Agendia BV Acquires Rights to the Discovery of a Major Drug Resistance Mechanism in Breast Cancer Potentially Leading to a Herceptin(R) Sensitivity Test

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 specific gene confers resistance to a cancer drug, cells harboring the inactivated gene can continue to grow in the presence of the cancer drug and can be readily identified. In the present study deregulation of the phosphatidylinositol 3-kinase pathway, which is mutated in up to half of all breast cancer tumors, was identified as a major mechanism of unresponsiveness to Herceptin-based therapies.

“We are very excited by these findings and pleased that we have been able to secure the rights”, comments Agendia’s CEO, Dr. Bernhard Sixt. “It is likely that a similar mechanism contributes to unresponsiveness to other cancer therapeutics that target the EGF receptor in colon and lung cancer”. Agendia will develop a microarray-based diagnostic to identify this drug resistance mechanism.

About Agendia

Agendia, located in Amsterdam, the Netherlands, is a world leader in gene expression analysis-based diagnostics with three products on the market. The company focuses on the development and commercialization of diagnostic tests using tumor gene expression profiling. Agendia was the first company to receive FDA approval for it’s breast cancer test - MammaPrint(R) - that predicts the risk of breast cancer recurrence. Its second microarray product, CupPrint(R)(*), is a diagnostic test to identify the origin of a metastasis in a cancer type called “Cancer of Unknown Primary”. Agendia recently also presented its new colon cancer prognosis profile, ColoPrint(R), which is currently undergoing further validation. Agendia maintains close ties with several leading academic centers to develop state of the art diagnostic tests for cancer. Agendia also offers its expertise to pharma companies focusing on development of highly effective personalized drugs in the area of oncology.

(*) CupPrint(R) is based on a license to the TUA database of AviaraDx

CONTACT: Contact Information: Agendia: Prof. Dr. Rene Bernards, Chief
Scientific Officer at +31-626-558-679

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