harles Giardina, an assistant professor of molecular and cell biology, has been awarded a $350,000 grant from the National Institutes of Health to investigate agents that augment the cell-death process, called apoptosis. His research could contribute to a deeper understanding of cancer biology.

Giardina, who came to UConn in 1998 from Cornell University, received the five-year grant as part of the New Investigator Award Program. It is his first NIH grant.

"This is major kudos for Charles," says David Knecht, head of the molecular and cell biology department's Cell Biology Program. "He is now one of the small select group of investigators on campus with an NIH award."

Giardina's research will explore the relationships between a number of chemopreventive agents in the human colon that have a role in sending signals to certain cells that it is time for them to die. Understanding the mechanism by which these agents kill colorectal cancer cells could lead to the development of more effective dietary guidelines and supplements, as well as chemotherapeutic agents to fight colon cancer.

The proper functioning of many tissues in the body requires an intricate balance between cell proliferation and programmed cell death (apoptosis). Comparing them to the leaves falling off a tree, Giardina explains that a healthy colon depends on a cycle of new cells being propagated, lasting five to seven days, and then undergoing apoptosis to be shed from the surface of the tissue.

Disturbing this sequence of events in the colon can result in cancer.

A number of colon cancer chemopreventive agents have been identified that appear to function, at least in part, by increasing cancer cell apoptosis. The most commonly known is aspirin, which reduces the risk of colon cancer by 50 percent. Another promising agent is found in fibrous foods such as grain cereals, common in many people's diets.

"But how these agents work to enhance cell death is not clear," Giardina says. "I want to study how these agents influence the activity of physiological death signals.

"That knowledge may provide valuable tools for the prevention and treatment of cancer, since these agents could rely on the body's ability to recognize transformed cells to target cell killing activity," he explains.

Giardina adds that a better understanding of how these agents sensitize cells to apoptotic signals could also facilitate the identification or design of pharmaceutical agents to trigger programmed cell death when medically desirable.

David Bauman