some known mechanism

一个关健调控点是
pyruvate

Cancers tend to have
- selective expression of PKM2 (instead of PKM1), causing return to FETAL phenotype.
[step: phosphoenolpyruvate -->pyruvate]

- inactivation of PDC (pyruvate dehydrogenase complex): basis for the controversial canadian DCA cancer therapy in that DCA inhibits PDH kinase by irreversible binding to the pyruvate site, which results in the re-activation of PDC, and eventual restoration of aerobic respiration, proper mitochondrial function hence apoptosis.
[step: pyruvate --> acetyl CoA]

- high expression of transcription factor HIF (hypoxia inducible factor): the expression of enzymes for both above steps, and many other key players, such as Glut-1 (gluocose transporter), VEGF and some MMPs/cathepsin, are regulated by HIF. I am sure you are familiar with avastin

glucose surge => enhanced tumor anaerobic metabolism => hypoxia => HIF => expression of cancer growth, angiogenesis, metastasis related proteins => aggressive cancer