ent, compared to control animals.
No one knows exactly how cromolyn works to control allergies. However, Dr. Logsdon has found that cromolyn can bind a specific protein produced by cancer cells and block that protein's ability to interact with a receptor that stimulates cancer cell growth, survival, and spreading. The relationship between how the drug controls allergies and its anti-tumor effect in pancreatic cancer remains unclear. "It may be possible that cromolyn has more than one target that influences cancer," he says.
Logsdon discovered the cancer-stimulating protein, determined how it triggers tumor growth and spread, and identified cromolyn as an inhibitor. "Through serendipity and basic science sleuthing we may now have something that helps patients," he says.
The study culminates Logsdon's five-year search for an agent to treat pancreatic cancer.
Logsdon searched for genes that produced proteins secreted only by cancer cells, which would then loop around and act on the cancer cell through a receptor on the cell surface. "That way, we could have two potential drug targets - the secreted protein and the receptor," he said.
Out of a long list of such genes, Logsdon and his research team selected one called "S100P" because it is a member of the large S100 gene family, some of which produce secreted proteins and some of which are associated with other cancers. Further work showed that S100P over-expression was very specific to pancreatic cancer; the protein was not found in normal pancreatic cells. "It is important to embryonic development, but no one knows its physiological role in adult biology," he says.
By using gene-silencing techniques, Logsdon found that when the protein is disabled, cancer growth is slowed. "S100P plays a role in tumor development because it causes cancer cells to grow faster, survive better, and be more invasive," he says.
Logsdon found that S100P interacts with a rePage: 1 2 3 Related medicine news :1
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