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Scientists identify overactive genes in aggressive breast cancers
Date:6/1/2011

their surfaces. They resemble stem cells, as they constantly renew themselves and make tumors likely to spread to distant organs.

As a result, Polyak and colleagues believe that new treatments aimed at specifically knocking out these CD44+CD24- cells with activated Jak2/Stat3 signaling could be useful in combating triple-negative cancers and potentially other tumors that contain these cells.

The investigators surveyed genes present in CD44+CD24- cells and found 1,576 genes that differed from those in other, more differentiated epithelial cancer cells within tumors. Additional experiments assessing the viability of CD44+CD24- cells when each of these genes was inhibited individually narrowed the field to 15 genes that were required for their growth and thus looked like promising targets for selective drugs. These 15 genes were linked to the overactive Jak2/Stat3 pathway, which in turn was triggered by a growth factor signal, interleukin-6, or IL-6.

When the activity of several of those genes was blocked in CD44+/CD24- tumor cells, the level of Stat3 signaling was reduced and cell growth was suppressed, the researchers said.

Polyak said that inhibitor drugs exist for five of the genes identified in the CD44+CD24- cell network, and two of those drugs are currently in advanced clinical testing.

Nancy Lin, MD, a Dana-Farber oncologist who will lead the clinical trial of a Jak2/Stat3 inhibitor in breast cancer patients, said women who volunteer for the trial will be tested to determine whether the pathway is abnormally activated in their cancer. Those who test positive will be candidates for treatment with the drug. According to Lin, the abnormal pathway is expected to be found in 50 to 60 percent of patients with triple-negative cancers.


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Contact: Bill Schaller
william_schaller@dfci.harvard.edu
617-632-5357
Dana-Farber Cancer Institute
Source:Eurekalert  

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