A new study has found that nearly all pancreatic cancers enslave and deform mitochondria, the powerhouses of cells, and force them to divide unnaturally, to lose their normal shape and collapse around the cell's nucleus. 

This creates an environment even more conducive to tumor growth. 

The researchers looked at tumors caused by mutations in the gene Ras, which is mutated in up to 30 percent of all cancers. Ras activates a cellular signaling pathway, the MAP kinase pathway, that was discovered years ago by University of Virginia researchers Michael J. Weber, PhD, and Thomas W. Sturgill, MD, PhD. That cellular communication, the new study determined, is prompting mitochondria to act very strangely, to divide with a frequency they normally wouldn't.

While mitochondria are popularly thought to resemble beans floating in the cellular cytoplasm, recent research has shown they're actually long, stringy interconnected networks. They constantly fuse and divide in response to bodily demands. Ras appears to send that division process into overdrive, both in mouse models and in cell lines created from human pancreatic cancer samples.  

By blocking this process, doctors one day may be able to block the growth of such tumors.

"Perhaps in combination with other inhibitors, we can target this process of mitochondrial division, mitochondrial fission," said David Kashatus, PhD, of the University of Virginia Department of Microbiology, Immunology and Cancer Biology. "Hopefully we can make a difference in some of these cancers."

That finding points to a promising new target for developing cancer drugs. "Over the years, the scientific community has identified vulnerabilities in some of the pathways activated by Ras, targets we can drug that can inhibit tumor growth for a short time," Kashatus said. "The problem is, the tumors always find a way to come back. We need additional targets. And what this new finding may provide is an additional target in Ras- and MAP kinase-driven cancers."

Published in Molecular Cell. Co-authored by Jennifer A. Kashatus, Aldo Nascimento, Lindsey J. Myers, Annie Sher, Frances L. Byrne, Kyle L. Hoehn, Christopher M. Counter and Kashatus.