Investigators in Dana-Farber's Center for Cancer Systems Biology (CCSB) have taken a novel approach to distinguish driver from passenger mutations. The key to their technique: viruses, the primal perpetrators of cellular havoc.
After a virus infects a cell, proteins made from the virus's genes begin interacting with the cell's own proteins. These interactions can interfere with the cell's normal functioning and the activity of its genes – so recklessly, sometimes, that the cell becomes cancerous.
The disruptions produced by cancer-causing viruses often mimic those triggered by gene mutations.
"That led us to ask, 'What if we systematically examine the interactions between normal cell proteins and the proteins made from cancer cell viruses?'" says Michael Cusick, PhD, of the CCSB, who helped lead the research. "Because viral proteins and gene mutations cause cancer by similar mechanisms, could we use the viral proteins as stand-ins for identifying proteins – and the underlying gene mutations – associated with cancer?"
To find out, researchers from the United States and Canada collected 144 proteins from four viruses linked to cancer and screened them one by one against 20,000 different proteins in human cells, recording which ones interacted. The end tally was the identification of roughly 950 viral targets, cell proteins potentially associated with cancer.
"Viruses have spent millions of years perfecting the art of interacting with cells – of taking advantage of gene pathways that are essential for the cell and may therefore be essential to cancer," Cusick remarks. "We're now using them as a guide to the mutations that are most important in cancer."
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Paths of Progress Spring/Summer 2013 Table of Contents
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