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Agendia Acquires Rights to the Discovery of a Major Drug Resistance Mechanism in Breast Cancer Potentially Leading to a Herceptin(R) Sensitivity Test
Date:10/15/2007

AMSTERDAM, October 15 /PRNewswire/ -- Agendia BV, world leader in the rapidly evolving field of molecular diagnostics, announced today that it has acquired the rights to the discovery of a major mechanism of resistance to the frequently-used breast cancer drug Herceptin(R), which is published in the October 15 issue of the journal "Cancer Cell".

The antibody drug Herceptin(R) targets the HER2 protein, which is hyper-active in about one in four breast cancers and the HER2 protein contributes to aggressive cancer behavior. Striking initial responses are observed in combination with chemotherapy in more than half of treated patients. However, the majority of responding patients eventually develop resistance to Herceptin-based therapies. The laboratory of Agendia's Chief Scientific Officer, Prof. Rene Bernards, today published a rapid method to identify biomarkers associated with non-responsiveness to cancer drugs in cell culture and used the technology to identify a mechanism of resistance to Herceptin-based cancer therapy. His work also demonstrated that these biomarkers indeed have predictive value in patients treated with this drug, thus validating the approach.

"The availability of biomarkers that predict responses to cancer therapy is instrumental to the rational use of cancer drugs in the clinic. Elucidating the molecular mechanism of drug resistance can be critical to identify patients that fail to respond to therapy and may help design more efficient treatment protocols", says Rene Bernards. "Although more work is needed to further validate our findings, the method is generally applicable to find mechanisms of drug resistance and should expedite the development of biomarkers that are associated with therapy non-responsiveness".

The technology used relies on the simultaneous inactivation of thousands of genes through a process known as RNA interference in cells that are sensitive to a specific cancer drug. If the inactivation of a specif
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SOURCE Agendia BV
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