Research Brief — September 2009

Researchers are increasingly recognizing that metabolic abnormalities play a role in cancer. These abnormalities often appear to involve abnormal glucose metabolism, an observation that first was made decades ago. However, the relationship between specific aspects of glucose metabolism and the development of tumors has not been clear.

In a paper published in Science Express, Dr. James K.V. Willson, director of the Harold C. Simmons Comprehensive Cancer Center, and colleagues at the Johns Hopkins Kimmel Cancer Center shed light on how glucose levels affect tumor progression.

They found that colorectal cancer cell lines with cancer-causing mutations in the KRAS and BRAF genes — two of the most common cancer genes — can survive better in low-glucose environments than normal cells. The scientists hypothesize that these mutations reprogram the cells so that their growth depends on this ability to convert low levels of glucose to energy.

To test this hypothesis, the researchers added to both mutated and normal cells an agent that inhibits glucose metabolism. The agent was toxic to the cells harboring the mutations, but was significantly less toxic to similar cells that did not contain the mutations. The researchers also tested the agent on tumors that contained KRAS and BRAF mutations that had been transplanted into mice; they found that the same agent slowed the growth of the tumors but did not affect normal cells.

“Our results raise a variety of questions, but also point to a potential strategy for preferentially targeting cells that harbor these mutations,” Dr. Willson said.

Connie Piloto

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