A strong positive correlation between energy intake and the incidence or growth of tumors has been reported in virtually every animal model system evaluated (6,10,40,41). Many studies have shown that an imposed restriction of total food intake or energy inhibits tumorigenesis (Fig. 1; 12). In addition, groups of mice or rats with free access to food, which is typical in most rodent studies, also show a striking positive correlation between self-selected energy intake and risk of cancer (Fig. 2; 40,42,43). Recent examination of data derived from the National Toxicology Program shows that chemicals reducing body weight, and presumably reducing self-selected energy intake, are associated with a lower cancer risk (44). Subsequent studies show that energy intake can have a profound influence upon the sensitivity of the bioassays used to identify health risks from environmental chemicals and define regulatory policy (45).
Readers of cancer therapy literature, including studies of antiangiogenic agents, must carefully evaluate the data, try to ascertain if the drug or therapeutic intervention alters food intake and body weight, and determine if energy intake has confounded the interpretation of the data. If food consumption is altered by the growth of a tumor, or changed by the anticancer treatments employed, it may be difficult to disentangle the results of the
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Thus far, few studies have focused on the role of energy intake and tumor vascular biology. A recent report showed that the transplantable Englebreth-Holm-Swarm (EHS) sarcoma (46), grown in young mice fed reduced-energy intake, contained fewer blood vessels and increased matrix, compared to those fed ad libitum (47). These observations are supported by the authors' recent unpublished experiments. The authors have completed a series of studies employing total diet or energy restriction with a variety of rodent tumor models, and assessed tumor growth and its relationship to microvessel density, based on factor VIII staining. These studies show that energy or diet restriction significantly reduces microvessel density in several transplantable tumor models, including murine MB49 bladder cancer, RT2 rat glioma, Dunning R3327H rat prostate cancer, and LNCaP human prostate carcinoma grown in nude mice (48).
Since the inhibition of tumor growth by energy restriction appears to be associated with a reduction in microvessel density, one can begin to speculate on the potential mechanisms involved. The endocrine system plays a significant role in the integration of nutritional status with the coordinated function of tissues and organs in mammals. Possible mediators of changes in tumor angiogenesis during dietary restriction are several hormones and growth factors that show changes with energy balance, and have been linked to angiogenesis.
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