APPLICATIONS OF TECHNOLOGY:
- Cancer diagnostics
- Cancer therapeutics
- Cancer research
- Provides markers correlated with increased metastases risk
- Provides for therapies that block or reverse cancer progression through adjusting glucose metabolism
Berkeley Lab researchers led by Mina Bissell have discovered that markers of higher glucose metabolism correlate with increased risk of metastatic cancer via specific biochemical pathways, including those of well-known oncogenes. These findings could lead to more accurate diagnostics that predict patient outcome and to new enzymatic therapies that block or reverse cancer progression through adjustment of glucose metabolism.
For decades, medical researchers have considered increased glycolysis a consequence of biological conditions that support the growth and survival of malignant cells. The Berkeley Lab team has provided compelling evidence that increased uptake of glucose may in fact be a driver of oncogenesis, and that reduction of glucose uptake in malignant cells has led to phenotypic reversion of those cells. Markers correlated with increased risk of metastases have been identified and may be useful for prognostic tests of cancerous tumors. The specific glucose metabolism pathways implicated in oncogenesis may serve as targets for therapeutics that could block or reverse tumor growth.
Gene expression tests of enzymes correlated with oncogenic signaling may prove to be more accurate than current assays to gauge the risk of metastasis in an individual. Inhibition of these enzymes in order to downregulate the expression of genes involved in glucose uptake and metabolism could prove a more effective strategy for interfering with tumor growth than more conventional approaches that attack tumors with chemotherapeutics or antibodies.
DEVELOPMENT STAGE: Proven principle
STATUS: Patent pending. Available for licensing or collaborative research.
FOR MORE INFORMATION:
Onodera, Y., Nam, J-M., Bissell, M.J., “Increased sugar uptake promotes oncogenesis via EPAC/Rap1 and O-GlcNAc pathways,”Journal of Clinical Investigation, doi:10.1172/JCI63146. Published online December 9, 2013.
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REFERENCE NUMBER: IB-2921