ABC2 Science Advisor Albert S. Baldwin has received a prestigious grant from the National Cancer Institute to support research considered to have breakthrough potential.
Baldwin, University of North Carolina Lineberger Comprehensive Cancer Center's associate director of basic research and the William Rand Kenan Professor of Biology at UNC, will receive nearly $5.9 million across seven years to study a cell signaling pathway called NF-kappaB that becomes dysregulated in many cancers. NCI designated its first class of award recipients in 2015.
“This grant gives us the freedom to take risks and to test innovative ideas that we probably wouldn’t have had the time or the funding to be able to do otherwise,” Baldwin said. “We are working to understand how NF-kappaB becomes activated by oncoproteins and by the loss of tumor suppressors, and how we can block its cancer-driving signaling with new drug approaches.”
Baldwin received his doctoral degree in biology from the University of Virginia in 1984. He went on to study gene expression as a postdoctoral research fellow at the Massachusetts Institute of Technology under the mentorship of Nobel Prize winner Phillip A. Sharp.
It was in Sharp’s laboratory that he began studying NF-kappaB, a transcription factor discovered at MIT in the laboratory of Nobel Laureate David Baltimore. Baldwin started his 27-year career at UNC in 1989. During that time, he has made significant contributions to the understanding of signaling pathways associated with NF-kappaB and to its role in both normal and cancer cells.
Normally, NF-kappaB plays an important role in immune cells to help them fight infection. In these cells, NF-kappaB promotes cell proliferation, survival and invasion to sites of infection. While those properties are critical in immune cells, those same functions are turned on abnormally to drive cancer cell growth.
“This pathway that does good things in an inflammatory cell to help the body fight disease gets co-opted to drive cancer,” Baldwin said. “In a normal immune cell, these functions become activated in response to infection, and then they’ll be turned off by a natural feedback process. The cancer cell is locked into this survival, proliferation and invasion program and can’t turn it off.”