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NDSU researcher studies why cells die

In the time it takes to read this sentence, approximately 4 million of your body’s cells have died. Approximately 4 million cells also have been created to replace them. 

It’s the mechanisms behind this orderly cell death and creation that John Wilkinson, assistant professor of chemistry and biochemistry, is studying in hopes of one day curing cancer.

Cancer develops when cells lose control of normal biochemical processes. Wilkinson’s lab examines how two such processes, cellular metabolism and the cellular suicide process known as apoptosis, contribute to the growth of cancer and other human diseases.

Cell death is controlled by certain types of molecules. Some molecules – proteins, in particular – can keep cancer cells alive longer than they should. Wilkinson is studying how a protein called apoptosis-inducing factor and its cellular partners work together to help prostate cancer cells grow.

His project is one of 82 studies funded by the American Cancer Society aimed at understanding how prostate cancer develops, the details of which remain somewhat of a mystery.

“Cancer isn’t one disease,” Wilkinson said. “Cancer is 1,000 different diseases. The challenge is figuring out how to identify in any one specific patient what kind of cancer they actually have, and then, based on that identification, how to tailor therapy in order to achieve the best possible outcome for that particular patient.”

Wilkinson discovered that advanced prostate cancer cells contain more apoptosis-inducing factor protein in them compared to normal cells. When he was able to remove the protein, the cancer cell’s ability to survive was decreased. The protein is surprisingly critical for the ability of the mitochondria of advanced prostate cancer cells to make enough energy for the cells to survive.

Exactly why is what Wilkinson is working to figure out.

“Our logic is that if we can figure out how to use apoptosis-inducing factor protein as a target for turning off cancer cell energy supplies without affecting normal cells, we may be one step closer to curing cancer,” he said.

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