Abdallah K Alameddine1, Frederick T Conlin2,3, Brian J Binnall1, Yvonne A Alameddine4, Khaled O Alameddine5. 1. Division of Cardiac Surgery, Baystate Medical Center, Springfield, MA, USA. 2. Anesthesiology, Baystate Medical Center, Springfield, MA, USA. 3. University of Massachusetts Medical School, Boston, MA, USA. 4. MassDerm associates, Beverly, MA, USA. 5. Swedish Covenant Hospital, Chicago, IL, USA.
Abstract
BACKGROUND: Multiple genetic changes, availability of cellular nutrients and metabolic alterations play a pivotal role in oncogenesis AIMS: We focus on cancer cell's metabolic properties, and we outline the cross talks between cellular oncogenic growth pathways in cancer metabolism. The review also provides a synopsis of the relevant cancer drugs targeting metabolic activities that are at various stages of clinical development. METHODS: We review literature published within the last decade to include select articles that have highlighted energy metabolism crucial to the development of cancer phenotypes. RESULTS: Cancer cells maintain their potent metabolism and keep a balanced redox status by enhancing glycolysis and autophagy and rerouting Krebs cycle intermediates and products of β-oxydation. CONCLUSIONS: The processes underlying cancer pathogenesis are extremely complex and remain elusive. The new field of systems biology provides a mathematical framework in which these homeostatic dysregulation principles may be examined for better understanding of cancer phenotypes. Knowledge of key players in cancer-related metabolic reprograming may pave the way for new therapeutic metabolism-targeted drugs and ultimately improve patient care.
BACKGROUND: Multiple genetic changes, availability of cellular nutrients and metabolic alterations play a pivotal role in oncogenesis AIMS: We focus on cancer cell's metabolic properties, and we outline the cross talks between cellular oncogenic growth pathways in cancer metabolism. The review also provides a synopsis of the relevant cancer drugs targeting metabolic activities that are at various stages of clinical development. METHODS: We review literature published within the last decade to include select articles that have highlighted energy metabolism crucial to the development of cancer phenotypes. RESULTS:Cancer cells maintain their potent metabolism and keep a balanced redox status by enhancing glycolysis and autophagy and rerouting Krebs cycle intermediates and products of β-oxydation. CONCLUSIONS: The processes underlying cancer pathogenesis are extremely complex and remain elusive. The new field of systems biology provides a mathematical framework in which these homeostatic dysregulation principles may be examined for better understanding of cancer phenotypes. Knowledge of key players in cancer-related metabolic reprograming may pave the way for new therapeutic metabolism-targeted drugs and ultimately improve patient care.
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