Effect of energy substrate manipulation on tumour cell proliferation in parenterally fed cancer patients

Fanelli, Filippo Rossi; Franchi, F; Mulieri, Massimo; Cangiano, C.; Cascino, A.; Ceci, Fabrizio; Muscaritoli, Maurizio; Seminara, Patrizia; Bonomo, Lorenzo

doi:10.1016/0261-5614(91)90043-c

Cited by 42 publications

(20 citation statements)

References 16 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Interestingly in the normal healthy hepatic tissue GTPN increased the FDG uptake by 62% and LTPN by 10%. These findings are in agreement with an early report of Rossi Fanelli et al [124] who investigated the thymidine labelling index on tumour samples of patients in basal conditions and after two weeks of administration of a glucose-based or a mixed glucose/fat (20/80) parenteral nutrition.…”

Section: Preclinical Experience In Humanssupporting

confidence: 93%

Toward a cancer-specific diet

Bozzetti

Zupec‐Kania²

2016

Clinical Nutrition

View full text Add to dashboard Cite

Section: Preclinical Experience In Humanssupporting

confidence: 93%

Toward a cancer-specific diet

Bozzetti

Zupec‐Kania²

2016

Clinical Nutrition

View full text Add to dashboard Cite

“…There is only anecdotal evidence that such a diet might be effective as a supportive treatment. One study investigated whether a high-fat diet (80% non-nitrogenous calories from fat) would inhibit tumor cell replication compared to a high-dextrose diet (100% non-nitrogenous calories from dextrose) in 27 patients with gastro-intestinal cancers [137]. Diets were administered parenterally and cell proliferation assessed using thymidine labeling index on tumor samples.…”

Section: The Benefits Of Mild Ketosismentioning

confidence: 99%

Is there a role for carbohydrate restriction in the treatment and prevention of cancer?

2011

View full text Add to dashboard Cite

Over the last years, evidence has accumulated suggesting that by systematically reducing the amount of dietary carbohydrates (CHOs) one could suppress, or at least delay, the emergence of cancer, and that proliferation of already existing tumor cells could be slowed down. This hypothesis is supported by the association between modern chronic diseases like the metabolic syndrome and the risk of developing or dying from cancer. CHOs or glucose, to which more complex carbohydrates are ultimately digested, can have direct and indirect effects on tumor cell proliferation: first, contrary to normal cells, most malignant cells depend on steady glucose availability in the blood for their energy and biomass generating demands and are not able to metabolize significant amounts of fatty acids or ketone bodies due to mitochondrial dysfunction. Second, high insulin and insulin-like growth factor (IGF)-1 levels resulting from chronic ingestion of CHO-rich Western diet meals, can directly promote tumor cell proliferation via the insulin/IGF1 signaling pathway. Third, ketone bodies that are elevated when insulin and blood glucose levels are low, have been found to negatively affect proliferation of different malignant cells in vitro or not to be usable by tumor cells for metabolic demands, and a multitude of mouse models have shown anti-tumorigenic properties of very low CHO ketogenic diets. In addition, many cancer patients exhibit an altered glucose metabolism characterized by insulin resistance and may profit from an increased protein and fat intake.In this review, we address the possible beneficial effects of low CHO diets on cancer prevention and treatment. Emphasis will be placed on the role of insulin and IGF1 signaling in tumorigenesis as well as altered dietary needs of cancer patients.

show abstract

“…Other data are more supportive for targeting tumor cell proliferation through CHO restriction. Rossi-Fanelli et al [69] showed that a high-fat diet (80 % non-nitrogenous calories from fat) inhibited tumor cell proliferation while a high-dextrose diet (100 % non-nitrogenous calories from dextrose) increased proliferation over 14 days in patients with gastrointestinal cancers, though patient numbers were too small to reach statistical significance. Diets were administered parenterally and cell proliferation was assessed using thymidine labeling index on tumor samples, which measures the fraction of cells in the S phase as a proxy for de novo DNA synthesis.…”

Section: How Calorie and Carbohydrate Restriction May Influence The Rmentioning

confidence: 99%

Calories, carbohydrates, and cancer therapy with radiation: exploiting the five R’s through dietary manipulation

Klement

Champ

2014

Cancer Metastasis Rev

View full text Add to dashboard Cite

Aggressive tumors typically demonstrate a high glycolytic rate, which results in resistance to radiation therapy and cancer progression via several molecular and physiologic mechanisms. Intriguingly, many of these mechanisms utilize the same molecular pathways that are altered through calorie and/or carbohydrate restriction. Furthermore, poorer prognosis in cancer patients who display a glycolytic phenotype characterized by metabolic alterations, such as obesity and diabetes, is now well established, providing another link between metabolic pathways and cancer progression. We review the possible roles for calorie restriction (CR) and very low carbohydrate ketogenic diets (KDs) in modulating the five R’s of radiotherapy to improve the therapeutic window between tumor control and normal tissue complication probability. Important mechanisms we discuss include (1) improved DNA repair in normal, but not tumor cells; (2) inhibition of tumor cell repopulation through modulation of the PI3K–Akt–mTORC1 pathway downstream of insulin and IGF1; (3) redistribution of normal cells into more radioresistant phases of the cell cycle; (4) normalization of the tumor vasculature by targeting hypoxia-inducible factor-1α downstream of the PI3K–Akt–mTOR pathway; (5) increasing the intrinsic radioresistance of normal cells through ketone bodies but decreasing that of tumor cells by targeting glycolysis. These mechanisms are discussed in the framework of animal and human studies, taking into account the commonalities and differences between CR and KDs. We conclude that CR and KDs may act synergistically with radiation therapy for the treatment of cancer patients and provide some guidelines for implementing these dietary interventions into clinical practice.

show abstract

Effect of energy substrate manipulation on tumour cell proliferation in parenterally fed cancer patients

Cited by 42 publications

References 16 publications

Toward a cancer-specific diet

Toward a cancer-specific diet

Is there a role for carbohydrate restriction in the treatment and prevention of cancer?

Calories, carbohydrates, and cancer therapy with radiation: exploiting the five R’s through dietary manipulation

Contact Info

Product

Resources

About