JERELL AGUILA, PhD

Jerell R. Aguila, PhD
Research Assistant Professor
Basic Science Tower, Level 9
Stony Brook Medicine
Stony Brook, NY 11794-8691

Phone: (631) 444-1533
Fax: (631) 444-1566
Email: jerell.aguila@stonybrookmedicine.edu

Research Summary:
Hematopoietic stem cells (HSCs) are rare cells that have the unique ability to self-renew and differentiate into cells of all hematopoietic lineages. The expansion of HSCs has remained an important goal to develop advanced cell therapies for bone marrow transplantation and many blood disorders. During the last three decades, in which the first hematopoietic growth factors were identified, there have been numerous attempts to expand HSCs in vitro using purified growth factors that are known to regulate HSCs. However, these attempts have been met with limited success for clinical applications. An innovative approach is urgently needed for the research community to succeed in unraveling HSC expansion biology and creating a breakthrough in the ability to expand HSCs in vitro to clinically useful numbers. This would have tremendous impact in the areas of bone marrow transplantation and gene therapy for hematologic cancers and disorders. My expertise is in cancer biology, hematopoietic stem cells, and molecular biology. My research focuses on the role of the SALL4 gene in hematopoietic stem cells and the expansion of HSCs to develop advanced cell therapies for bone marrow transplantation and many blood cancers and disorders. My research deals with stem cell self renewal, proliferation, and differentiation. I am interested in optimizing a system utilizing a TAT-SALL4 fusion protein (SALL4 protein fused with the TAT cell-penetrating peptide) that has been shown to rapidly expand HSCs/HPCs, coupled with a stem cell-like niche extracellular matrix which may make it feasible to translate these finding into the clinical setting. I also have interest in working with both human embryonic stem cells and induced pluripotent stem cells. I played a key role in the first study to correct the phenotype of hemophilia A and diabetes in mouse model systems using iPS cells.

Peer Reviewed Publications: