IMAGE: This is a depiction of the structure of protein form KRAS4b. view more
Credit: Kelleher Research Group, Northwestern University
EVANSTON, Ill. — When a RAS gene operates normally, it acts as an on/off switch for cell signaling to control cell proliferation. But when the gene mutates, the switch jams into the “on” position, allowing cells to proliferate uncontrollably.
This unstoppable cascade inevitably leads to cancer.
“The mutation in the gene is very common in pancreatic and colon cancer,” said Neil Kelleher, the Walter and Mary Elizabeth Glass Professor of Chemistry, Molecular Biosciences and Medicine at Northwestern University. “But there are currently no drugs that can target the mutation and fix the broken switch.”
Now Kelleher’s team has gathered insights that could potentially lead to new treatments for this historically “undruggable” target. An expert in proteins and director of Northwestern’s Proteomics Center of Excellence, Kelleher has developed a new technology that can — in precise detail — detect and quantify the effect of RAS mutations on RAS proteins.
Responsible for the signaling that controls cell growth and death, these proteins have been directly implicated in promoting tumor formation and cancer progression. Understanding how RAS proteins function in cancer could
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