Professor Irving Weissman, Stanford University

Single-cell genetic and epigenetic determinants of developmental potential

Characterization of Extracellular Vesicles Isolated from Canine Placental-derived Mesenchymal Stem/Stromal Cells

The essence of a cell’s identity and function lies in its transcriptomic landscape, including the variety of protein isoforms that arise from alternative splicing (AS). Of all protein-coding genes in the human genome, greater than 90% undergo post-translational AS, giving rise to many unique isoforms from a single gene. Through rearrangement of functional domains prior to translation, AS allows a single gene to encode a variety of proteins that may function in varying degrees of similarity or differ entirely in their activity.

Diffuse intrinsic pontine gliomas (DIPG) are the leading cause of childhood brain cancer-related deaths and have limited therapeutic options. A novel approach to treating DIPG is CAR T-cell therapy, a therapy already in use for acute lymphoblastic leukemia (ALL). Patients that undergo CAR T-cell therapy often experience important side effects, including cognitive dysfunction. Here we sought to understand how cancer immunotherapy impairs cognition, and how to restore cognition following CAR T-cell therapy.

Deciphering the Crosstalk within Human Coranary Atherosclerosic Plaques

Developing a three-dimensional culture system to improve the yield of placental mesenchymal stem cell derived extracellular vesicles

Reducing polyamine levels favors osteogenic differentiation of MSCs

Understanding the origins of hematopoietic stem cells has been a challenge due to the lack of a marker specific to this cell type. Recently, our lab has functionally proven that HoxB5 is a unique marker for long-term HSCs in adult murine models. Whether HoxB5 is also a marker for HSCs in development, has not been studied. Here, we are labeling HoxB5+ cells found in the yolk sac blood islands at E7.5 by using a genetic tool we generated. We will then analyze all marked cells at several time points during development and in adulthood.

Acute Myeloid Leukemia (AML) is an aggressive cancer of the bone marrow that results from the uncontrolled growth of abnormal hematopoietic stem cell (HSC) populations. The goal of this project is to characterize the mechanisms for the transformation of genetically engineered human primary HSCs to AML. My aim is to validate FLT3-ITD CRISPR-Cas9 reagents to contribute to the sequential editing matrix scheme of the larger project of investigating preleukemic stem cells as therapeutic targets in AML.