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Targeting brain cancer cell metabolism may provide new treatment
Date:12/15/2009

Inhibiting fatty acid synthesis in brain cancer cells may offer a new option to treat about 50 percent of deadly glioblastomas that are driven by amplified signaling of the epidermal growth factor receptor (EGFR), according to a first-of-its-kind study by researchers at UCLA's Jonsson Comprehensive Cancer Center.

Rapidly dividing cancer cells require fatty acids for the formation of new membranes. The fatty acids also provide an alternative energy source for the cancer cells, and may be important for regulating cell signaling, said Dr. Paul Mischel, a professor of pathology and laboratory medicine and senior author of the study, which appears in the Dec. 15 issue of the journal Science Signaling.

While healthy cells take up the fat they need to function through the blood stream, the cancer cells prefer to be autonomous of the body and convert glucose for the fatty acids they need to multiply out of control.

"This suggests an important link between cancer progression and fatty acid synthesis and has raised the idea that targeting fatty acid synthesis could be an effective way to block cancer growth," said Mischel, a Jonsson Cancer Center researcher. "Understanding the molecular links between oncogenes such as EGFR and the process by which simple sugars such as glucose are converted to fatty acids could lead to new treatments. It could also potentially be used to identify the subsets of patients most likely to benefit from treatment targeting fatty acid biosynthesis."

Although about half of glioblastomas involve amplified and mutated EGFR, which is clearly playing a role in the development and progression of the disease, clinical trials testing EGFR inhibitors have not been successful, with only about 10 to 15 percent of patients responding, Mischel said. The cancer, it appeared, finds a way to work around the inhibitor. Something more had to be going on. Previous studies have suggested that EGFR signaling needs to "team
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Contact: Kim Irwin
kirwin@mednet.ucla.edu
310-206-2805
University of California - Los Angeles
Source:Eurekalert

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