Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027651 (tumor)
 685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The water-soluble carbodiimide salt 1-ethyl-3-(3'-dimethylaminopropyl)carbodiimide. HCl (EDCI-HCl) has been shown to increase the complement-dependent lysis of cultured mouse neuroblastoma C1300 cells by two types of antibody: (1) natural antibodies in the sera of normal (nonimmunized) rabbits, and (b) serum antibodies from snygeneic tumor-bearing A/HeJ mice. In the latter case, both the level of serum antibodies and the extent of carbodiimide enhancement of immune lysis were demonstrated in vitro to be substantially greater with sera from mice bearing 21-day-old tumors relative to 4-day-old tumors. The carbodiimide EDCI-HCl has also been found to increase the complement-dependent lysis of cultured TA3 carcinoma cells by serum antibodies from isogeneic LAF1/J mice bearing ascites tumors in advanced stages of growth. Finally, it has been shown that EDCI-HCl exerts an antitumor activity in vivo that is significantly greater against 21-day-old than against 4-day-old neuroblastoma c1300 tumors. The increase in EDCI-HCl activity with tumor age is contrary to the response that would be expected if this drug were serving as an antimetabolite. This is evidenced by data showing that the antimetabolite 6-thioguanine is most effective against young rapidly growing neuroblastoma C1300 tumors. The correlation between carbodiimide antitumor activity and host production of cytotoxic antibodies suggests that EDCI-HCl may operate in vivo by an immunological mechanism comparalbe to that demonstrated in vitro.
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PMID:Carbodiimide enhancement of complement-dependent antibody-mediated tumor cell lysis in vitro and antitumor activity in vivo. 111 28

A cell-free protein synthesis system derived from Ehrlich ascites tumor cell ribosomes (S30) plus rabbit reticulocyte tRNA was developed and the activity of the system was dependent on rabbit reticulocyte ribosomal salt (0.5 M KC1) wash factors, The exogenous mRNAs from BALB/c mouse liver and the mammary gland were translated with a high efficiency in this heterologous cell-free system. Furthermore, the RNA from the lactating mammary gland faithfully directed the synthesis of casein. The presence of mouse casein in the reaction product was identified by radioimmunoprecipitation with mouse casein antiserum, co-electrophoresis of the reaction product and mouse casein the urea-polyacrylamide gel and by electrophoresis in sodium dodecyl sulfate (SDS) polyacrylamide gel. The major portion of the lactating mammary gland RNA directed synthesis of the milk protein in the cell-free system appeared to be analogous to alphas casein,
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PMID:Murine mammary gland RNA directed synthesis of casein in a heterologous cell-free protein synthesis system. 116 23

Tumour-bearing mice, 248 in number, have been injected with 5-methyl-cytidine dissolved in physiological salt solution. The mice were divided into 5 series depending upon the amount of 5-methyl-cytidine they received. Mice of a successive series received 43.2, 28.8, 14.4 and 7.2 mg/kg body weight. There was a progressive increase in the percentage of mice showing regression of tumours in the successive series, as follows: 45%, 50%, 65%, 60%, and 67.8% respectively, giving an average percentage of regressions of 59.7%. The incidence of mice developing multiple primary tumours increased in the same successive series respectively as follows: 25%, 43.8%, 58.3%, 73.3%, and 70%, thus giving an average of 58.3%. The evidence obtained indicates an inverse correlation (dose-response) between the amount of the 5-methyl-cytidine injected and the percentage of regressions of spontaneous tumours.
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PMID:An inverse correlation (dose-response between 5-methyl-cytidine and the fate of spontaneous tumours in mice. 117 91

Tumor-bearing mice of the C3H/ST inbreds were used in this investigation. Of the 598 mice, 290 were controls, 248 received injections of 5-methyl cytidine dissolved in physiological salt solution, and 60 received injections of three nucleosides - adenosine, 6-methyl adenosine, and 5-methyl cytidine - also dissolved in physiological salt solution. The mice were divided into 6 groups based upon the number of generations of descent from a mouse injected with an alcohol-soluble liver extract. The criterion of tumor growth is the average increment of growth at the 20th observation period in the 7th week (3 per week). There is a cumulative inhibition of tumor growth, compared with controls, when 5-methyl cytidine is added to the effect of a transmissible entity which occurs in the lineal descendants of a tumor-bearing mouse injected with an alcohol-soluble liver extract and when the combination of three nucleosides in the same ratio of molar concentrations as in the liver extract is added to the effect of the transmissible entity.
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PMID:Further studies on a transmissible entity in relation to the control of cancer in mice. 117 69

Peritoneal effusions of patients with ovarian cancer contain sizable amounts of free and complexed immunoglobulins. By means of salt precipitation procedures, antibodies were recovered that after purification and concentration displayed a high degree of specificity against ovarian carcinoma cells. In indirect immunofluorescence, immunoglobulins recovered from seven different peritoneal effusions showed bright cytoplasmic staining with tissue cultures and fresh suspensions of ovarian carcinoma cells but not of normal ovaries or non-ovarian tumors. Immunoglobulins isolated from fluids of benign ovarian cysts or from effusions of non-ovarian tumors were negative in immunofluorescence tests. Autologous antibodies recovered from peritoneal effusions will be hopefully utilized in sensitive radioimmunoassay tests that are greatly needed for the early detection of ovarian cancer, the leading cause of death from gynecologic neoplasia.
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PMID:Isolation of tumor-specific antibodies from effusions of ovarian carcinomas. 118 43

Ten series mice of C3H/ST inbreds with spontaneous tumors have received 5-methyl cytidine (total 500 mice). Graded single doses of (1) 3.86, (2) 2.57, (3) 2.06, (4) 1.54, (5) 1.03, (6) 1.54, (7) 1.03, (8) 0.51, (9) 0.26, and (10) 0.13 mg/injection (three times weekly) were used. In series 1-5 the 5-methyl cytidine was dissolved in distilled water, and in series 6-10, the nucleoside was dissolved in physiological salt solution. In doses administered, series 4-5 overlapped with series 6-7. The number of mice that showed a regression of tumor increased in the successive series (48%-63% in series 1-5 and 25%-73% in series 6-10). As the number of mice with regressing tumors increased, the percentage of mice showing multiple primary tumors also increased. The administration of the nucleoside in physiological salt solution altered the inhibitory effect of 5-methyl cytidine on spontaneous tumors. For example, in physiological salt solution the 0.51 mg/injection gave as much inhibitory action as 1.03 mg/injection in distilled water. An inverse dose response is thus indicated between the amount of 5-methyl cytidine injected and the inhibition of spontaneous tumors in mice (percentage of regression and number of multiple primary spontaneous tumors are the criteria of inhibition considered).
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PMID:An inverse dose response of 5-methyl cytidine on multiple primary spontaneous tumors and their regressions in mice. 118 70

The membrane-bound polyribosomes in Ehrlich ascites tumor cells can be separated into a loosely bound and a tightly bound fraction by means of a high salt treatment. Both membrane fractions as well as the free polyribosomes in the supernatant synthesize about the same set of proteins, suggesting a close relationship between these polyribosome fractions in the Ehrlich cell. Relatively high concentrations of cycloheximide do not prevent newly synthesized poly(A)-containing mRNA from entering the tightly bound polyribosome fraction. Nor had treatment of the cells with puromycin in the presence of cycloheximide, which released about 70% of the nascent chains, any significant effect on the entrance of newly synthesized mRNA into tightly bound polyribosomes. These results suggest that in ehrlich ascites tumor cells nascent polypeptide chains are not involved in the binding of polyribosomes to membranes.
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PMID:Transport of messenger RNA into different classes of membrane-associated polyribosomes in Ehrlich-ascites-tumor cells. 123

The distribution of injected [3H]testosterone into nuclear (Nt) mitochondrial-microsomal (Mp) and cytosolic fractions (Cs) obtained from hormone-dependent R-3327 Dunning tumor, dorsal prostate, ventral prostate and heart ventricle, as a non-target tissue, was studied. Since it has been suggested that salt resistant steroid receptor complexes may represent acceptor sites, extractability of nuclear androgen complexes with high KCl (0.6 M) solution was also determined. Both orchiectomized (Or) and estrogen treated (E2) rats were used. The distribution of bound radioactivity between Nt and Cs fractions was very similar in tumors, dorsal and ventral prostate, being approximately 50% and 10% in Nt and Cs, respectively. In heart the corresponding figures were 15% and 12%, respectively. The concentration of radioactivity/mg protein in nuclear KCl-extract (Ne) from tumors was approximately 10-fold higher than that in the salt-resistant (Nr) fraction and also nearly 10-fold higher than that in Cs. Similar distribution patterns were observed in dorsal and in ventral prostate, but the concentration in Ne from ventral prostate was higher than that from tumors or dorsal prostate. Both total and bound radioactivity in Cs from heart was similar to that in the tumors, whereas the concentration in Ne from heart was < 2% of that in Ne from tumors. No significant differences were found in the distribution of radioactivity in tumors or tissues obtained from Or or E2 rats.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Subcellular distribution in vivo of testosterone and salt extractability of nuclear androgen complexes in the prostate and prostatic adenocarcinoma: effect of estrogen treatment. 129 4

The isolated laminin receptor (LN-R) labeled by 125I was reconstituted into liposomes. 125I-LN-R-liposomes and free 125I-LN-R were separated by Sepharose 4B column chromatography. The LN-R-liposomes showed affinity for laminin (LN) and were capable of binding to immobilized LN substrate. In order to make transplantation of LN-R, LN-R-liposomes were fused with cultured murine Lewis lung carcinoma cells with the help of polyethylene glycol (PEG) induction. The radiation with the fused cells was not removed by salt solution. The binding of the fused cells enriched in foreign LN-R to LN substrate increased by 87.5%. Furthermore, the murine Lewis lung carcinoma cells with and without transplanted LN-R were injected into C57BL/6J mice through tail veins (5 x 10(5) cells/each mouse) respectively. The mice in the test group died earlier than those in the control group. The total weight of lung tumor in the test group remarkably increased in comparison with those in the control group. The results taken together directly demonstrated that LN-R on carcinoma cell surface were involved in the recognition and binding of the cancer cells to LN in basement membranes, and also LN-R was of a crucial biological molecule in cancer metastasis.
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PMID:Studies on transplantation of the laminin receptor and its roles in experimental metastasis of murine Lewis lung carcinoma cells. 130 46

The retinoblastoma tumor suppressor gene product (pRb) is a nuclear protein subject to cell cycle-regulated hyperphosphorylation. I constructed a recombinant vaccinia virus vector that expresses both the underphosphorylated and hyperphosphorylated forms of pRb and purified the recombinant protein by using immunoaffinity chromatography directed toward a synthetic carboxy-terminal epitope. To investigate the hypothesis that hyperphosphorylation of pRb is a means of controlling its growth-regulating activity, I tested purified pRb for the ability to be reincorporated into pRb-deficient nuclei in vitro. The underphosphorylated form of pRb efficiently reassociated with nuclei, but the hyperphosphorylated form remained soluble in this assay. Nuclear binding of pRb was enhanced by phosphatase treatment and reduced by phosphorylation of pRb effected by using a preparation of the cell cycle-regulatory kinase p34cdc2. Mutant-encoded proteins with altered E1A-binding domains failed to bind to nuclei. Pretreatment of target nuclei with nucleases and high-salt extraction did not alter the specificity of binding for underphosphorylated pRb. These observations demonstrate that hyperphosphorylation of pRb can regulate its interaction with nuclei, supporting the hypothesis that hyperphosphorylation controls the growth-regulatory activities of pRb. Further, at least one target of pRb binding appears to be an integral component of the nuclear envelope.
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PMID:Nuclear binding of purified retinoblastoma gene product is determined by cell cycle-regulated phosphorylation. 131 Jan 46


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