Monica Buzzai

TL;DR: It is shown that proliferating mammalian cells have a cell-cycle checkpoint that responds to glucose availability and is regulated by AMP-activated protein kinase (AMPK), acell-cycle arrest that occurs despite continued amino acid availability and active mTOR.

TL;DR: It is suggested that activation of the Akt oncogene is sufficient to stimulate the switch to aerobic glycolysis characteristic of cancer cells and that Akt activity renders cancer cells dependent on aerobic glyCOlysis for continued growth and survival.

TL;DR: Metformin is selectively toxic to p53-deficient cells and provides a potential mechanism for the reduced incidence of tumors observed in patients being treated with metformin.

TL;DR: It is suggested that activation of Akt blocks the ability of cancer cells to metabolize nonglycolytic bioenergetic substrates, leading to glucose addiction.

TL;DR: It is reported that p53 can directly upregulate expression of Bnip3L, a cell death inducer that mediates p53-dependent apoptosis under hypoxia, which provides a novel understanding of p53 in tumor suppression.