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Query: UMLS:C0027651 (tumor)
 685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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.
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PMID:Kinetics of G1 progression in 3T6 and SV-3T3 cells following treatment by 25-hydroxycholesterol. 394 95

We evaluated the effects of chronic massive elevations of serum GH and PRL on calcium metabolism in rats bearing the MStT/W15 and 7315a transplantable pituitary tumors. MStT/W15 tumor rats manifest elevated serum GH and PRL levels, hypercalcemia, hypercalciuria, and elevated serum levels of PTH and 1,25-dihydroxyvitamin D. The hypercalcemia was not reversed by dexamethasone or propranolol treatment, but was ameliorated by starvation. Parathyroidectomy produced hypocalcemia in the MStT/W15 tumor rats, confirming the parathyroid dependence of the hypercalcemia. The 7315a tumor produced a milder degree of hypercalcemia, along with elevated serum levels of PRL, ACTH, and corticosterone; serum GH was normal. In high concentrations, PRL and/or GH may stimulate the secretion of PTH as well as enhance dietary calcium absorption, in part through the mediation of 1,25-dihydroxyvitamin D.
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PMID:Hypercalcemia in rats bearing growth hormone- and prolactin-secreting transplantable pituitary tumors. 402 91

The highly increased fibrinolytic activity of HeLa cells, treated with the tumor promoting phorbol ester, phorbol myristate acetate (PMA), correlates with equally increased levels of tissue-type plasminogen activator (t-PA) antigen in the conditioned media of these cells and concomitantly increased steady state levels of t-PA-specific mRNA. The effect of PMA on t-PA mRNA levels is completely blocked by pretreatment of the cells with the inhibitor of translation, cycloheximide, indicating that it requires the biosynthesis of at least one protein intermediate. In contrast, mRNA of the oncogene product c-myc can be induced for a brief period immediately following serum starvation in the presence and absence of PMA, and in the presence of cycloheximide. Our results suggest that increased t-PA biosynthesis in HeLa cells, probably through an increased rate of translation of the t-PA gene, forms part of the "late" events of the pleiotropic response to tumor promoters.
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PMID:Induction of fibrinolytic activity in HeLa cells by phorbol myristate acetate. Tissue-type plasminogen activator antigen and mRNA augmentation require intermediate protein biosynthesis. 403 26

Tumor and host tissue DNA synthesis in C3H female mice with MA16/C tumors were examined for the effects of starvation and refeeding. Animals with subcutaneously implanted tumors were randomized to either regular diet or starvation for 48 hr followed by refeeding for 6, 12, 24, 48, or 72 hr. With starvation, both tumor and host tissues demonstrated a decrease in DNA synthetic activity. After refeeding, resumption in DNA tumor synthesis preceded that of host tissues and was greatest within the first 6-12 hr. Host tissue DNA synthetic activity resumed at different times in the various tissues examined with bone marrow being earlier than spleen or liver. The differential time course between induction of tumor and host DNA synthesis could allow a more precise modeling in studies dealing with the interaction of nutritional repletion and antitumor therapy.
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PMID:Refeeding differentially affects tumor and host cell proliferation. 406 92

Thyroid-stimulating hormone (TSH) alpha- and beta-subunit glycosylation was investigated in mouse thyrotropic tumor and in normal and hypothyroid pituitary cells for various periods of time in the presence of [3H]mannose or [3H]galactose. After sequential precipitation with anti-alpha and anti-beta sera, subunits were treated with Pronase followed by endo-beta-N-acetylglucosaminidase H (Endo H) and analyzed by paper chromatography. In primary cultures of thyrotropic tumor cells incubated for 60 min with [3H]mannose, primarily Man9GlcNAc and Man8GlcNAc were found on TSH + alpha subunits, whereas Glc1Man9GlcNAc and Man9GlcNAc were prominent on free beta subunits. After preincubation of cells for 16 h in the presence or absence of glucose followed by a 60-min pulse of [3H]mannose, there was an 8-fold increase in labeled TSH + alpha but only a minimal change in free beta or total proteins. In the absence of glucose, there was a selective accumulation of Man8GlcNAc on TSH + alpha but not on free beta or total proteins; however, there was no detectable accumulation of Endo H resistant forms during glucose starvation on TSH subunits or total proteins. Normal mouse and rat pituitary minces incubated for 60 min with either [3H]mannose or [3H]galactose showed no glucose-containing species on TSH subunits, but equal amounts of Man9GlcNAc and Man8GlcNAc on TSH + alpha, and mostly Man9GlcNAc on free beta subunits. In contrast, hypothyroid mouse and rat pituitaries exhibited an increase in Glc1Man9NAc and Glc1Man8GlcNAc on free beta but not on TSH + alpha or total proteins.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Differential processing and regulation of thyroid-stimulating hormone subunit carbohydrate chains in thyrotropic tumors and in normal and hypothyroid pituitaries. 407 17

Enhancement of hexose uptake seems well correlated with transformation of cell cultures by tumor viruses and the absence of contact inhibition. Enhancement of sugar uptake has also been observed as a result of hexose starvation. Both types of enhancement can clearly be demonstrated in cultures of hamster cells when uptake of (14)C-labeled galactose is monitored after 10 or 20 min. The profiles of accumulation products are strikingly different. In cultures of hamster NIL cells transformed with polyoma virus much of the (14)C is accumulated as UDPhexose. Untransformed cells accumulate galactose-l-phosphate as well as UDPhexose. Hexose-starved cells show enhanced uptake of galactose; however, this marked enhancement was only observed in NIL cultures close to contact inhibition. The novel and common feature seen in hexose-starved cells when incubated briefly with (14)C-labeled galactose is the occurrence of a marked accumulation of [(14)C]UDPglucuronic acid at the expense of UDPhexose. The ratio [(14)C]UDPglucuronic acid/UDPhexose in cultures fed glucose or galactose was invariably low (0.15-0.2) regardless of the presence or absence of contact inhibition. 20 hr of hexose starvation invariably changed this ratio by a factor of 10 or more, due to accumulation of UDPglucuronic acid. This result was also observed in cultures transformed with polyoma virus. The presence of 3-O-methylglucose in the growth medium did not alter the typical "sugar starvation pattern" (i.e., the UDPglucuronic acid/UDPhexose ratio averaged 1.7). Enhancement of galactose uptake by hexose starvation was very pronounced in NIL cultures that were close to contact inhibition, but was not a prominent feature in the polyoma-transformed cultures. The transformed cells grown on glucose or galactose growth medium showed the usual enhanced rate of uptake of galactose as compared with nontransformed near-confluent cultures that had been fed hexose. The polyoma-induced enhancement showed none of the features characteristic of hexosestarved cells.
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PMID:Two distinct types of enhancement of galactose uptake into hamster cells: tumor-virus transformation and hexose starvation. 451 63

Billen, Daniel (University of Texas M. D. Anderson Hospital and Tumor Institute, Houston, Tex.), and Roger Hewitt. Influence of starvation for methionine and other amino acids on subsequent bacterial deoxyribonucleic acid replication. J. Bacteriol. 92:609-617. 1966.-A study has been made of the subsequent replicative fate of deoxyribonucleic acid (DNA) synthesized during amino acid starvation by several multiauxotrophic strains of Escherichia coli. Using radioisotopic and density labels and a procedure whereby total cellular DNA is analyzed, we have confirmed and extended a recent report that the DNA made during amino acid starvation behaves anomalously during subsequent DNA replication. When 5-bromouracil (BU) serves as the density lable, 40% or more of the DNA synthesized during starvation will subsequently fail to replicate during three cell generations. Selective amino acid effects were noted. In two methionine-requiring bacteria, methionine deprivation appeared to be of singular importance in influencing the subsequent replicative fate of the DNA made in its absence. When a non-BU density label (N(15), C(13)) was utilized, the effects of amino acid starvation were less obvious. Although the DNA synthesized during complete amino acid starvation in a methionine-requiring E. coli was subsequently more slowly replicated, most of the DNA was finally duplicated during three generations of growth. If methionine was present during starvation for other required amino acids, the subsequent replication rate of the DNA synthesized during this time was more nearly normal, and complete replication was observed. The results have been interpreted as indicating that DNA synthesized during amino acid starvation, and especially during methionine starvation, is somehow altered, and that BU substitution for thymine may interfere with the restoration of such DNA to its replicative state.
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PMID:Influence of starvation for methionine and other amino acids on subsequent bacterial deoxyribonucleic acid replication. 533 80

Fixation of (131)I-serum albumin by Ehrlich ascites tumor cells in suspensions and sarcoma S-180 monolayers was measured under experimental conditions. Anaerobic incubation and inhibitors of the oxidative metabolism critically restricted the range of glucose concentrations capable of supporting cell life; in glucose concentrations higher than 10(-2)M, Ehrlich cells suffered from their own acid production; in concentrations 10(-2)M, lower than they underwent damage by starvation. Both types of damage were accompanied by increased albumin fixation unrelated to pinocytosis. Different procedures recommended to enhance the uptake of infectious viral RNA by animal cells in culture were tested for their ability to increase albumin uptake. They enhanced the penetration of both albumin and vital dyes and decreased the viability of cell populations. Their effect, therefore, is related to cell damage. It was postulated that reversible damage to cells favors RNA infection by leading to abnormal uptake processes and by decreasing intracellular digestion. This abnormal uptake is different from pinocytosis and also from the massive fixation of albumin to dead cells. The latter phenomenon is due to adsorption by intracellular sites exposed by disruption of the cell membrane. Polycations are able to induce all three forms of fixation depending on the experimental conditions.
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PMID:Studies on protein uptake by isolated tumor cells. 3. Apparent stimulations due to pH, hypertonicity, polycations, or dehydration and their relation to the enhanced penetration of infectious nucleic acids. 603 87

The importance of decreased food intake as the mechanism behind altered protein metabolism in skeletal muscle in cancer was evaluated. A methylcholanthrene-induced sarcoma (MCG 101) transplanted in weight-stable and nongrowing mice (C57BL/6J) was used as the tumor-animal model. Three study groups with appropriate control groups were used: sarcoma-bearing mice; pair-fed mice; and starved mice. The synthesis of myofibrillar and sarcoplasmic proteins was decreased in sarcoma-bearing mice. This was correlated to decreased content of RNA in the muscles and caused a net loss of muscle tissue was measured by dry weight of skeletal muscles. The incorporation rate of amino acids into myofibrillar and sarcoplasmic proteins was decreased to the same extent in the pair-fed mice as that in the sarcoma-bearing mice. This probably reflected decreased protein synthesis, since the radioactivity (dpm/mg) did not differ significantly in the crude transfer RNA fraction between the groups. Separation of soluble proteins from muscle tissue by means of ion-exchange chromatography showed that the pattern of decreased protein synthesis was not tumor specific when compared to muscle affected by starvation. The decrease in protein synthesis was more or less selective, since the synthesis of basic proteins was considerably decreased and was influenced more than were neutral and acidic proteins in both cancer and starvation. Anorexia of a tumor-bearing host is a sufficient trigger to induce decreased protein synthesis in skeletal muscles, but other factors may also be of quantitative importance.
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PMID:Evaluation of anorexia as the cause of altered protein synthesis in skeletal muscles from nongrowing mice with sarcoma. 616 32

Seven strains of normal human cells (fibroblastic, skin epithelioid, and amniotic) ceased to proliferate in medium depleted of free calcium ion by titration with ethylenebis(oxyethylenenitrilo)tetraacetic acid (EGTA), whereas the growth of 9 of 10 human melanoma cell lines was not affected. Fibroblasts showed a rapid drop in thymidine pool size and decreased incorporation of thymidine and uridine when treated with EGTA, followed during the next 48 hr by a decrease in plasma membrane potential and by development of a proliferative block in the G1 phase of the cell cycle. The calcium-independent melanoma line MM96 exhibited an early decrease in thymidine pool size and enhanced incorporation of nucleosides but continued to proliferate with little perturbation of the cell cycle or change in membrane potential. Tumor cell DNA may therefore be selectively labeled in the presence of normal cells. The anomalous, calcium-dependent melanoma line (MM170) showed an immediate increase in the thymidine pool size and in nucleoside incorporation and subsequently accumulated in G1 and G2 with diminution of membrane potential and of DNA and RNA synthesis. The proliferative block in MM170 cells could be reversed by addition of calcium ion or by replacement with control medium. Addition to the medium of all 8 nucleosides (50 microM), singly or together, did not prevent EGTA-induced cytostasis in fibroblasts or MM170; transport of thymidine across the cell membrane was enhanced by 24-hr EGTA treatment in fibroblasts, MM96, and MM170. Thus, although calcium affected thymidine utilization rapidly and differently in each of the three cell types, nucleoside starvation per se did not appear to be responsible for either type of proliferative block.
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PMID:Effects of calcium depletion on human cells in vitro and the anomalous behavior of the human melanoma cell line MM170. 618 41


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