Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0598934 (tumor growth)
 58,965 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The results of nonspecific immunotherapy with BCG vaccine in 98 cases of melanoma, breast cancer and other malignancies were used in evaluating the frequency and degree of side-effects and complications arising in cancer patients during this treatment. The procedure proved to be safe irrespective of patients' age. Prevention and treatment of side-effects such as fever, water-salt disorders, anorexia, interstitial hepatitis and promotion of tumor growth are discussed.
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PMID:[Treatment of the complications occurring in BCG vaccine immunotherapy of patients with malignant neoplasms]. 646 96

The effects of carbohydrate-deficient diets on the growth of the Walker carcinosarcoma 256 in rats and on the carcinostatic action of the glucose analogue 2-deoxyglucose were studied. All diets contained 13.0% casein with glucose levels as indicated and the balance of calories present as corn oil free fatty acids. The growth of the tumor was directly related to the glucose level in such diets; after 16 days rats fed 0.0, 1.5 and 4.5% glucose had tumors weighing 7.0, 11.1 and 13.3 g, respectively. The decrease in tumor weight was related to dietary glucose level rather than the anorexia produced by the diets low in glucose, as shown by the fact that tumors in rats fed 4.5% glucose were larger than rats fed 1.5% glucose even when the rats fed 4.5% glucose were pair-fed to the levels consumed by those fed 1.5% glucose. 2-Deoxyglucose (0.2%) also caused a reduction in tumor growth in a manner independent from the anorexia produced by its presence in the diet. This carcinostatic effect was potentiated by low glucose levels in the diets in the rats fed 4.5% glucose plus 0.2% 2-deoxyglucose had proportionally greater reductions in tumor weights due to the glucose analogue than did rats fed 20% glucose plus 0.2% 2-deoxyglucose.
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PMID:Effects of diets deficient in glucose and glucose precursors on the growth of the Walker carcinosarcoma 256 in rats. 649 63

A modified learned food aversion paradigm simulated the prolonged food and illness exposure likely to characterize nutrient deficiencies or tumor growth. In this paradigm, a continuously available food was associated with a slow, continuous infusion of LiCl provided by osmotic minipump. Significant aversions were acquired when the available diet was novel but not when it was familiar. Effects of drug infusions on daily food intake were found to parallel those on aversion formation. Marked, persistent suppression of food intake was seen in drug-treated animals consuming a novel diet, but only transient declines were seen in those with a familiar diet. By separating the direct from the conditioned effects on food intake of chronic drug infusions, these studies provided strong evidence that learned food aversions can lead to anorexia.
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PMID:Chronic lithium chloride infusions: conditioned suppression of food intake and preference. 657 80

This study was designed to ascertain whether the overall availability of whole-body lipids and nitrogen is a limiting factor for survival in tumor-bearing mice suffering from anorexia and cachexia. Three-month-old nongrowing mice (C57BL/6J) were given s.c. transplants of a methylcholanthrene-induced sarcoma. Freely fed, starved, and pair-fed animals were used. Body and lipid composition, tumor growth, and survival time were measured. Freely fed sarcoma-bearing mice died with profoundly altered body composition. This was not explained by the anorexia assessed in pair-feeding experiments. Starvation had caused a more severe depletion in body composition in both tumor-bearing and nontumor-bearing animals than the tumor alone did in freely fed tumor-bearing mice. Freely fed tumor-bearing animals had normal proportions of whole-body triglycerides, cholesterol, and polar lipids, but they lost palmitic acid quantitatively more than any other fatty acid. It is unlikely that any single fatty acid became limiting during tumor growth. The results show that the overall availability of lipids, nitrogen, and glucose precursors is not a limiting factor for survival in experimental tumor cachexia. Other factors considered to be more likely as determining factors for the death of tumor-bearing animals are discussed.
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PMID:Role of whole-body lipids and nitrogen as limiting factors for survival in tumor-bearing mice with anorexia and cachexia. 657 17

The role of nutrition support as an adjunct to cancer treatment is discussed. Many patients with advanced cancer have demonstrable nutritional deficits, the reason is still unclear. Anorexia, taste abnormalities, pain and obstruction of the gastrointestinal tract can lead to malnutrition. Different modes of therapy, like surgery, radiotherapy and chemotherapy, sometimes deteriorate nutritional status. Several investigators have indicated, that nutritional support provides some benefit. There is no indication at the present time of any disadvantage of this method of treatment in relation to tumor growth. The potential indications and methods of nutritional support are pointed out.
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PMID:[The role of enteral and parenteral feeding in cancer therapy]. 680 86

The time course of energy metabolism has been studied in weight-stable and nongrowing mice with a transplantable methylcholanthrene-induced sarcoma. Daily oxygen consumption and carbon dioxide production were measured in relation to the tumor growth from the time of tumor implantation. The time course of energy dynamics was related to the end-state changes in body composition. Freely fed sarcoma-bearing mice decreased their whole-body energy expenditure in proportion to the tumor growth. This was due to the accompanying anorexia. The alteration in oxygen consumption and carbon dioxide production was continuously evident 24 hr/day in sarcoma-bearing mice. The tumor-bearing mice lost body fat and had decreased respiratory quotient, while pair-fed controls maintained their body composition, and their respiratory quotients agreed with the food respiratory quotient. Loss of body lipids in freely fed sarcoma-bearing mice reflected a negative energy balance, accompanied with increased fat oxidation, while maintenance of body composition in pair-fed controls reflected a decreased metabolic rate. Sarcoma-bearing mice showed a significantly higher energy expenditure in relation to their food intake compared to that of pair-fed controls. Estimates of partition of oxygen uptake in sarcoma-bearing mice support that both the host and the tumor account for the elevated energy expenditure. This study has confirmed a small but significantly increased energy expenditure in sarcoma-bearing mice, which was continuously present 24 hr/day in spite of unlimited availability of food. This illustrates the fatal outcome of experimental cancer.
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PMID:Energy metabolism in nongrowing mice with sarcoma. 686 Nov 35

Anorexia can occur when a specific diet is associated with a developing illness. The studies reported here show that the decline in food intake which accompanies tumor growth is accompanied by the development of aversions to the specific diet consumed during tumor growth. An immediate elevation in food consumption occurred when a novel diet was introduced. Therefore, the development of learned aversions to the specific diet eaten during tumor growth may be a causal factor in the development of tumor anorexia.
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PMID:Tumor anorexia: a learned food aversion? 693 Jan 6

Walker carcinoma 256/B transplanted sc in CD-COBS rats induce a decrease of food intake when the tumor size is less than 5% of the body weight. This anorexia is accompanied by a decrease of the adipose tissue and, to a lesser extent, of muscular tissue. The mechanism involved in cancer-induced anorexia seems to be different from that of classic centrally acting anorectic agents. Among the drugs tested to counteract this anorexia only cyproheptadine shows a modest effect. Cyclophosphamide reduces tumor growth and prevents decrease in food intake. It is suggested that Walker carcinoma 256/B may be a useful animal model to study problems related to cancer-induced anorexia and cachexia.
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PMID:Animal models for the study of cancer-induced anorexia. 695 17

The present study was designed to determine whether alterations in host metabolism associated with progressive tumor growth were a result of the anorexia frequently observed with cancer or could be attributed to other direct tumor effects. Rates of tyrosine flux, oxidation, and incorporation into protein, as well as fractional protein-synthetic rates in nonsecretory liver, muscle, and tumor, were determined in overnight-fasted rats, 5 to 6 (Stage I), 10 to 11 (Stage II), and 15 to 16 (Stage III) days following s.c. implantation of RNC-254 fibrosarcoma. Tumor-bearing rats were allowed to consume a purified diet containing 20% protein ad libitum, and results were compared to non-tumor-bearing rats pair fed quantities of food equivalent to tumor-bearing animals or allowed to consume the diet ad libitum. Results demonstrate that during later stages of tumor growth (Stage III) calorie intake and nontumor body weight gain were reduced in tumor-bearing rats (p less than 0.05). Fifteen and 16 days following implantation, there were significant changes in amino acid kinetics that were not observed after earlier periods of tumor growth and that could not be explained by any reduction in dietary intake. Rates of tyrosine appearance in the plasma and subsequent incorporation into whole-body protein were increased 33 and 34%, respectively (p less than 0.05), when compared to non-tumor-bearing rats fed equivalent quantities of food. Whole-body tyrosine oxidation rates were unchanged. Skeletal protein synthesis, as reflected by gastrocnemius or rectus abdominus muscle, was reduced from 10.5 and 10.1%/day to 7.4 and 6.0%/day, respectively (p less than 0.05), in tumor-bearing compared to pair-fed animals. The findings suggest that significant alterations in protein metabolism occur in advanced stages of experimental neoplastic disease which cannot be explained by reductions in dietary intake and are aimed at providing adequate quantities of endogenous amino acids for net tumor growth.
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PMID:Altered amino acid kinetics in rats with progressive tumor growth. 705 80

Mouse fibrosarcoma cells were grown in vitro and incubated with L-2,4 diaminobuturic acid, a non-metabolizable amino acid. The tumor cells were irreversibly and totally damaged by incubation with 10 mM DAB for 24 h at 37 degrees C. The cell-destructive effect by DAB was probably due to an osmotic lysis induced by the non-saturated intracellular accumulation of DAB. The harmful effect of DAB could be abolished by concomitant incubation with L-alanine and L-methionine, that compete with DAB for the same transport system, while the D-forms of the same amino acids as well as sarcosine had a weak effect. The fibrosarcoma cells were also transplanted s.c. into mice that were subsequently treated with i.p. injections of an isotonic 0.1 M DAB solution. The neoplastic cells were transplanted into totally 90 animals. The mean tumor weight of 42 treated animals was 1.16 g (+/- 0.77 g) compared with the corresponding figures of the 27 untreated mice, that were 2.05 g (+/- 1.22 g), i.e., a 43.4% reduction of tumor growth. There were, however, 17 drug-related deaths. Treatment with DAB generally resulted in weight reduction, at least partly due to loss of appetite, in animals. In addition, neurological symptoms of a specific character could develop among several of the treated animals. The side effects apparently restrict the usefulness of DAB alone as an anti-tumor agent, but since the principle of action of DAB is unique and not shared by other known chemotherapeutics it might offer new possibilities in the combined treatment of neoplastic growth.
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PMID:Antitumor activity of L-2,4 diaminobuturic acid against mouse fibrosarcoma cells in vitro and in vivo. 743 Feb 41


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