Future advances in cancer drug development may come from targeting cancer metabolism and the pathways associated with this.
That was one of the key messages of Tak Wah Mak (Princess Margaret Hospital, Toronto) in his plenary presentation at the recent ESMO/ECCO multidisciplinary cancer congress in Stockholm.
An examples of this is the PI3-Kinase RAS axis that also inhibits glycolysis.
Sally Church in today’s post on Pharma Strategy Blog picks up on this, and how “understanding the process of tumorigenesis, ie tumour formation and growth, is critical to figuring out how to stop it.”
She discusses recent research from MD Anderson Cancer Center on Pyruvate Kinase M2 (PKM2) that is highly expressed in human cancer.
PKM2 plays an important role in glycolysis (Warburg effect) but also has a non-metabolic effect on tumor formation and growth.
The MD Anderson researchers showed how epidermal growth factor (EGFR) activation led to translocation of PKM2, but not PKM1.
You can read more on Pharma Strategy Blog about the significance of these findings and how this might lead to new biomarkers and treatment approaches.
Targeting Tumor Metabolism is one of the plenary sessions at the forthcoming AACR-NCI-EORTC Molecular Targets and Cancer Therapeutics Congress in San Francisco.