cancer nutrition latest reviews
Selectively starving cancer cells
through dietary manipulation:
methods and clinical implications (March 2013)
Brittany A Simone 1 , Colin E Champ 1 , Anne L Rosenberg 2 , Adam C Berger 2 ,
Daniel A Monti 3 , Adam P Dicker 1 & Nicole L Simone*
1 Department of Radiation Oncology, Kimmel Cancer Center & Jefferson Medical College of ThomasJefferson University, Philadelphia, PA, USA.
2 Department of Surgery, Kimmel Cancer Center & Jefferson Medical College of Thomas Jefferson University,Philadelphia, PA, USA.
3 Myrna Brind Center of Integrative Medicine, Thomas Jefferson University Hospital, Philadelphia, PA, USA*Author for correspondence: Tel.: +1 215 503 0554 n Fax: +1 215 955 0412n email@example.com
As the link between obesity and metabolic syndrome and cancer becomesclearer, the need to determine the optimal way to incorporate dietarymanipulation in the treatment of cancer patients becomes increasingly important.Metabolic-based therapies, such as caloric restriction, intermittent fasting anda ketogenic diet, have the ability to decrease the incidence of spontaneoustumors and slow the growth of primary tumors, and may have an effect on distantmetastases in animal models. Despite the abundance of preclinical datademonstrating the benefit of dietary modification for cancer, to date there arefew clinical trials targeting diet as an intervention for cancer patients. Wehypothesize that this may be due, in part, to the fact that several different typesof diet modification exist with no clear recommendations regarding the optimalmethod. This article will delineate three commonly used methods of dietarymanipulation to assess the potential of each as a regimen for cancer therapy.
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R EVI EW Open Access
Cancer as a metabolic disease
Thomas N Seyfried*
, Laura M Shelton
Emerging evidence indicates that impaired cellular energy metabolism is the defining characteristic of nearly all
cancers regardless of cellular or tissue origin. In contrast to normal cells, which derive most of their usable energy
from oxidative phosphorylation, most cancer cells become heavily dependent on substrate level phosphorylation
to meet energy demands. Evidence is reviewed supporting a general hypothesis that genomic instability and
essentially all hallmarks of cancer, including aerobic glycolysis (Warburg effect), can be linked to impaired mitochondrial function and energy metabolism. A view of cancer as primarily a metabolic disease will impact
approaches to cancer management and prevention.