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DNA discovery opens new door to develop tools, therapies for hereditary cancers
Date:7/8/2010

l as very aggressive brain tumours.

"The reason why it can lead to cancer is because if you don't have mismatch repair proteins that correct these errors, you're going to accumulate mutations," said Guarn. "People with defective mismatch repair genes develop cancers at very early ages. You would see a family that in their 30s has colorectal cancer and in their 40s they have it again. There's no way you can prevent that you can't correct your DNA. As you grow older, you're going to accumulate mutations."

To determine how MutL is regulated, the researchers characterized the functional and structural domain of the protein that is involved in DNA mismatch repair. By mapping out MutL, they were able to unveil how the replication machinery turns MutL into an enzyme that cuts the error from the DNA. They also discovered that PCNA, another protein within the pathway, allows DNA to bind to MutL so it can be repaired.

"This is especially important because we've known for more than a decade that the PCNA protein is necessary to correct mismatches, but we didn't know its concrete function," Guarn said. "We're starting to understand that one of the roles of these replication proteins is to license the cutting activity of MutL."

The findings have profound implications in understanding the molecular mechanisms that predispose to cancer and Turcot syndrome development. In particular, it allows scientists to pinpoint mutations on the MutL protein in order to determine severity and long-term outcomes.

The results also provide new avenues to develop alternative cancer treatments, as the hope is future cancer therapies may be focused at the molecular level and involve blocking specific pathways within the cell.


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Contact: Veronica McGuire
vmcguir@mcmaster.ca
90-552-591-402-2169
McMaster University
Source:Eurekalert

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