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Laboratories, cancer researcher Stephen W. Fesik is excited about a compound that shows promise in enabling the body to activate a natural process to kill cancer cells.

Abbott's early-stage research on the drug has incorporated the use of pharmacogenomics, a science that identifies genetic factors that cause a drug to work or not work in certain patients.

Abbott's research has also been advanced by the use of so-called biomarkers -- indicators that can be measured via tests, such as the presence of certain proteins or enzymes.

WHAT IS BIO 2006?

The annual meeting of the Biotechnology Industry Organization runs through Wednesday at McCormick Place.

The gathering, which is closed to the general public, brings together more than 20,000 researchers, corporate executives, investors and regulators from 60 countries. They are the leading minds in the research and development of biotechnology products in health care, agriculture, industry and environment.

Pharmacogenomics and the use of biomarkers will be among the subjects of discussion at the Biotechnology Industry Organization 2006 convention under way here this week.

The science is aiding developers of tomorrow's medicines in selecting patients for clinical drug trials and in determining the dosage to give in those trials. It's also aiding them in determining which compounds are ineffective and shouldn't be pursued, explained Fesik, who will speak on the topics at the convention.

Abbott's research of cancer cells derived from patients has shown success in using its compound, called a "Bcl-2 inhibitor," to kill small cell lung cancer cells, and lymphoma and leukemia cancer cells -- but not all.

Through its research, Abbott discovered that if certain proteins called Bcl-2 and Bcl-xL are present in the cancer in large amounts, they block a process called apoptosis -- the body's natural process of destroying damaged cells. Abbott's compound binds to the proteins, enabling the destruction of cancer cells to take place.

In some cancer cells, the proteins are present at lower amounts. Another protein within the same family, called Mcl-1, is abundant, making its compound ineffective.

That discovery should aid the North Chicago-based medical products maker in conducting human clinical trials of the compound.

It might allow the company to predict that if a patient has large amounts of the Mcl-1 proteins, the patient is not likely to respond to treatment by the compound, Fesik said.

Such technology allows for improvement in the way drugs are tested, he said.

"Each patient that walks in the door has a different set of characteristics that define (his or her) individual cancer at the gene level," he said. "What we're trying to do is to figure out what those differences are at the molecular level, to understand what patients are going to be effectively treated by our agent.

"You don't want to be treating people with an agent when you're not going to be effectively treating the patient."

By identifying patients who are more likely to respond, the company should have greater response rates in its human clinical trials.

The technology should lead to more effective treatment, Fesik added.

"We'll know what patient should be getting the drug," he said. "When a patient comes in and says 'I have cancer. I have a lump' and the doctor examines that, instead of just saying 'Oh, you have breast cancer,' that cancer will be analyzed at the genomic level, providing a better understanding at the molecular level what's driving and what's really important to that cancer. This will allow us to more effectively treat that patient."

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