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)

Lectin binding [concanavalin A, biotinylated ricinus communis agglutinin, and biotinylated succinylated wheat germ agglutinin (B-SWGA)] was used to detect the glycosylated proteins associated with a residual protein fraction [insoluble in 4% sodium dodecyl sulfate and termed the nuclear residual fraction (NRF)] or with nuclear matrix preparations from normal rat liver, azo dye (3'-MeDAB)-induced rat hepatoma, and Walker 256 transplantable carcinosarcoma. One- and two-dimensional gel electrophoresis were used with lectins, polyclonal antisera, and monoclonal antibody binding to characterize some of the glycoconjugates. Two polypeptide bands with approximate molecular weights of 95,000 and 55,000, shown previously to be present only in the induced tumor cells and the Walker 256 tumor, were reactive with lectins. In addition, a Mr 62,000 protein reacted only with B-SWGA in the nuclear matrix fractions from normal rat liver and the induced hepatoma. A polypeptide band (approximate molecular weight, 213,000) in the Walker 256 NRF reacted with concanavalin A and biotinylated ricinus communis agglutinin. One polypeptide band (approximate molecular weight, 182,000) reacted with concanavalin A in all three tissues, with biotinylated ricinus communis agglutinin and B-SWGA in the Walker NRF, and with B-SWGA in the hepatoma NRF. Another polypeptide band (approximate molecular weight, 138,000), reactive with all three lectins, was present in all three tissues. Our findings are consistent with previous reports of lectin binding proteins in the eukaryotic cell nucleus and indicate that certain glycoproteins isolated in nuclear preparations are found specifically in 3'-MeDAB-induced hepatoma and Walker 256 transplantable carcinosarcoma.
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PMID:Lectin-binding proteins in nuclear preparations from rat liver and malignant tumors. 333 20

PSK is a protein-bound polysaccharide prepared from cultured mycelium of the Basidiomycete Coriolus versicolor. Effects of PSK on the immunologic responsiveness in tumor-bearing animals were investigated using syngeneic or allogeneic tumors in mice (Lewis lung carcinoma, B16 melanoma, Meth A fibrosarcoma, adenocarcinoma 755, X5563 plasmacytoma, colon 26, MOPC 31C myeloma, sarcoma 180 and Ehrlich carcinoma), rats (BC47 bladder carcinoma, Walker 256 sarcoma and AH7974 hepatoma), hamsters (HA-1T tumor and RPMI 1846 melanoma), guinea pigs (line-10 hepatoma) and rabbit (VX2 and VX7 tumor). Oral or intraperitoneal administration of PSK restored the depressed delayed hypersensitivity against sheep erythrocytes to a normal level in these tumor-host systems. Also, oral administration of PSK lowered the activity of immunosuppressive substances in the serum of tumor-bearing animals. These results suggest that PSK exhibits antitumor effects by restoring the depressed immunologic responsiveness in tumor-bearing animals.
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PMID:[Restoration of immunologic responsiveness by PSK in tumor-bearing animals]. 378 58

These experiments were performed to determine the factor(s) that regulate lactic acid production and utilization by rat tumors in vivo. Arteriovenous differences for glucose and lactic, pyruvic, 3-OH-butyric, and acetoacetic acids were measured across "tissue-isolated" Walker 256 sarcocarcinomas and Morris 5123C hepatomas in fasted rats anesthetized with sodium pentobarbital. Twenty-six per cent of the sarcocarcinomas (n = 53) and 48% of the hepatomas (n = 29) utilized blood lactic acid. The remainder released lactic acid into the venous blood. The steady-state rate of glucose consumption was similar in both lactate-producing and lactate-utilizing tumors. The range of lactate concentrations in the blood leaving the tumors was narrower than the range of lactate concentrations in the blood entering the tumors. This difference was caused by tumor lactic acid production at low arterial lactate concentrations and tumor lactic acid utilization at high arterial lactate concentrations. Individual tumors changed from lactic acid production to lactic acid utilization in a matter of minutes in response to an increase in the arterial lactic acid concentration. Mean lactic plus pyruvic acid concentrations and lactic/pyruvic acid ratios in the tumor venous blood were 2.15 +/- 0.22 and 23.4 +/- 3.7 mM, respectively, for Walker sarcocarcinoma 256 (n = 18) and 1.28 +/- 0.13 and 48.1 +/- 5.1 mM, respectively, for hepatoma 5123C (n = 11). The results suggest: that a steady-state lactic plus pyruvic acid concentration and lactic/pyruvic acid ratio are maintained in the tumor cell cytoplasm by the active glycolytic pathway and by lactic acid dehydrogenase; that the tumor intracellular concentrations equilibrate with the arterial blood and that the tumor steady state is expressed in the tumor venous blood; and that tumor lactic acid production or utilization results from the equilibration between the variable arterial lactic acid concentration and the more constant tumor intracellular steady-state lactic acid concentration. Since the arterial lactate concentration may be less than, greater than, or equal to the intracellular steady-state concentration, an individual tumor may produce, utilize or neither produce nor utilize lactic acid.
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PMID:Regulation of lactate production and utilization in rat tumors in vivo. 399 85

Cultured Novikoff rat hepatoma and Walker 256 carcinoma cells have previously been reported to express only nitrobenzylthioinosine (NBTI)-resistant uridine transport and to lack high affinity NBTI-binding sites, whereas the latter are common on all other types of cultured mammalian cells from different species [1-7) X 10(5) sites/cell) which have been investigated with the exception of a transport-deficient cell variant which lacks high-affinity NBTI-binding sites. The present study shows that lack of NBTI sensitivity of transport and of NBTI-binding sites in Novikoff and Walker 256 cells are not related to the species or tissue origin of these cells. Uridine transport in a variant (NRM) of Novikoff hepatoma cells, in HTC rat hepatoma cells, normal rat kidney (NRK) cells, rat erythrocytes and rat hepatocytes was inhibited 15-60% by 10-500 nM NBTI and the cells expressed high-affinity NBTI-binding sites (Kd = 0.1-0.6 nM). The apparent turnover numbers for the NBTI-sensitive nucleoside carriers fell into two classes, with those for transformed cells about 10-times higher than those for the normal rat cells.
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PMID:Nitrobenzylthioinosine-sensitive and -resistant nucleoside transport in normal and transformed rat cells. 400 49

The cell cycle of Walker carcinoma, Zajdela's hepatoma and their metastases into regional lymph nodes are studied. It is shown that cell cycle of metastases is shorter and the labeling index is higher than in primary tumours. The cell cycle shortening in Walker carcinosarcoma metastases is associated with a decrease in the duration of all its phases. The cell cycle of Zajdela's hepatoma metastases decreases with the S-phase length. The cell loss factor of primary tumours is less than that of their metastases. The results of the autoradiographic study correlate with the previously studied sensitivity of primary tumours and metastases to chemotherapy.
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PMID:[Cellular proliferation kinetics of Walker carcinosarcoma, Zajdela's ascitic hepatoma and their metastases to the lymph nodes]. 406 18

The paper deals with a study of the effect of a single challenge with living tularemia vaccine on the growth of such transplantable tumors as Zajdela's hepatoma, Pliss' lymphosarcoma, Walker's carcinosarcoma, Schwetz' erythromyelosis and sarcoma 45 in Wistar rats. Immunization was followed by a significant (37.2-86%) inhibition of the rate of growth of the said tumors. Ascites was detected in half the vaccinated animals of Zajdela's hepatoma series, this being matched by 100% in controls.
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PMID:[Effect of immunization with live tularemia vaccine on the growth of various tumor strains in rats]. 407 86

Spin echo nuclear magnetic resonance measurements may be used as a method for discriminating between malignant tumors and normal tissue. Measurements of spin-lattice (T(1)) and spin-spin (T(2)) magnetic relaxation times were made in six normal tissues in the rat (muscle, kidney, stomach, intestine, brain, and liver) and in two malignant solid tumors, Walker sarcoma and Novikoff hepatoma. Relaxation times for the two malignant tumors were distinctly outside the range of values for the normal tissues studied, an indication that the malignant tissues were characterized by an increase in the motional freedom of tissue water molecules. The possibility of using magnetic relaxation methods for rapid discrimination between benign and malignant surgical specimens has also been considered. Spin-lattice relaxation times for two benign fibroadenomas were distinct from those for both malignant tissues and were the same as those of muscle.
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PMID:Tumor detection by nuclear magnetic resonance. 554 70

We have investigated the appearance of specific nonhistone proteins during azo dye-induced hepatocarcinogenesis in the rat. Groups of animals fed azo dye-containing diet were sacrificed at approximately 3-week intervals, portions of their livers were examined histologically, and the remaining material was fractionated into chromatin and cytoplasmic fractions. Livers of the azo dye-fed animals exhibited histological changes that have been classically attributed to the course and development of cancer; by 28 to 30 weeks of treatment, nearly all animals had developed hepatomas. Heterogeneous rabbit antisera were prepared to dehistonized chromatin from several azo dye-induced hepatomas. These antisera were then used to assess various chromatins for the appearance of antigens specific for neoplasia during inducing carcinogenesis using immunodetection of antigens separated electrophoretically and transferred to nitrocellulose. Changes in the immunoreactivity of liver chromosomal proteins during carcinogen treatment were evident after 3 weeks, and the antigenic profiles of various chromatin samples gradually assumed the characteristics of the hepatoma. The transformation was accompanied by qualitative changes in chromosomal protein antigens, and although these antigenic species were not directly quantitated, noticeable enrichment of tumor-specific species occurred with treatment time. Immunotransfer assays of cytoplasmic fractions indicated most antigens to be specific for chromatin. Normal tissue chromatin exhibited minimal immunoreactivity, and slightly more antigenic homology was noted with regenerating liver and most transplantable tumor chromatins. Interestingly, the transplantable tumor Walker 256 carcinosarcoma was highly enriched in antigens recognized by antisera to azo dye hepatoma dehistonized chromatin. These studies establish a define chronological correlation between the chemical induction of cancer and sequential changes in the immunological specificity of nonhistone protein antigens.
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PMID:Antigenic changes in nonhistone proteins during azo dye hepatocarcinogenesis. 617 4

The sequences specifically transcribed in tumor cells are believed to be closely related to transformed phenotypes. For the isolation of such sequences, a cDNA clone library was constructed by using poly(A)+ RNAs from azo-dye-induced rat ascites hepatomas. Thirty-one tumor RNA-responsive clones were isolated by screening 4,000 clones of this library with conventional techniques, differential colony hybridization, and RNA blot hybridization. These clones were categorized into two groups with respect to their size distribution of mRNAs from which clones were derived. The first group was complementary to a single distinct species, either about 1.5 or 0.6 kilobases in length, of poly(A)+ RNA, and the second showed no distinct bands but a smear on a RNA blot. Semiquantitative RNA dot blot assays revealed that the sequences of these clones were expressed very little, if at all, in normal and regenerating livers, while generally high in ascites hepatomas. This specificity was also true for other solid lines of tumors, such as Morris hepatoma 5123D of Buffalo rat and Walker 256 carcinosarcoma of Wistar rat. The smear class sequences were transcribed from middle-repetitive sequences of DNA, indicating that a class of middle-repetitive sequences is specifically transcribed in tumor cells.
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PMID:Cloning of sequences expressed specifically in tumors of rat. 620 Aug 76

Protamine sulfate reversibly inhibits serum-induced mitogenic stimulation of several nontransformed and neoplastic cell types in vitro. Fifty percent inhibition was induced by approximately 120-150 micrograms protamine sulfate/ml. Cells were affected directly, and inhibition depended on the duration of cell exposure. Heparin, chondroitin sulfate, heparan sulfate, and dextran sulfate neutralized protamine sulfate effects during the early stages of treatment. Nontransformed cells [bovine aortic endothelial cells, adult human gingival fibroblasts (strains 423 and 1101), fetal rat skin (strain 921-K) and muscle fibroblasts] required longer exposure to induce inhibition than did neoplastic cells [rat 3-methylcholanthrene-induced fibrosarcoma cell lines (MCA-6 and MCA-9), a macrophage-like cell line (NCTC-3749), Walker 256 rat carcinoma cells (ATCC-CCL-38), rat Morris hepatoma cells (ATCC-CCL-144), murine melanoma cells (B16), and rat bladder squamous cell carcinoma cells (804-G)]. Other polycationic compounds, including histone type VIII-S, poly-L-lysine, poly-L-arginine, and protamine (free base), were also effective inhibitors, whereas the basic proteins cytochrome c and lysozyme had no effect. Poly-L-histidine, poly-L-glutamic acid, poly-L-aspartic acid, and dextran blue also had no inhibitory effect.
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PMID:Protamine sulfate inhibition of serum-induced mitogenic responses: differential effects on normal and neoplastic cells. 621 Mar 90


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