentorship of Dr. Jennifer Gillette.

My dissertation project investigated the role of the tetraspanin CD82 in Acute Myeloid Leukemia (AML) chemosensitivity and disease relapse. AML is a cancer of blood cells of myeloid lineage that causes accumulation of white blood cells in the bone marrow, which interfere with the normal production of blood and immune cells. Relapse and resistance to therapeutics are among the most challenging obstacles in the management of AML. The interactions between AML cells and the bone marrow microenvironment are critical for AML disease progression and relapse. Interestingly, the membrane scaffolding protein CD82 is known to be involved in several biological processes including cell adhesion, migration, and survival. My central hypothesis was that CD82 expression in AML cells promotes chemoresistance and AML/bone marrow interactions contributing to minimal residual disease. My research assessed how CD82 regulates response to chemotherapeutics through modifications of downstream signaling molecules and interactions within the bone marrow.