Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019204 (hepatocellular carcinoma)
 71,386 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Activities of pyrimidine nucleoside phosphorylase in brain tumors were measured and their relationship to a clinical course of the patients was investigated. Pyrimidine nucleoside phosphorylase is said to exist more quantitatively in malignant tumors such as Sarcoma 180, Ehrlich ascites carcinoma, Walker 256, and hepatoma, and very little in normal tissues. In brain tumors the activities were measured by bioassay and compared to that of Sarcoma 180. When the activity of Sarcoma 180 was expressed to be 100%, those of brain tumors were as follows: ten cases of normal brain less than 8.5; six cases of glioblastoma 39.3 +/- 30.7; five cases of astrocytoma 22.0 +/- 13.8; five cases of meningioma 22.4 +/- 13.7; two cases of oligodendroglioma 8.1 and 11.3; two cases of sarcoma 94.3 and 145.4; chordoma 48.0; ependymoblastoma 3.7; plexus papilloma 22.5; parotid cancer 43.4; ten cases of metastatic brain tumors from lung cancer 61.5 +/- 41.6; two cases from breast cancer 28.0 and 68.8; that from thyroid cancer 10.0; that from gastric cancer 13.5; malignant melanoma 77.2. In 12 cases of gliomas (glioblastoma, astrocytoma, oligodendroglioma) the mean activity was highest in glioblastoma (39.3), followed by astrocytoma (22.0) and oligodendroglioma (9.7). The postoperative survival time became shorter in gliomas with the higher activities. In metastatic brain tumors from lung, breast, and gastric cancer, the average time from the diagnosis of primary cancer to brain metastasis was shorter in cases with high activities and longer in cases with low activities.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Activities of pyrimidine nucleoside phosphorylase in brain tumors and antitumor effect of 5'-DFUR]. 622 41

The 1H NMR spin-lattice relaxation time (T1), spin-spin relaxation time (T2), and spin-lattice relaxation time in the rotating frame (T1rho) were determined for Novikoff hepatoma, Walker-256 Carcinosarcoma, Sarcoma-180 and Ehrlich Ascites tumor as well as for 7 normal tissues in the rat at 2.18 MHz. T1 values yielded improved discrimination of normal and malignant tissue compared to previous results at higher frequencies.
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PMID:Improved discrimination of normal and malignant tissue using 1H NMR relaxation time measurements at 2.18 MHz. 654 47

The metabolism of deoxycytidine (dCyd) and dCyd nucleotides in Yoshida ascites sarcoma (YS) cells and the host rat liver was investigated with reference to the increased excretion of urinary dCyd. Incorporation of [14C]orotic acid into the livers of rats at the fifth day after the transplantation of YS cells, the time when the amount of excretion of dCyd in urine was near maximal, was 2 times higher than that into the normal rat livers. After the injection of [14C]orotic acid, the ratio of the specific radioactivity of cytidylate to uridylate moieties of the host liver RNA was measured and found to be higher than that of normal rat liver RNA and to be similar to that of YS cell RNA. When [14C]orotic acid was injected into rats followed by the transplantation of YS cells, the radioactivities present in the livers disappeared more rapidly than those in the control rat livers. The activities of pyrimidine de novo synthesis enzymes, such as cytidine triphosphate synthetase (EC 6.3.4.2) and cytidine diphosphate reductase (EC 1.17.4.1), in YS were higher than those in both rat ascites hepatoma AH 7974 and Walker 256 carcinosarcoma, the transplantations of which did not induce increased excretion of dCyd into urine of the hosts. The activities of dCyd kinase (EC 2.7.1.10) and dCyd deaminase (EC 3.5.4.5) in YS cells were lower than those in the other two tumors investigated. The activities of cytidine triphosphate synthetase and cytidine diphosphate reductase in the livers of YS-bearing rats were elevated compared with those in the livers of rat ascites hepatoma AH 7974- or Walker 256 carcinosarcoma-bearing rats and normal rats, while the activities of dCyd kinase, 5'-nucleotidase (EC 3.1.3.5), and dCyd deaminase were similar between normal rat livers and tumor-bearing rat livers. These results suggest that the increased excretion of urinary dCyd in YS-bearing rats could be caused by both the stimulation of the synthesis of dCyd nucleotides and the low activity of dCyd deaminase in YS cells as well as in the host liver.
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PMID:Origin of increased deoxycytidine excretion into urine of rats bearing Yoshida ascites sarcoma. 672 78

The metabolism, antitumor activity, and acute toxicity of 5-fluoro-1,3-bis-(tetrahydro-2-furanyl)-2,4-pyrimidinedione (FD-1) were investigated in animals, compared with 5-fluoro-1-(tetrahydro-2-furanyl)-2,4-pyrimidinedione (FT). It was found that after oral administration of FD-1, the level of 5-fluorouracil (5-FU) was maintained higher and longer than after administration of FT, and that a large amount of 5-FU was released from FD-1 by liver microsomal drug-metabolizing enzymes or spontaneous hydrolysis via 5-fluoro-3-(tetrahydro-2-furanyl)-2,4-pyrimidinedione (3-FT) and FT. FD-1 had a significant activity against the solid form of Ehrlich carcinoma, sarcoma-180, hepatoma AH130, Yoshida sarcoma, Walker carcinosarcoma-256, and leukemia L1210 and P388, but not the ascitic forms, and it produced greater inhibition of tumor growth than FT. The acute toxicity of FD-1 was less than that of FT.
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PMID:Metabolism, antitumor activity, and acute toxicity of 5-fluoro-1,3-bis(tetrahydro-2-furanyl)-2,4-pyrimidinedione by oral administration to animals. 676 37

Succinylacetone (SA, 4,6-dioxoheptanoic acid) inhibits d-aminolevulinic acid dehydrase, the second enzyme of the heme biosynthetic pathway and thereby inhibits heme biosynthesis. In the present study SA is shown to inhibit the growth of the Walker carcinosarcoma (W256) in vitro and in vivo, the Novikoff hepatoma in vivo, and L1210 leukemia in vitro, but only slightly in vivo. Rats can tolerate significantly larger doses of SA for at least twice as long as were administered in the present study without gross evidence of toxicity. In contrast to findings in previously published studies with murine erythroleukemia cells, the inhibition of growth of L1210 and W256 cells by SA in vitro is not accompanied by a decrease in cellular heme and is not reversed by addition of hematin to the medium. This suggests a second mechanism of growth inhibition of tumor cells unrelated to heme biosynthesis. Although the growth of both W256 and L1210 cells was markedly inhibited by the same concentration of SA in culture, there was a great difference in responsiveness in vivo, in that much greater inhibition of the growth of the Walker tumor was produced by SA.
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PMID:Growth inhibitory activity of succinylacetone: studies with Walker 256 carcinosarcoma, Novikoff hepatoma and L1210 leukemia. 682 92

The Walker 256 carcinosarcoma growing in Sprague-Dawley rats and the Morris 5123 hepatoma growing in Buffalo rats both produce cachexia but have widely differing patterns of host metabolism and tumor growth. Both organisms respond to exogenous insulin with increased food intake and rate of weight gain of host. The insulin treatment response of food intake was 1.5 to 2 times and of body weight gain was 2 to 3 times that of tumor-free controls. Insulin does not accelerate tumor growth. On withdrawal of insulin, the reactive hypophagia seen in tumor-free rats does not occur in tumor bearers, and the host weight does not return to the expected untreated value as it does in tumor-free rats. Most of the weight gained during insulin treatment of tumor bearers above that gained by tumor-free rats is retained after withdrawal of insulin. A computer model based on the inference from these results, that the tumor-bearing host is blind to body weight error, indicates that this abnormality of feeding control could account for only about one-third of the observed depression of host weight and food intake.
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PMID:Feeding response of tumor-bearing rats to insulin and insulin withdrawal and the contribution of autonomous tumor drain to cachectic depletion. 704 59

This study investigates the specificity of two antigenic proteins with molecular weights of 39,000 and 49,000, respectively (p39 and p49), present in Novikoff ascites hepatoma. Chromatins and cytosol fractions were assayed from a number of tumorigenic cell lines by identifying antigenic species immunologically on nitrocellulose transfers containing proteins separated electrophoretically. Immunoreactivity was confirmed with complement-fixation. Although the p49 antigen was present only in Novikoff ascites hepatoma and a tissue culture line derived from these ascites cells, the p39 antigen was found in every carcinoma cell line examined. In contrast, neither antigen was present in a representative sarcoma, fibrosarcoma, or Walker 256 carcinosarcoma. These results suggest that the p39 antigen is a protein specific for malignant cells derived from the epithelium. The overall expression of the p39 antigen by the various cell lines examined did not appear to be influenced by in vivo or in vitro growth of homologous cell lines. This latter feature suggests that the p39 antigen is a stable, possibly structural component of neoplastic cells.
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PMID:Distribution of Novikoff ascites hepatoma antigens p39 and p49 in various tumorigenic cell lines. 706 17

In this paper the recognition of various rat tumor cells by rat liver cells is demonstrated in vitro. A liver cell receptor involved in the binding process has been identified. The ultrastructure of the cell contacts was examined by transmission electron microscopy. Hepatocytes and Kupffer cells were isolated from rat liver by collagenase treatment and cell adhesion tests were performed with 4 different tumor cells types. Hepatocytes were found to bind Walker sarcoma cells, lymphoma cells and Yoshida hepatoma cells but not leukemia 5222 cells. Kupffer cells bound all tumor cell types. Normal blood cells were not bound under the same conditions. Recognition of tumor cells by hepatocytes was mediated by a galactose specific lectin on the liver cell surface as shown by hapten inhibition experiments with specific saccharides. Although Kupffer cells express a similar lectin-like receptor adhesion of tumor cells could not or only slightly be inhibited by galactose or related saccharides. It is concluded that the spontaneous adhesion of tumor cells to liver cells in vitro is a specific recognition event which in part is mediated by lectin-carbohydrate interactions.
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PMID:Galactosyl specific receptor on liver cells: binding site for tumor cells. 728 63

A new anthramycin-group antitumor antibiotic, neothramycin, isolated from a Streptomyces culture, showed activity against experimental tumors such as lymphocytic leukemia P388 ascites sarcoma-180, hepatoma AH130, Walker carcinosarcoma-256 and mouse mammary adenocarcinoma (CCMT). In particular, the tumor growth inhibition ratio was as high as 96% when neothramycin was injected intraperitoneally at a daily dose of 2 mg/kg into Wistar strain rats previously inoculated with Walker carcinosarcoma-256 by the subcutaneous route. Successive intraperitoneal injections of the compound were more effective than a single injection with the P388 system.
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PMID:Antitumor effect of a new antibiotic, neothramycin. 741 76

The human beta-galactoside alpha 2,6-sialyltransferase (EC 2.4.99.1) (SiaT-1) gene is localized to human chromosome 3 (q21-q28) by Southern analysis of somatic cell hybrids and by in situ hybridization of metaphase chromosomes. Comparative analysis between the human and the previously reported rat SiaT-1 genomic sequences demonstrates precise conservation of the intron/exon boundaries throughout the coding domains. Furthermore, there is extensive inter-species sequence similarity in some of the exons that contain information only for the 5'-leader regions. Human genomic sequences were also analyzed to reconcile reported differences in the 5'-untranslated region in SiaT-1 mRNAs. In cultured cell lines of the B-lineage, Reh, Nalm-6, Jok-1, Ball-1, Daudi, and Louckes, the study demonstrates that three upstream exons, Exons(Y+Z) and Exon(X), are mutually exclusively utilized, resulting in at least two distinct populations of SiaT-1 mRNA being synthesized. None of these exons is present in the SiaT-1 mRNA isotype expressed in HepG2 human hepatoma cells. In all B-lymphoblastoid cell lines examined, the basal level SiaT-1 mRNA is maintained by the expression of an isotype containing the Exons(Y+Z) sequence. The slightly smaller SiaT-1 mRNA, which contains the Exon(X) sequence but not Exons(Y+Z) sequence, is synthesized at a high level and found only in Jok-1, Daudi, and Louckes, the cell lines with mature B-cell phenotype. The study also provides further evidence that induced SiaT-1 expression accompanies the appearance of CDw75, a putatively sialylated cell surface epitope and a marker of human mature B-lymphocytes. The SiaT-1 induction is the result of the appearance of a novel form of SiaT-1 mRNA isotype.
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PMID:Chromosome mapping and organization of the human beta-galactoside alpha 2,6-sialyltransferase gene. Differential and cell-type specific usage of upstream exon sequences in B-lymphoblastoid cells. 778 24


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