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

Histone mRNA was isolated from mengovirus-infected Ehrlich ascites tumor cells at various times postinfection and quantitated in a reticulocyte cell-free protein-synthesizing system. The amount of translatable histone mRNA decreases during the first hour postinfection by 30%, rises during the following 1-1.5 h by 10-15%, drops progressively in the further course of infection, and reaches 20% of the control at the end of the infectious cycle (8-9 h postinfection). On the basis of the relative histone mRNA contents, the histone-synthesizing potentials of mengovirus-infected Ehrlich ascites tumor cells are substantially higher throughout infection than actually expressed in vivo. This result indicates that the virus-induced shutoff of histone synthesis is not directly the consequence of inactivation or degradation of histone mRNA. Most of the histone mRNA recovered from mengovirus-infected Ehrlich ascites tumor cells is bound to ribosomes. Late in infection, certain mRNAs are co-isolated with histone mRNAs, very likely due to loss or shortening of poly(A) occurring after release of the mRNAs from polyribosomes.
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PMID:Fate of histone messenger RNA in mengovirus-infected Ehrlich ascites tumor cells. 20 58

Dimethylbenzanthracene-induced rat carcinomas possess activities binding cyclic adenosine 3':5'-monophosphate (cAMP) and estrogen. When dimethylbenzanthracene-induced tumors regress after ovariectomy of the host, a change in the specific binding of cAMP and estrogen occurs in the tumors. Six days after ovariectomy, cAMP binding increases 5-fold in the nuclei and 2-fold in the cytosol of tumors, while nuclear and cytoplasmic estrogen binding decreases by 80% and 50%, respectively. These changes in activities binding cAMP and estrogen are detectable within 1 day after ovariectomy and the changes are reversed when resumption of tumor growth is induced by the injection of 17beta-estradiol. When dimethylbenzanthracene-induced tumors fail to regress after ovariectomy, the change in activities binding cAMP and estrogen does not occur. Significant increases in the cAMP level as well as in adenylate cyclase and cAMP-phosphodiesterase activities are also found in the regressing tumors. Concomitant with the increase of cAMP-binding activity is an increase in histone kinase activity in the regressing tumor. These data suggest the involvement of cAMP in the growth control of a hormone-dependent mammary rumor.
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PMID:Cyclic AMP-binding proteins: inverse relationship with estrogen-receptors in hormone-dependent mammary tumor regression. 20 18

Cyclic AMP dependent protein kinase activity was depressed in whole thymus and spleen as well as isolated splenic lymphocytes from B16 melanoma bearing C57B1/6J mice as compared to control animals. A similar loss of enzyme activity was observed in human peripheral blood lymphocytes from melanoma bearing patients as compared to normal subjects. An unaltered level of activity in the heart of tumor bearing mice suggested some specificity for the lymphoid system. This depressed enzyme activity was the result of a diminished Vmax for cAMP stimulated calf histone phosphorylation. The tumor bearing state in the mouse was also accompanied by a depletion of small lymphocytes from both thymus and spleen and it is hypothesized that the losses of lymphocytes and cAMP dependent protein kinase activity are related.
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PMID:Loss of lymphocyte cyclic AMP dependent protein kinase activity in malignant melanoma. 20 55

During the growth arrest of 7,12-dimethylbenz(alpha) anthracene-induced rat mammary carcinomas following ovariectomy or N6, O2'-dibutyryl cyclic adenosine 3':5'-monophosphate (DBcAMP) treatment, a change in the specific estrogen and cAMP binding to tumor proteins is observed. Three days after ovariectomy or DBcAMP treatment of the hosts, cAMP binding increases 5- and 2-fold in the nuclei and cytosol of tumors, respectively, whereas nuclear and cytoplasmic estrogen binding decreases by 70 and 25%, respectively. These changes in cAMP- and estrogen-binding activities are detectable within 1 day after ovariectomy or DBcAMP treatment, and the changes are reversed when resumption of tumor growth is induced by the injection of estradiol valerate or cessation of DBcAMP treatment. When 7,12-dimethylbenz(alpha)anthracene-induced tumors fail to regress after ovariectomy or DBcAMP treatment, the change in estrogen and cAMP binding does not occur. Concomitant with the increase of cAMP-binding activity in regressing tumors are increases in histone kinase activity and the cAMP content of the tumors. These increases in cAMP-binding and protein kinase activities are blocked by cycloheximide. These data suggest an interaction between a steroid hormone and cAMP in the growth control of a hormone-dependent mammary tumor.
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PMID:Inverse relation between estrogen receptors and cyclic adenosine 3':5'-monophosphate-binding proteins in hormone-dependent mammary tumor regression due to dibutyryl cyclic adenosine 3':5'-monophosphate treatment or ovariectomy. 21 Sep 38

The effect of mengovirus infection on the extent of phosphorylation of histone H1 was studied in Ehrlich ascites tumor cells. After prelabeling of the nuclear protein with [32P] orthophosphate, the excorporation of radioactivity was followed as a function of time postinfection. Employing high-resolution polyacrylamide gradient slab gel electrophoresis and autoradiography, it was found that, compared to a relatively slow turnover of phosphate groups in histone H1 in mock-infected cells, in mengovirus-infected cells the excorporation of radiolabel from histone H1 was significantly enhanced. In the latter case, the decrease of histone-bound radioactivity was paralleled by a reduction of the band multiplicity in the histone H1 region of the electrophoresis profile. It was also shown that the microheterogeneity in the histone H1 complements isolated at various times postinfection was reduced to the same basal 3-band level by incubation of the nuclear protein fractions in the presence of alkaline phosphatase. After this treatment, the band multiplicity equaled that found in histone H1 from stationary cells.
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PMID:Dephosphorylation of histone H1 after mengovirus infection of Ehrlich ascites tumor cells. 21 3

Approximately 70% of primary 7,12-dimethylbenz(alpha)-anthracene-induced mammary tumors regressed when (tumor-bearing) rats were made diabetic after treatment with streptozotocin. In the intact animal, cyclic adenosine 3':5"-monophosphate (cAMP) levels of tumors that regressed following the induction of diabetes were initially 4-fold lower than in unresponsive tumors but increased 4-fold during regression. The insulin-independent tumors showed no statistically significant changes. cAMP binding in cytosol of regressing tumors was about 80% above the initial values at 36 hr after therapy but decreased to about 45% 1 week later. On the contrary, the binding capacity of the nuclei showed a 56% increase at 36 hr and increased gradually to about 3-fold 1 week later. Within 36 hr after treatment, total histone kinase activity increased 127% in the cytosol and 153% in the nuclei of regressing tumors. The increment of histone kinase activity was almost totally in the cAMP-dependent component of the enzyme. These changes were not apparent in insulin-independent tumors. The results are interpreted to indicate that mammary tumor regression due to diabetes involves the cAMP system and occurs through a sequence of events similar to those observed during regression induced by either ovariectomy or dibutyryl cAMP (cyclic adenosine 3':5'-monophosphate) treatment.
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PMID:Cyclic adenosine 3':5'-monophosphate and protein kinase activity in insulin-dependent and -independent mammary tumors. 22 Nov 6

Cyclic-AMP-dependent protein kinase activity was depressed in whole spleen as well as in isolated splenic lymphocytes from 3-methylcholanthrene (MCA), R3230 AdCa mammary adenocarcinoma, N-hydroxy-2-acetylaminofluorene, and 4-dimethylaminoazobenzene (DMAAB) tumor-bearing Fischer rats as compared to control animals. The magnitude of depression increased with the immunogenicity of the tumor. The depressed enzyme activity was the result of a reduced Vmax for adenosine 3',5'-monophosphate (cAMP)-stimulated histone phosphorylation.
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PMID:Correlation of immunogenicity with suppression of lymphocyte adenosine 3',5'-monophosphate-dependent protein kinase. 22 14

Injection of L-1-tosylamido-2-phenylethyl chloromethyl ketone (TPCK) at a level of 10 mg/100 g body weight inhibited the incorporation of 3H-labeled amino acids into protein in Morris hepatomas 7777and 9618A2. The degree of inhibition was similar in cytoplasmic proteins and in histone and nonhistone nuclear protein fractions. There was no inhibitory effect on 3H-labeled amino acid incorporation in the livers of the tumor-bearing rats. The inhibitory effect of N-tosyl-L-lysine chloromethyl ketone (TLCK) on incorporation of 3H-labeled amino acids was observed in both the slowly growing hepatoma 7787 and the rapidly growing hepatoma 7777. In hepatoma 7777, TLCK (2.5 mg/100 g body wt) exerted a greater inhibitory effect on incorporation when administered 60 minutes before [3H]leucine injection than when injected simultaneously. Studies on tissue uptake of amino acids, thymidine, and phosphate indicated that inhibitory effects of TPCK and TLCK on active transport may be a major factor in the action of these drugs on macromolecular synthesis. The inhibitory effects of TPCK and TLCK seen in transplanted hepatomas and a colon tumor were not generally seen in normal tissues of the tumor-bearing rats.
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PMID:Selective effects of two chloromethyl ketones on amino acid and phosphate uptake in rat liver and tumors. 28 72

The chromosomal proteins from a number of transplantable hepatocellular carcinomas (THC) induced by a single carcinogen or its derivatives and varying greatly in their growth rates were examined by sodium dodecyl sulfate (SDS) polyarcylamide gel electrophoresis. Before extraction and analysis of proteins, chromatin from hepatomas, as well as from normal and regenerating liver was fractionated into rapidly and slowly sedimenting gradient components. Ten non-histone chromosomal proteins (NHCP) present in the tumors and ranging in molecular weight from 220,000 to 55,000, were absent from normal liver. Further, each rapidly growing tumor possessed more non-histone protein bands in the most rapidly sedimenting chromatin fractions than did corresponding, slowly growing tumor fractions. A number of single protein occurrences common only to normal liver and/or rapidly or slowly growing tumors were also found. In contrast, NHCP banding patterns of rapidly growing 70% hepatectomized rat liver were identical to those of non-dividing liver. Of particular interest was the finding that the prototypic "minimal deviation tumor" 9618A varied more in its NHCP-banding pattern when compared to liver than did those tumors which were rapidly growing and poorly differentiated. These studies represent an initial attempt at seeking NHCP which might be uniquely related to the malignant process.
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PMID:Analysis of chromosomal proteins of fractionated chromatin from rat liver and transplantable hepatocellular carcinomas. 52 72

The chromosomal proteins from chromatins of normal and background liver and spontaneous primary hepatocellular carcinomas (PHC) of C3H/HeN mice were examined by high resolution acid-urea and sodium dodecyl sulfate (SDS) polyacrylamide gel electrophoresis. Before gel analysis, the histone and non-histone chromosomal proteins (NHCP) from the various tissues studied were separated by affinity chromatography. No qualitative or quantitative differences in histone content were detected in any of the chromatins studied. Tumor and background chromatins did, however, exhibit higher NHCP content than normal tissues. When NHCP were fractionated on SDS polyacrylamide gels, the appearance of 10 new unique NHCP, many of which were of high molecular weight, was found to accompany the manifestation of malignancy in these C3H/HeN mice. Conversely, the abundance of a number of individual NHCP decreased precipitiously in PHC chromatin; and, additionally, two high-molecular-weight NHCP present in normal chromatins were not detectable in background and PHC chromatin. A number of NHCP were found to be unique to each of the chromatins studied. The progressive increase in total number of NHCP in background and PHC chromatin when compared to normal chromatin suggested that such changes in NHCP might indicate progression towards malignancy. The acquisition of new high-molecular-weight NHCP, the loss of some high-molecular-weight NHCP, and the decrease in individual NHCP found for mouse PHC correlate well with findings of previous studies in other systems in which malignant transformation was induced with some agent. It appears then that changes in NHCP accompany both spontaneous and induced malignant transformation, and that such changes may reflect alterations in gene expression known to accompany malignancy.
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PMID:Alterations in chromosomal proteins in C3H/HeN mice with spontaneous primary hepatocellular carcinomas. 54 34


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