Glucose metabolism and cancer

@article{citeulike:2999210, abstract = {The first identified biochemical hallmark of tumor cells was a shift in glucose metabolism from oxidative phosphorylation to aerobic glycolysis. We now know that much of this metabolic conversion is controlled by specific transcriptional programs. Recent studies suggest that activation of the hypoxia-inducible factor (HIF) is a common consequence of a wide variety of mutations underlying human cancer. HIF stimulates expression of glycolytic enzymes and decreases reliance on mitochondrial oxidative phosphorylation in tumor cells, which occurs even under aerobic conditions. In addition, recent efforts have also connected the master metabolic regulator AMP-activated protein kinase (AMPK) to several human tumor suppressors. Several promising therapeutic strategies based on modulation of AMPK, HIF and other metabolic targets have been proposed to exploit the addiction of tumor cells to increased glucose uptake and glycolysis.}, author = {Shaw, Reuben J. }, booktitle = {Cell division, growth and death / Cell differentiation}, citeulike-article-id = {2999210}, doi = {http://dx.doi.org/10.1016/j.ceb.2006.10.005}, journal = {Current Opinion in Cell Biology}, keywords = {cancer, glucose, metabolism, review}, month = {December}, number = {6}, pages = {598--608}, posted-at = {2008-07-14 17:44:53}, priority = {2}, title = {Glucose metabolism and cancer}, url = {http://dx.doi.org/10.1016/j.ceb.2006.10.005}, volume = {18}, year = {2006} }

TY - JOUR ID - citeulike:2999210 L3 - citeulike-article-id:2999210 N2 - The first identified biochemical hallmark of tumor cells was a shift in glucose metabolism from oxidative phosphorylation to aerobic glycolysis. We now know that much of this metabolic conversion is controlled by specific transcriptional programs. Recent studies suggest that activation of the hypoxia-inducible factor (HIF) is a common consequence of a wide variety of mutations underlying human cancer. HIF stimulates expression of glycolytic enzymes and decreases reliance on mitochondrial oxidative phosphorylation in tumor cells, which occurs even under aerobic conditions. In addition, recent efforts have also connected the master metabolic regulator AMP-activated protein kinase (AMPK) to several human tumor suppressors. Several promising therapeutic strategies based on modulation of AMPK, HIF and other metabolic targets have been proposed to exploit the addiction of tumor cells to increased glucose uptake and glycolysis. IS - 6 JF - Current Opinion in Cell Biology EP - 608 TI - Glucose metabolism and cancer VL - 18 T2 - Cell division, growth and death / Cell differentiation SP - 598 KW - cancer KW - glucose KW - metabolism KW - review AU - Shaw, Reuben PY - 2006/12// UR - http://dx.doi.org/10.1016/j.ceb.2006.10.005 ER -