Final Report Summary - TUMOR-HOST GENOMICS (Genome-wide analysis of signaling pathways in regulation of the interactions between tumor and host cells: Applications for cancer therapy)
The ultimate aim of the TUMOR-HOST GENOMICS project was to unravel and validate new targets for anticancer therapy, and new strategies for delivering therapy to tumours. Its specific aims were to:
- develop targeted lentiviral libraries for inhibition of selected major cell signalling pathways;
- identify tumour-derived factors that lead to increased angiogenesis and recruitment of stromal cells contributing to a microenvironment permissible for tumour growth;
- identify host-derived factors that induce tumor cell growth and tumor stem cell self-renewal;
- identify endothelial/bone marrow (BM) cell-specific cis-regulatory elements for use in lentiviral in vivo targeting vectors;
- test in vivo the effect of targeted lentiviruses in inhibition of tumor growth and metastasis.
The project studied major signalling pathways in mesenchymal and hematopoietic cells and formed a concerted effort to understand tumour-host interactions, and to identify novel therapeutic targets. The work plan entailed development of novel advanced functional genomics instruments, technologies and methods to study tumour-host interactions in cancer, and to apply these techniques to the identification of molecules and processes in normal cells which could be targeted by novel anti-cancer therapeutic agents.
In addition, the project would develop targeted lentiviruses which would allow in vivo delivery of therapeutic agents into tumours. Functional validation of the discovered targets and developed delivery systems will be performed in vivo models of murine tumor growth and dissemination.
The project was designed to increase understanding concerning central mechanisms on which tumor growth is depended on. Therefore, the findings may potentially combat all types of human cancer, since tumor-host interactions including but not limited to tumour angiogenesis are universally essential for the growth and dissemination of any malignant disease. Unravelling the molecular basis of tumour-host interactions not only increases knowledge about these pathophysiological processes, but also allows affecting cancer by targeting normal cells that are genetically stable, and would not be expected to develop resistance to the novel therapeutic agents.
Therefore, the work had significant exploitation potential and relevance for health in the understanding of the molecular mechanisms of tumour-host interactions, and in the treatment of cancer.
- develop targeted lentiviral libraries for inhibition of selected major cell signalling pathways;
- identify tumour-derived factors that lead to increased angiogenesis and recruitment of stromal cells contributing to a microenvironment permissible for tumour growth;
- identify host-derived factors that induce tumor cell growth and tumor stem cell self-renewal;
- identify endothelial/bone marrow (BM) cell-specific cis-regulatory elements for use in lentiviral in vivo targeting vectors;
- test in vivo the effect of targeted lentiviruses in inhibition of tumor growth and metastasis.
The project studied major signalling pathways in mesenchymal and hematopoietic cells and formed a concerted effort to understand tumour-host interactions, and to identify novel therapeutic targets. The work plan entailed development of novel advanced functional genomics instruments, technologies and methods to study tumour-host interactions in cancer, and to apply these techniques to the identification of molecules and processes in normal cells which could be targeted by novel anti-cancer therapeutic agents.
In addition, the project would develop targeted lentiviruses which would allow in vivo delivery of therapeutic agents into tumours. Functional validation of the discovered targets and developed delivery systems will be performed in vivo models of murine tumor growth and dissemination.
The project was designed to increase understanding concerning central mechanisms on which tumor growth is depended on. Therefore, the findings may potentially combat all types of human cancer, since tumor-host interactions including but not limited to tumour angiogenesis are universally essential for the growth and dissemination of any malignant disease. Unravelling the molecular basis of tumour-host interactions not only increases knowledge about these pathophysiological processes, but also allows affecting cancer by targeting normal cells that are genetically stable, and would not be expected to develop resistance to the novel therapeutic agents.
Therefore, the work had significant exploitation potential and relevance for health in the understanding of the molecular mechanisms of tumour-host interactions, and in the treatment of cancer.
