The EU FP6 (Framework Program 6) research project entitled GROWTHSTOP started in October 2006. Prof. Lukas A. Huber, Director of the Biocenter Innsbruck, Medical University is the coordinator of the project:

<< IDENTIFICATION, DEVELOPMENT AND VALIDATION OF NOVEL THERAPEUTICS
TARGETING PROGRAMMED CELL DEATH IN TUMORS >>

Funding body

Cancer is a major challenge to European healthcare. Each year nearly two million people are diagnosed with cancer in the EU, and over one million deaths results from this disease. Each case can have a tremendous impact on the health and well being of the affected person, his or her family and personal enviroment. In addition, a high percentage of cases have major economics impacts, both for the individual and for the health care provider.
As a result, improvements in cancer therapy remain of prime importance for the well being of the Europeans and for the future development of the community.

Cancer can be viewed as a disease of the genes. Importantly, however, mutations in individual genes do not cause tumors, since the human genome harbors failsafe mechanisms that protect normal cell from the consequences of deregualted proliferative stimuli. Two failsafe mechanisms are known:

• an irreversible growth arrest, termed senescence, which is activated by deregulated oncogenic signals provided through the Ras pathway: one key example is the often lifelong lack of proliferation of melanocytic naevi despite the presence of mutations on B-Raf, a downstream effector of Ras proteins.

• apoptosis, or programmed cell death, which is activated by many forms of deregulated proliferative signals. Tumors can only develop when secondary mutations that disable these failsafe programms arise; as a consequence, many mutations that are found in human tumors are involved in pathways that control either senescence or apoptosis.

The GROWTHSTOP consortium applies a combination of high resolution bio-imaging techniques, proteomics, cellular models, and in vivo tumor models towards the understanding of the pathways that signal apoptosis in solid tumours, with the goal of establishing the manipulation of apoptotic pathways as a viable therapeutic strategy that is applicable to the wide variety of tumors where propapototic signalling mechanisms are still intact.