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Query: UMLS:C0038187 (starvation)
 24,951 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

It has been suggested that adaptation to starvation may be impaired in patients with malignant disease and that this may contribute to the development of cancer cachexia. We have investigated this by comparing the body composition, as well as the tissue composition of weight loss, of a group of 49 patients with gastrointestinal carcinomas and 91 patients with benign gastrointestinal disease all of whom had sustained a weight loss greater than 10% of their recalled pre-illness weight. Total body protein was calculated from total body nitrogen measured by in vivo neutron activation analysis which also provided absolute values of sodium, chlorine, phosphorus, and calcium. The masses of muscle and nonmuscle protein were estimated using a validated compartmental analysis. Total body fat was derived using anthropometry. Total body water was estimated from the difference between body weight and the sum of body protein, fat, and minerals. The loss of body weight incurred by patients with both benign and malignant disease was primarily muscle mass and body fat. Both groups of patients retained nonmuscle protein. All patients manifested, with increasing weight loss, a progressive loss of muscle protein, fat, and water, which must represent the tissue composition of weight loss. No significant differences between patients with benign or malignant disease were demonstrated for any of the body composition parameters measured. The results of this study do not support the hypothesis that adaptation to starvation in patients with cancer is in anyway different from that which occurs in patients with benign disease.
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PMID:Body composition in malignant disease. 382 8

The metabolic responses associated with the tumor-bearing state, as compared to states of sepsis and prolonged starvation, were examined. Tumor-bearing rats manifested significant elevation of triglycerides, significant reduction of glucose and insulin levels, significantly increased plasma skeletal muscle proteolysis-inducing activity, and an unchanged hepatic protein synthetic activity compared to control rats. Prolonged starvation produced an adaptation characterized by significant hypoglycemia and hypoinsulinemia, reduced hepatic protein synthesis, and increased peripheral protolysis compared to controls. Septic animals had glucose, insulin, and lipid levels similar to control animals but had increased hepatic protein synthesis. Each state manifested its own unique metabolic response compared to controls. It appears that the metabolic consequences of cancer in this sarcoma rat model is different than septic and prolonged starvation states.
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PMID:Tumor-associated metabolism in the rat is a unique physiologic entity. 388 27

In summary, anemia developing in a patient with cancer can be due to several different factors. A relative failure of erythropoiesis, in conjunction with a modestly shortened erythrocyte survival, is the most likely explanation for the anemia and can occur in patients with or without bone marrow invasion. Several theories have been proposed to explain the mechanism of limited red cell production in cancer. Internal iron starvation and cancer toxic factors have been widely implicated. Immunoglobulin inhibitors of erythropoiesis occur in the rare entity, pure red cell aplasia, which is sometimes associated with thymomas. Autoimmune hemolytic anemia and microangiopathic hemolytic anemia can also occur in patients with solid cancers, pointing out the need for a complete evaluation of anemia in any patient with recent-onset anemia. Successful treatment and prognostic implications of anemia in cancer is dependent on proper diagnosis.
Cancer Invest 1985
PMID:Anemia in cancer. 389 Oct 30

Starvation-induced hypoglycaemia and streptozotocin-induced diabetes suppressed the growth of Ehrlich ascites tumor in mice. The suppression of tumor growth by diabetes was alleviated by administration of insulin. The number of glucose carriers on tumour cells was found to be reduced in diabetes and partial resumption of glucose carriers was observed in tumour cells of diabetes after insulin administration. Insulin had no direct effect on tumour growth in vivo and did not affect the number of glucose carriers on tumour cells in vitro. The physiological significance of these observations is discussed.
Cancer Lett 1985 Sep 30
PMID:Suppression of Ehrlich ascites tumor growth in mice by starvation and streptozotocin-induced diabetes. 390 10

There are many tumors that have paraneoplastic syndromes. Furthermore, location of certain tumors can result in very specific effects on the host, especially tumors in the hypothalamus, the intestinal tract, or the liver. Finally, tumors of the immune system can have significant distant consequences. However, from direct experimental evidence, from model systems, and from the utilization of nutritional manipulation in the treatment of cancer, the data suggest very strongly that there is no unique cancer malnutrition. Early diagnosed cancer does not show malnutrition as a presenting symptom. Furthermore, all metabolic disturbances can be explained on the basis of the metabolic differences of tumor cells and normal cells and are very frequently proportional to the bulk of the tumor. The cachexia that is associated with malignancies is more likely cachexia in cancer patients than it is a specific cancer cachexia, unless the tumor burden is very large. This point was clearly made in a short review of the causes of cachexia in nearly 1500 cancer patients in Russia (145). Brennan also feels that most cases of malnutrition are uncomplicated starvation, and cancer cachexia has many features seen in major injury or sepsis (16). This distinction has great implications in the management of cancer patients.
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PMID:Nutrition and cancer: physiological interrelationships. 392 50

Tumor-bearing animals provided with intravenous glucose and amino acids (TPN) exhibit enhanced response to S-phase-specific chemotherapeutic agents (H. M. Reynolds, J. M. Daly, B. Rowlands, S. J. Dudrick, and E. M. Copeland. Cancer 45: 3069, 1980; M. H. Torosian, J. L. Mullen, E. E. Miller, et al. J. Parenter. Enteral Nutr. 7: 337, 1983). To determine the mechanism of this response, DNA synthesis rate during starvation or a 48-hr infusion of glucose/amino acids (Glu/AA) was evaluated in tumor, liver, and terminal ileal cells of 68 rats. Tumor cells exhibited a rapid increase in DNA synthesis following the initiation of an infusion of Glu/AA. This increase was most marked after 2 hr of infusion and returned to control levels within 24 hr. Liver DNA synthesis rate increased in both starved and Glu/AA animals over 48 hr with a larger increase in animals receiving Glu/AA. Ileal DNA synthesis decreased equally in both groups. Short pulse Glu/AA produced transient increases in tumor DNA synthesis. Changes in host tissues occurred but followed a different temporal sequence. This may indicate the existence of a period of time following initiation of metabolic manipulation when tumor susceptibility to phase-specific chemotherapeutic agents will be enhanced while host tissues will be spared from increased toxicity.
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PMID:The effects of glucose and amino acids on tumor and host DNA synthesis. 393 82

The kinetics of cell cycle progression in continuously proliferating 3T3 fibroblasts and two tumor transformed derivatives (3T6 and SV 3T3 cells) following treatment by growth-factor deprivation (serum starvation) or 25-hydroxycholesterol were studied. Normal 3T3 cells were found to respond immediately (in the first cycle) to growth factor deprivation by leaving the cell cycle from G1, whereas the tumor transformed derivatives did not. However, all three cell types were forced to stop the progression through the beginning of G1 when treated by 25-hydroxycholesterol. It was ensured that the doses of 25-hydroxycholesterol used really induced substantial decrease of HMG CoA reductase activity. However, the effects of serum starvation on HMG CoA reductase activity varied considerably. In 3T3 cells HMG CoA reductase activity was substantially depressed, in 3T6 cells it was moderately depressed, and in SV-3T3 cells it was not depressed at all. This difference of HMG CoA reductase activity between 3T6 and SV-3T3 cells was related to the difference of growth activity in serum-free medium. The data indicate that a certain activity of HMG CoA reductase is required for the proliferation of normal as well as tumor transformed cells but also that impairment of the control of HMG CoA reductase, leading to increased enzyme activity, may result in uncontrolled growth in tumor transformed cells.
Cancer Res 1986 Mar
PMID:Kinetics of G1 progression in 3T6 and SV-3T3 cells following treatment by 25-hydroxycholesterol. 394 95

While malnutrition attending cancer cachexia may be associated with variable losses of body fat, lipid metabolism has been only minimally studied. To clarify potential aberrations of lipid metabolism in weight losing cancer patients, the whole body rate of lipolysis was determined in 9 cancer patients in the postabsorptive state and compared to that in 5 normal subjects. A primed-three stage infusion of glycerol was used to measure plasma glycerol clearance and turnover. A positive correlation between glycerol turnover and plasma concentration was demonstrated in both cancer patients (r = 0.72) and in normal subjects (r = 0.81). Glycerol turnover rate in cancer patients (2.05 +/- 0.14 mumol X kg-1 X min-1) was not different from that in normals (2.31 +/- 0.50); while glycerol clearance in cancer patients (1.72 +/- 0.13 L/min) was significantly lower (P less than 0.025) by 32% than that in normals. This study demonstrates that the whole body lipolytic rate in cancer patients is not different from healthy normals. As a consequence, the loss of body fat in patients with cancer cachexia may be due to a reduced rate of lipogenesis rather than augmented lipolysis as is observed in nonmalignant malnutrition, starvation, or injury.
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PMID:Cancer cachexia and the rate of whole body lipolysis in man. 395 2

The growth of MCF-7 cells was arrested by 24 h of isoleucine deprivation. Following replenishment of the medium, the incorporation of uridine and thymidine into trichloroacetic acid-precipitable material began to increase slowly and gradually rose to the level of cycling cells. The addition of 5 X 10(-9) M estradiol to growth-arrested cells dramatically shortened the time of onset of macromolecular synthesis and increased the overall amount of precursor incorporation 2- to 4-fold over the level obtained by arrested control cells. The increase in uridine incorporation preceded the increase in thymidine incorporation by 6 h. Inhibition of protein synthesis with cycloheximide blocked the recovery of macromolecular synthesis in both control and estrogen-treated cells. Actinomycin D was ineffective in blocking the estrogen-stimulated recovery of macromolecular synthesis at concentrations known to inhibit pre-rRNA synthesis (10(-8) M). At higher concentrations, uridine and thymidine incorporation were inhibited in a dose-dependent manner. Inhibition of RNA polymerase II activity with alpha-amanitin similarly blocked both the recovery of the cells from isoleucine starvation and the potentiation of this by estradiol. Dihydrofolate reductase and thymidine kinase activities are both stimulated by estradiol in MCF-7 cells. In cycling cells, estrogen stimulates a 2-fold increase in their messenger RNAs (mRNAs) within 24 h. The level of dihydrofolate reductase mRNA is unaffected by isoleucine starvation, and estrogen caused no change in dihydrofolate reductase mRNA levels over a 24-h period following reversal of growth arrest. Similar results were observed for the 600-nucleotide pS2 mRNA that has been identified as an estrogen-induced RNA in MCF-7 cells. In contrast, thymidine kinase mRNA was found to be increased by estrogen at 24 h, but not at 12 h, following reversal of growth arrest. This increase correlates with increases in thymidine, but not uridine incorporation. These data indicate that the estrogen-stimulated increase in thymidine incorporation following release from growth arrest is dependent on new RNA synthesis. However, the hormone did not increase the levels of three estrogen-regulated mRNAs coordinately with the increases observed in uridine incorporation.
Cancer Res 1985 Jun
PMID:Relationship between the expression of estrogen-regulated genes and estrogen-stimulated proliferation of MCF-7 mammary tumor cells. 398 99

To investigate the effects of 1-beta-D-arabinofuranosylcytosine (ara-C) at high doses as applied in human acute leukemia, the cytotoxic effect of high-dose ara-C was studied in L1210 leukemia cells grown in tissue culture or as tumors in syngeneic mice. Exponentially growing cells displayed the expected S-phase specificity and dose saturation properties of drug action. In contrast, in stationary cultures, progressively more cells were killed by increasing the concentration of the drug. Moreover, the fraction of cells killed at high doses exceeded by 2- to 3-fold the number of cells in drug-sensitive S phase detectable by flow cytometry or [3H]thymidine radioautography. To identify these apparent non-S targets of ara-C at high doses, L1210 cells were separated according to cell cycle position by velocity sedimentation at unit gravity. Large fractions of cells, accumulating at the G1-S boundary by nutrient starvation, were detected in stationary tissue culture cells as well as in ascites or solid tumor cells. The cells located in this cell cycle compartment (termed S1 cells) were sensitive to the cytotoxic effect of high-dose ara-C. The putative presence of similar S1 fractions in advanced human acute nonlymphocytic leukemia may explain in part the clinical efficacy of a high-dose application of the drug.
Cancer Res 1985 Jul
PMID:S1-phase cells of the leukemic cell cycle sensitive to 1-beta-D-arabinofuranosylcytosine at a high-dose level. 400 48


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