Epigenetic Regulation of the Immune Synapse in Melanoma
Abstract
Melanoma is a deadly skin cancer associated with sun exposure. As such, both active-duty Service Members and Veterans have increased risk of developing melanoma and there is significant unmet need to understand the underlying biology of this aggressive cancer. More recently, immunotherapy has redefined the way we treat melanoma, but majority of patients remain resistant, and understanding how tumors evade the immune system is of pivotal importance. Methylation is an epigenetic mechanism controlling gene expression by chemically modifying the DNA. Among various ways that melanoma suppresses our body’s immune system to escape immune killing, our recent studies have demonstrated methylation of genes involved in the interaction between tumor and the immune cells as crucial. In this context, we will address the Melanoma Research Program Focus Areas; Understanding the tumor microenvironment: Primary Tumor, Regional Nodes, Distal Nodes and Prevention of melanomagenesis and precursor lesions (e.g., novel genetic and epigenetic drivers, oncogene induced senescence). In other words, we will investigate how methylation modulates the tumor microenvironment to suppress the immune system from attacking the tumor. Further, the pattern of methylation in melanoma can also inform us it will respond to immunotherapy. These studies will be performed by analyzing the methylation patterns of tumor tissues obtained from melanoma patients treated with immunotherapy at the Moffitt Cancer Center and correlating with their clinical outcome following immunotherapy. The resultant methylation-based biomarker will be a valuable tool for clinicians to make optimal decisions in treating melanoma patients with immunotherapy.
Document Details
- Document Type
- DoD Grant Award
- Publication Date
- Dec 28, 2022
- Source ID
- W81XWH2210860
Entities
People
- Sungjune Kim
Organizations
- H. Lee Moffitt Cancer Center & Research Institute
- United States Army