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Massachusetts Institute of Technology IDs new cancer drug target
Date:11/8/2010

CAMBRIDGE, Mass. -- Suppressing cancer cells' ability to replicate damaged DNA could dramatically enhance the effectiveness of chemotherapy drugs such as cisplatin, according to a new pair of papers from MIT biologists.

In studies of mice, the researchers found that slowing down a specific system for tolerating DNA damage not only prolonged survival but also prevented relapsed tumors from becoming resistant to chemotherapy, and made tumors much less likely to spread to other parts of the body.

Two enzymes that play key roles in a cell's response to DNA damage could be an enticing target for new cancer drugs, according to Michael Hemann and Graham Walker, senior authors of the two papers. Their new findings will appear in the Proceedings of the National Academy of Sciences during the week of Nov. 8.

Many cancer drugs, including cisplatin, kill cancer cells by damaging their DNA. This damage can impair a cell's ability to copy its DNA before cell division, resulting in cell death. However, cancer cells use enzymes known as translesion DNA polymerases to copy over damaged DNA and prevent the newly replicated DNA from having gaps in its normal sequence of nucleotide bases (the "rungs" of the ladder that forms the DNA double helix).

In these studies, the MIT researchers focused on two proteins, known as Rev3 and Rev1, which are subunits of translesion DNA polymerases.

In one of the PNAS papers, Hemann and Walker studied mice with a particularly aggressive form of lung cancer. Among mice treated with cisplatin, mice whose Rev3 levels were reduced by 60 to 70 percent lived twice as long as mice with the normal amount of Rev3. (Mice with reduced Rev3 lived an average of 22.5 days following cisplatin treatment; mice treated with cisplatin alone lived 11 days.) This is the first alteration shown to sensitize these tumors to front-line chemotherapy.

Translesion polymerases can be highly error-prone and thus i
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Contact: Jennifer Hirsch
jfhirsch@mit.edu
617-253-1682
Massachusetts Institute of Technology
Source:Eurekalert

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