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Breast Cancer Cells Leave Gene Sign That can Predict Treatment Prognosis

by Rajashri on  September 1, 2008 at 4:52 PM Cancer News   - G J E 4
 Breast Cancer Cells Leave Gene Sign That can Predict Treatment Prognosis
Genetic response to insulin-like growth factor 1 (IGF-I) in breast cancer cells can help predict aggressive tumours that are less likely to respond to treatment, researchers from Baylor College of Medicine have revealed.
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They believe that the new findings will help in determining which patients will respond to these drugs.

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In the study led by Dr. Adrian Lee, associate professor in the Lester and Sue Smith Breast Centre at BCM, the researchers stimulated breast cancer cells with IGF-I in the laboratory and defined how more than 800 genes in the cells responded to the growth factor.

They then examined the samples of patient breast tumours with this "gene signature" and correlated the gene signatures with the fate of the patients.

"We have technology now to allow us to globally assess what IGF is doing in breast cancer at the whole gene expression level," said Lee.

"This is one of the first studies to do that. We know that IGF is bad in cancer, but now we can globally understand it in a more comprehensive manner. It could lead to finding biomarkers for patients response to breast cancer treatments.

"We found that IGF-I is a major regulator of cell growth and cell survival. It also regulates DNA repair," he added.

The researchers found that tumours in which IGF (insulin-like growth factor) affected the way in which genes were activated or translated into messages were more aggressive and more likely to grow.

"These findings come at a critical time," said Lee.

"Our goal is to identify biomarkers that will help predict which patients will respond to therapy against insulin-like growth factor. Several inhibitors of the IGF pathway are in patient studies right now. There's a large movement to understand which patients will respond to these drugs. This is a step toward that goal," he added.

Source: ANI
RAS/L
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