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Flipping the angiogenic switch

A new paper in the September 15th issue of G&D reveals how pancreatic tumors get the blood supply they need to thrive and spread.

"150 years ago, the German pathologist Rudolf Virchow first proposed the idea that cancers are wounds that never heal. Our data present a stark example of the remarkable molecular overlap between the biology of cancers and the biology of chronic inflammation, potentially suggesting strategies by which both can be treated," explains Dr. Evan.

Using a mouse model of pancreatic cancer, Dr. Gerard Evan (UCSF) and colleagues determined how the Myc oncoprotein drives tumor angiogenesis. The researchers demonstrated that Myc activation in pancreatic cells induces expression of the pro-inflammatory cytokine protein interleukin 1beta (IL-1beta). Rising IL-1beta levels promote the release of sequestered vascular endothelial growth factor (VEGF) molecules, thereby stimulating new blood vessel formation and cell proliferation.

The authors also show that tumor angiogenesis can be thwarted by blocking IL-1beta activity. Since IL-1beta is upregulated in several human cancers, this discovery of IL-1beta as a key mediator of Myc-induced tumor angiogenesis provides experimental evidence to support the design of cancer drug therapies targeted at affecting IL-1beta activity.

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