In 1920, Walburg described the Walburg effect which characterizes the CANCER CELL MODE.
Indeed in cancer there is a dissociation of Glycolysis and with Catabolism. In Cancer mode, the cell adopts Glycolysis and Anabolism. Glycolysis is to escape the normal requirements of constant feeding, be in a stress like while Making new proteins (Anabolism) to allow cell division and proliferation. One hundred years after the Walburg effect was described, it is now molecularly explained by Researchers. Indeed, to do this the cell induces a genetic controlled hypoxia by suppressing SIRT3 which overexpresses HIF. This induces Hypoxic conditions in the Mitochondria.
The Cancer mode can now be measured
1 Pyruvate Dehydrogenase kinase
2. Over-expression of GLUT1
3. level of vascular endothelial growth factor
4. level of suppression of SIRT3 and related Increase in ROS1
5. level of HK2, IDH, and SOD3
and if you are very smart, start by including c-JUN, HIF, Myc and TCA (fatty acid)
And as you progress with the clues given you will understand why overexpression of ROS1 could predict resistance to MTOR Inhibitors. And I believe it predicts of low participation of MAPK as a driver of pathogenesis therefore decreasing the value of MTOR inhibitors. more detail to come.
ANOTHER WAY OF INDUCING HIF: