Responses of hepatoma-bearing rats to total parenteral hyperalimentation and to ad libitum feeding

Cameron, Ivan L.; Ackley, William; Rogers, William E.

doi:10.1016/0022-4804(77)90020-8

Cited by 55 publications

(12 citation statements)

References 15 publications

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“…7777 rat system with total parenteral feeding alone [10]. Our earlier failure to maintain carcass mass was not attributed to mechanical or surgical problems or to inadequacies in the liquid formula diet in that we have shown that our parenteral feeding procedures do indeed permit body weight gain [17] and maintenance of carcass mass [10] when given to nontumorous rats.…”

Section: Discussionmentioning

confidence: 99%

“…An increased rate of tumor growth has been previously noted in this laboratory as associated with i.v. hyperalimentation [14,17], HS therapy by itself appears to have reduced voluntary food intake and inhibited gluconeogenesis to the extent that tumor growth was inhibited. Total parenteral nutrition appear ed to overcome this inhibition of tumor growth simply by making more nutrition (glucose, etc.)…”

Section: Discussionmentioning

confidence: 99%

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Total Parenteral Nutrition and Inhibition of Gluconeogenesis on Tumor-Host Responses<sup>1</sup>

Grubbs¹,

Rogers²,

Cameron³

1979

Oncology

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Rats bearing the Morris hepatoma No. 7777 were randomized into three treatment groups. Two of the groups received a nutritionally complete liquid formula diet per os ad libitum. One of these two groups received hydrazine sulfate (HS; an inhibitor of gluconeogenesis) twice daily (15 mg/kg) for 5 days. A third group of tumorous rats received the HS therapy and was given the liquid diet parenterally for 5 days. Tumorous rats fed per os, especially with HS therapy demonstrated inhibition of tumor growth, reduction of body and carcass weight, anorexia and decreased nitrogen retention. The combination of parenteral feeding and HS therapy sustained body and carcass weight with high nitrogen retention but stimulated tumor growth and was associated with liver toxicity. These results support the concept that cancer cachexia involves ‘a systemic energy-losing cycle dependent on an interplay of tumor glycolysis and gluconeogenesis’.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Total Parenteral Nutrition and Inhibition of Gluconeogenesis on Tumor-Host Responses<sup>1</sup>

Grubbs¹,

Rogers²,

Cameron³

1979

Oncology

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“…3 In tumor-bearing animals, PN has been demonstrated to increase tumor mitotic activity, tumor volume and weight, weight/carcass ratio, and metastases. [3][4][5][6][7][8][9][10][11][12][13] In humans, numerous studies have been conducted to try to determine if NS stimulates tumor growth and causes cancer progression [14][15][16][17][18][19][20][21][22][23][24][25][26][27] ; however, after almost 30 years, the question remains, at least in part, unresolved. No conclusive answer exists because of ethical and study design barriers, including the complexity of quantifying tumor growth characteristics in vivo.…”

mentioning

confidence: 99%

Does Nutrition Support Stimulate Tumor Growth in Humans?

et al. 2011

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Many studies have been conducted to ascertain if nutrition support (NS), either as parenteral nutrition (PN) or enteral nutrition (EN), stimulates tumor growth and causes cancer progression, but after almost 30 years, the question remains at least in part unresolved. In this study, previous studies were reviewed to evaluate the effect of NS on tumor growth, tumor proliferation, tumor apoptosis, and cancer-related survival in humans. MEDLINE and PubMed were searched using combinations of the following keywords: PN, EN, tumor growth, tumor proliferation, tumor apoptosis, arginine, ω-3 fatty acids, and glutamine. Unfortunately, the effect of nutrition support on tumor growth has been assessed only in terms of tumor proliferation, whereas the interferences on tumor apoptosis have never been determined. Overall, the results seem conflicting and inconclusive. Similarly, it remains unknown if PN or EN enriched with specific nutrients such as arginine, ω-3 fatty acids, and glutamine can affect tumor growth in humans. It is hoped that further studies will elucidate if NS with conventional or specific nutrients stimulates tumor proliferation, interferes with tumor apoptosis, and causes cancer progression.

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“…These data demonstrate that for tumors differing only in antigenicity the influence of malnutrition is on that tumor which induces an immunologic antitumor response. ( Journal of Parenteral and Enteral Nutrition 10: [21][22][23][24][25][26][27][28]1986) Nutritional support for the cancer patient, though frequently written about, remains a confusing topic since there is little uniformity practiced clinically. Although the cancer patient frequently can be shown to be malnourished and aggressive nutritional support can be shown to correct such malnutrition as well as its associated immunosuppression,2 the bigger question of what influence such therapy has on outcome from the disease is less clear.…”

mentioning

confidence: 99%

Tumor Immunogenicity—The Prime Determinant of the Nutritional Influence on the Host‐Tumor Relationship

McCarrick

Ikeda

Ziegler

1986

J Parenter Enteral Nutr

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The influence which malnutrition plays on the host-tumor relationship is controversial because of the disparity of human and rodent tumors, a critical difference being the minimal immunogenicity of human tumors and the variable antigenicity of rodent tumors. The hypothesis we tested is that the influence of malnutrition on tumor growth is a result of the immunogenicity of the host's tumor. C-1300 neuroblastoma (NB) is an immunogenic tumor by in vivo and in vitro assessment while the histologically identical TBJ-NB clone is non-immunizing. Isogeneic A/J mice were malnourished with 2.5% protein chow and were inoculated with C-1300-NB or TBJ-NB; either serial tumor volumes were assessed by three-dimensional measurement or animals were serially killed and tumor weight/carcass weight ratios (TW/CW) were calculated. Non-immunogenic TBJ-NB grew more rapidly than C-1300-NB in both control and malnourished groups, but there was no difference in either tumor size or TW/CW ratios between the two TBJ-NB nutritional groups. Contrasting with these data were immunogenic C-1300-NB in that the tumor grew significantly better in malnourished mice (tumor volume p less than 0.05 day 12 and 14; TW/CW p less than 0.026 by day 21). Prior whole-body irradiation abrogated this difference. These data demonstrate that for tumors differing only in antigenicity the influence of malnutrition is on that tumor which induces an immunologic antitumor response.

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Responses of hepatoma-bearing rats to total parenteral hyperalimentation and to ad libitum feeding

Cited by 55 publications

References 15 publications

Total Parenteral Nutrition and Inhibition of Gluconeogenesis on Tumor-Host Responses<sup>1</sup>

Total Parenteral Nutrition and Inhibition of Gluconeogenesis on Tumor-Host Responses<sup>1</sup>

Does Nutrition Support Stimulate Tumor Growth in Humans?

Tumor Immunogenicity—The Prime Determinant of the Nutritional Influence on the Host‐Tumor Relationship

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