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Query: UMLS:C0598934 (tumor growth)
 58,965 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An aplastic mammary carcinoma (AMC) grew slower in hypoglycemic mice (caused by fasting or by daily insulin injections) and in hyperglycemic mice (caused by alloxan or streptozotocin, or by daily injections of glucose) than in normoglycemic mice. The tumor was able to adapt to the unfavourable conditions of the diabetes; cells, when transplanted from diabetic donors into diabetic recipients, secreted immunoreactive insulin (IRI) and immunoreactive glucagon (IRG), which are deficient in the diabetic hosts. In the terminal (hypoglycemic) phase of tumor growth, the concentrations of glucose, IRI and IRG decreased. The immunological reactivity of the host animals was reduced in the hypoglycemic terminal phase. The tumor cells taken from hosts in this phase behaved differently from the cells taken in the normoglycemic phase. The "hypoglycemic" cells grew more slowly in healthy mice; the intensity of their DNA synthesis was diminished, their response to antitumor therapy was weaker. Furthermore, it was necessary to transplant more of these cells to obtain tumors in all recipients, and they lost their ability to adapt to diabetic conditions (i.e. secreted neither IRI nor IRG). Hypoglycemia was apparently the immediate cause of death in mice with AMC. Injections of glucose or glucagon into mice with AMC eliminated the hypoglycemia temporarily and postponed the death by 4 days. Mice treated with glucagon and with chemotherapy or immunotherapy survived 6-9 days longer than mice treated with chemo- or immunotherapy alone. Some of these differences between the end-stage and the progressively growing tumors could be explained in terms of tumor cell kinetics but some could be attributed to metabolic conditions of the host caused in part by the tumor.
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PMID:Different endocrinological properties, growth rate and sensitivity to chemotherapy of aplastic mammary carcinoma in normo- and hypoglycemic phase of tumor growth. 675 72

Two experiments were conducted with male rats weighing 170 to 190 grams. In experiment 1, some nutritional parameters were determined in tumor-bearing (TB) (Walker 256 carcinosarcoma) rats fed a 23.6% casein diet for 4 weeks after the tumor inoculation. Cumulative weight gain and food intake were less in TB rats than in nontumor-bearing (NTB) rats. At 3 and 4 weeks after the tumor inoculation, plasma histidine, alanine, and glycine levels were higher in TB rats than in NTB animals. The arginine level was lower in the plasma of TB rats at 4 weeks after the inoculation. The significance of decrease in plasma arginine with regard to tumor growth is discussed. In experiment 2, the effects of total parenteral nutrition (TPN) on TB rats were evaluated as compared with those of 5% glucose (Glc) solution. Body weights of TPN rats were maintained and their nitrogen (N) balances were positive during a 7-day experimental period, while 5% Glc animals showed severe body weight loss and apparent negative N balance. After the end of infusion, the plasma urea level of the TPN group was within normal range, whereas that of 5% Glc group showed a markedly high value. The plasma albumin level was higher in the TPN group. Liver and spleen weights were increased in TPN rats. Absolute tumor weight was somewhat greater in TPN rats than in 5% Glc rats, but the difference in tumor weight:body weight ratios became more slight. These results indicate that TPN was effective for maintaining the nutritional status of TB host without significant acceleration in tumor growth.
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PMID:Nutritional responses of tumor-bearing rats to oral or intravenous feeding. 681 15

The effect of hyperglycemia on the cytotoxic effect of a chemotherapeutic agent was studied at elevated temperature. The seventh generation of a spontaneous C3Hf/Sed mouse fibrosarcoma, FSa-II, was transplanted into the footpads of the same strain of mice. Hyperthermia was given by immersing animal feet into a water bath where 41.5 +/- 0.1 degrees (range) was maintained by a constant temperature circulator. Cyclophosphamide (CY), an alkylating agent, was selected as a test agent. Single i.p. doses of glucose and of CY were given 60 and 30 min before the initiation of hyperthermia. Tumor response was assayed by determining the median tumor growth time (time required for one-half of the treated tumors to reach 1000 cu mm), and the dose-response curve was obtained. Hyperthermia enhanced tumor response to CY. The enhancement was greater when a glucose dose of 10 mg/g was administered before CY and heat treatments. The enhancement ratio, calculated as a ratio of the tumor growth time following CY (200 mg/kg) with heat or with glucose and heat to that following CY alone, was 1.31 or 2.86, respectively. Glucose given at ambient temperature did not enhance the effect of CY. A dose-response curve obtained for a glucose dose with fixed CY (200 mg/kg) and heat (90 min at 41.5 degrees) doses demonstrated that a significant enhancement was obtained following a glucose dose as low as 2 mg/g, suggesting that the glucose enhancement could be safely achieved for human cancer treatment.
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PMID:Effect of hyperglycemia on thermochemotherapy of a spontaneous murine fibrosarcoma. 685 Jun 14

Arteriovenous differences for acetoacetate, beta-hydroxybutyrate, glucose, lactic acid, and glutamine and other amino acids were measured across Morris hepatomas 5123C, 7777, and 7288CTCF and Walker sarcocarcinoma 256 in vivo in rats fasted for 2 days. The acetoacetate and beta-hydroxybutyrate concentrations in arterial whole blood of fasted tumor-bearing rats were 0.52 +/- 0.06 and 1.82 +/- 0.19 mM (S.E., n = 38), respectively. Both ketone bodies were utilized by the tumors, and the rates of utilization were directly related to the rates of supply. The mean utilization rates for acetoacetate and beta-hydroxybutyrate were 13.9 +/- 2.9 (range, 0 to 64; n = 30) and 24.7 +/- 4.4 (range, 0 to 145; n = 38) nmol/min/g tumor wet weight, respectively. Eight of the tumors produced acetoacetate, presumably from utilized beta-hydroxybutyrate. An average of 52% of the acetoacetate and 30% of the beta-hydroxybutyrate carried in the arterial blood was removed during one pass through the tumors. The concentrations of glucose and glutamine in the arterial whole blood of fasted tumor-bearing rats (n = 38) were 6.55 +/- 0.3 and 0.76 +/- 0.02 mM, respectively; both of these substrates were utilized at rates that were directly proportional to the rates of supply. The mean rates of glucose and glutamine utilization for all tumors in fasted rats were 101 +/- 11 (range, 3 to 313) and 8.2 +/- 1.1 (range, 0 to 25.1) nmol/min/g tumor wet weight, respectively. Thirty-six % of the glucose and 25% of the glutamine supplied to the tumors was utilized. Comparison (by linear regression and analysis of covariance) of the rates of supply and utilization of glucose and glutamine in tumors growing in fasted versus fed rats indicated that these substrates are utilized more efficiently by tumors growing in fasted animals. Lactic acid was either produced or utilized, depending on the arterial whole-blood concentration. Production or utilization occurred, respectively, when the arterial lactate concentration was less or greater than 1 to 3 mM. The arterial whole-blood amino acids (except glutamine) were utilized at rates that ranged from 1 to 4 nmol/min/g tumor wet weight. The results indicate that energy production for tumor growth in fasted rats is supported, in part, by an increased availability of ketone bodies, by an increased efficiency of utilization of glucose and glutamine, and, under certain circumstances, by utilization of lactic acid.
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PMID:Ketone body, glucose, lactic acid, and amino acid utilization by tumors in vivo in fasted rats. 686 Nov 21

Observations were carried out in rats with transplantable Geren's carcinoma or sarcoma induced by 3,4-benz (a) pyrene. The contents of plasma immune-reactive insulin (IRI), the glucose tolerance and response of the insular apparatus to the glycemia level were found to change at all stages of the tumor growth. Most of animals had low levels of IRI in blood, the glucose tolerance was decreased. Some rats with Geren's carcinoma showed the signs of increased functioning of the insular apparatus. It was shown that disorders in the insular apparatus function in tumor-bearing animals were due to changing of its response to the level of glycemia.
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PMID:[State of the insular apparatus in rats with transplanted and induced tumors]. 698 9

Some features of energy metabolism in two strains of Ehrlich ascites tumor cells are presented in this paper. A correlation between malignancy and activity of aerobic glycolysis was observed. In the Roma strain, ammonium ions (1-10 mM) enhance the aerobic glycolysis and the Crabtree effect induced by 5 mM glucose. In spite of the activation of glycolysis, the total amount of pyruvate and lactate decreased in the presence of ammonium, because a drain of pyruvate takes place through the pyruvate dehydrogenase complex. Ammonium ions fail to modify the Crabtree effect or the aerobic glycolysis in CBM strain. In these cells, NH4+ did not affect the pyruvate and lactate produced from glucose. It is suggested that ammonium effect on the aerobic glycolysis in Roma strain could be adventageous for tumor growth, because there is an increase in the availability of carbon skeleton from glucose to account for the assimilation of NH4+ and consequently for the synthesis of aminoacids.
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PMID:[Effect of ammonia on the Crabtree effect of 2 strains of Ehrlich ascites tumor]. 714 71

Melanoma B-16 grew slowly in mice with hyperglycemia induced by alloxan, glucagon, or glucose. The mechanism of retarded tumor growth is different and depends on the origin of hyperglycemia. The concentration of immunoreactive insulin in blood of mice with melanoma and in the tumor tissue is increased in nondiabetic as well as in diabetic mice. The chemotherapy of melanoma in diabetic mice is as effective as in nondiabetic mice whereas immunotherapy in diabetic mice is not effective. Combined chemoimmunotherapy of melanoma in diabetic mice is more effective than either therapy alone only when mice are given a daily dose of insulin.
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PMID:Growth and treatment of B 16 melanoma in hyperglycemic mice. 740 88

We have determined rates of fatty acid (FA) synthesis from glucose carbon and all two-carbon units in control mice and in mice bearing Ehrlich ascites carcinomas. Using [U-14C]glucose and 3H2O as tracers under three nutritional conditions (24-hr fasted, 24-hr fasted-refed, and ad libitum fed-refed), we found that lipogenic regulatory mechanisms in adipose tissue and livers of mice bearing advanced tumors were similar to those of control mice. FA synthesis from glucose carbon and from all two-carbon units in livers of tumorous (8-day tumors) mice was at least as fast as that in control mice in the fasted and fasted-refed states but only about one-half that of controls in the fed-refed condition. The rate of FA synthesis from two-carbon units in carcasses of mice with 8-day tumors was not significantly different from that of controls in any of the 3 dietary states studied; however, in fed-refed mice with 8-day tumors, the rate of FA synthesis in the whole body was only one-half that of controls. The rate of FA synthesis from glucose carbon in carcasses of these tumorous mice was significantly depressed compared to that of controls in both the 24-hr-fasted and the fed-refed states. In well-nourished mice with early (5-day) tumors, the whole-body lipogenic rate from all two-carbon units was not depressed. Thus, decreased lipogenesis observed in host tissues of mice with advanced tumors is due to malnourishment; this secondarily depressed lipogenic activity probably contributes significantly to the loss of body fat that may occur at later stages of tumor growth. De novo FA synthesis in Ehrlich ascites cells, although small compared to that of the whole-body rate, was substantial in relation to lipids needed for tumor nutrition.
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PMID:Dietary control of lipogenesis in vivo in host tissues and tumors of mice bearing Ehrlich ascites carcinoma. 743 94

Zinc homeostasis was studied during the induction, growth, and methotrexate (MTX) treatment of Dark Agouti rat mammary adenocarcinomas (DAMA). A progressive fall in plasma Zn concentration (pZn), significant at a tumor burden of less than 1% body weight (bw), was sustained during tumor enlargement to give a 54% reduction in pZn at 16.3% bw (n = 6/group). The hypozincemia was attributed to the increasing Zn demand for tumor growth. Zn content of the 16.3% bw tumors equaled that of muscle (normally 60% of total body Zn). Tumor metallothionein (tMT) was sufficient to bind < 3% of total tumor Zn, and hepatic MT (hMT) remained at basal concentrations during early tumor growth, doubling only in the presence of significant necrosis in large tumors. Methotrexate (MTX, 0.5 mg/Kg im x 2 d) at respective tumor burdens of 5 and 10% bw (n = 9, 10/group) gave 2 therapeutic effects, dependent on tumor size: 1.5% bw tumors in 7 rats remained close to their original size until experiment end when pZn, hMT, and tMT were typical of 5% bw untreated tumors. 2. Tumors in 5 rats given MTX at 10% bw had marked subcapsular necrosis and regression to a size similar to those in group 1; pZn returned toward normal, whereas hMT was 6 times its 5% bw counterpart. Host weight loss was significantly reduced, as were tumor-associated changes in plasma glucose and calcium. In summary, neither tMT nor hMT appears to play a role in the hypozincemia that follows DAMA Zn sequestration and growth. Critically timed MTX can result in tumor regression and return of plasma Zn, Ca, and glucose toward normal. This is associated with an increase in hMT and reduction in host weight loss, suggesting a flow of Zn from the resorbing tumor to the host, enabling the synthesis of hMT and retention of host structural proteins.
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PMID:Metallothionein and zinc homeostasis during tumor progression. Effect of methotrexate treatment. 751 67

This study examined the effect of Walker 256 tumor growth in vivo on the metabolism of glucose, glutamine and pyruvate in lymphocytes. A comparison between the metabolism of Walker 256 tumor cells obtained in vivo with that of lymphocytes was also carried out. Lymphocytes and tumor cells were isolated and incubated for 1 h for the following measurements: lactate production from glucose (5.6 mM) and pyruvate (3 mM), glutamate and aspartate formation from glutamine (3 mM) and decarboxylation of [U-14C]-glucose, [U-14C]-glutamine, [1-14C]-pyruvate and [3-14C]-pyruvate. The presence of the tumor increased lactate production (2.7-fold from glucose and 2-fold from pyruvate), decarboxylation of [U-14C]-glucose (3.7-fold) and [1-14C]-pyruvate (4.4-fold) and the formation of aspartate (6.3-fold) and glutamate (4.6-fold) from glutamine. The conversion of glucose to lactate and CO2 was higher in tumor cells as compared to lymphocytes. Tumor cells also showed a higher production of glutamate and an 8-fold increased decarboxylation rate of [U-14C]-glutamine in tumor cells, which was more active than that of lymphocytes even from tumor-bearing rats. Tumor growth stimulated glucose and glutamine metabolism in lymphocytes; however, the importance of this fact for the function of these cells remains to be elucidated.
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PMID:Metabolism of glucose, glutamine and pyruvate in lymphocytes from Walker 256 tumor-bearing rats. 754 73


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