David Soto-Pantoja, Ph.D.

Funded by the Stuart Scott Memorial Cancer Research Fund

Our immune system operates on a balance of cells that can destroy infected or cancerous tissue and cells that prevent attacking healthy tissue. This balance is affected during cancer where cells that attack the tumor become inactivated. This allows further growth, cancer spread (metastasis) and eventual death of the patient. To address this problem researchers have developed drugs known as immune checkpoint inhibitors. These drugs activate T cells, a type of immune cell, to attack the tumor. Cancer patients treated with these drugs have seen major increases in survival. However, due to these drugs tipping the balance to a more active immune system, it can cause harmful side effects. These side effects cause interruptions in treatment plans which can result in disease progression. Currently, we do not have tests in the clinic that are able to predict these side effects. Therefore, there is an urgent need to understand how these side effects develop. Cancer cells consume abnormal levels of nutrients and release factors that can be sensed by blood circulating cells. We believe that these changes can be sensed by mitochondria. The mitochondria are organelles in cells that regulates energy metabolism. With new technological advancements, we can measure how this organelle changes in function in patients’ blood cells. We propose to test how patient blood cells energy changes. We predict that patients that develop side effects will have a lower cellular energy levels. Our study will provide a marker to predict side effects before they develop. We will also study genes that regulate cell energy metabolism to identify drug targets aimed at reducing the onset of side effects. Therefore, our studies will provide a personalized approach to cancer treatment to improve outcomes while preserving their quality of life.

Location: Comprehensive Cancer Center of Wake Forest University - North Carolina
Proposal: Metabolic & Immune Endpoints as Biomarkers of Immune Checkpoint Therapy Response
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