Maria Figueroa, MD

Funded in partnership with Miami Dolphins Foundation

Like computers, the cells that make up our bodies also have specialized ‘software’ that runs their specific functions. When cells in the blood become cancerous -known as leukemia-, they hijack this biological software. By doing this, the leukemia cells can grow very fast and quickly multiply. Despite the many different types of leukemia that exist, they all share certain defects in their biological software. We call these shared defects a ‘biological common denominator’ across all of them. As part of this biological common denominator of leukemia we have identified the abnormal loss of PDZD2. Although PDZD2 is a gene capable of stopping the growth of other types of cancers it has never been studied in leukemia. Normally, PDZD2 is present in healthy blood cells. However, when blood cells become malignant, they lose PDZD2. We will explore how loss of PDZD2 helps turn healthy blood cells into leukemia. Importantly, we will determine if treatment of cells with a synthetic version of PDZD2 can help stop the growth of leukemia cells. Our long-term goal is to develop a novel way to treat patients with leukemia. We expect that this synthetic PDZD2 will kill the leukemia cells while having no effect on healthy blood cells.

Location: University of Miami, Sylvester Comprehensive Cancer Center - NC
Proposal: sPDZD2: A novel tumor suppressor in AML
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