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atugen AG Discovers Novel Cancer Target

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21.01.2003

atugen AG, a private company focused on the elucidation of disease pathways, today announced the identification of a novel cancer target that appears to play an important role in tumor growth and metastasis. atugen’s research group has demonstrated that inhibition of the novel target, Atu027, which has homology to protein kinases, results in blockage of tumor growth of human prostate carcinoma cells in orthotopic mouse models. atugen has demonstrated that human prostate tumor cells engineered to express siRNA molecules against the kinase shows significant reduction or even complete lack of secondary tumors indicating a role of the kinase in tumor progression and metastasis.

The novel target, Atu027, is the result of the company’s internal research program on the phosphatidylinositol 3-OH kinase (PI 3-K) pathway. The approach was presented at the Cold Spring Harbor Laboratory’s Tumor Suppressor August 2002 Meeting in Cold Spring Harbor, NY. PI 3-K is a central signal transduction molecule controlling a wide range of cellular responses including contributing to increased malignant behavior of cancer cells.

The identification and functional validation of the kinase as PI 3-K downstream effector molecule underscores the strength of the atugen approach to find novel targets. The use of the company’s proprietary mRNA knockdown technologies (GeneBlocs® antisense molecules, improved synthetic siRNA, vector expression systems for siRNA, ribozymes and superior transfection reagents) together with atugen’s expertise in gene function elucidation has to date resulted in 19 functionally validated cancer targets that act in the PI 3-K pathway.

“We are in the process of out-licensing this novel kinase target to partners,” said Dr. Klaus Giese, atugen’s Chief Scientific Officer and Vice President of Research. “The breakthrough in this complex pathway endorses our approach, which aims at providing our partners and in-house projects with the best targets for therapeutic intervention within a given disease cascade. We have already started to dissect a complementary pathway, the TGF-beta/Smad pathway.”

Caroline Stupnicka | Source: alphagalileo
Further information: www.atugen.de

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