"We hope to use these models to understand how mutations in the EGFR gene initiate lung tumors, which are the most common cause of cancer mortality . In addition, these models will allow us to evaluate the effectiveness of new drugs and drug combinations and to study the molecular basis of resistance to existing tyrosine kinase inhibitors," explains Dr. Politi.

Lung cancer patients who harbor mutations in the human epidermal growth factor receptor (EGFR) gene generally have a better response to drugs that inhibit EGFR (like Iressa and Tarceva). Dr. Politi and colleagues have engineered a strain of mice with a mutated form of EGFR that can be turned on or off in lung cells at will. These inducible EGFR-mutant mice allow the researchers to evaluate the contribution of EGFR mutations to lung cancer formation, progression and response to chemotherapeutics.

The researchers found that mutations in EGFR drive lung tumorigenesis, and that either turning off the mutant EGFR gene or inhibiting it with drug can effectively force the tumors into regression. Thus, their model not only lends mechanistic insight into the genetic factors involved in lung cancer, but also serves as a paradigm to develop, test, and hopefully improve targeted cancer therapies.

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MCPIP is formed when an often-studied protein called MCP-1 binds to receptors. The MCP-1 protein helps to attract white blood cells known as monocytes to infected and injured areas of the body. The monocytes then attack bacteria and help the body fight diseases.

But that process also produces several known and unknown proteins. The researchers focused on MCPIP, one of the previously unknown proteins, because they discovered links between it and the deaths of healthy cells adjacent to the infected ones.

This finding could lead to advances in treating other inflammatory diseases such as arthritis and some forms of cancer.

Cardiovascular research is one of four main specialties at the Burnett College of Biomedical Sciences, which laid the foundation for the recently approved medical college at UCF. Kolattukudy began his research at Ohio State University before he moved to UCF in 2003.

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