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)

The growth of allogeneic ascites hepatoma is accompanied by involution of the thymus, leukemoid response and anemia. Tumor cells disseminate throughout the body appearing in many organs including the spleen, liver, bone marrow and lymph nodes. The activity of adenosine deaminase and the adenosine deaminase/purine nucleosidephosphorylase ratio decrease in the host thymus as well as in the cellular elements of the spleen. The above phenomena reflect the impairment of lymphocyte differentiation and presumably contribute to the decreased efficiency of the host immune response.
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PMID:[Morphologic and biochemical changes in the lymphoid and hematopoietic tissues of rats with Zajdela hepatoma]. 679 89

The basis of the differential effect of anionic polysaccharides on replicative DNA synthesis in liver and hepatoma cell nuclei was investigated. The differential effect of heparin was lost when more than 40% of its sulfate was removed. DNA synthesis in liver nuclei was optimally stimulated by heparin of molecular weight 22600 and sulfate to hexosamine ratio 2.42, but inhibited by heparin of molecular weight 4300 and sulfate to hexosamine ratio 2.35. A heparin fragment (molecular weight 2800 and sulfate to hexosamine ratio 1.81), prepared by partial nitrous acid treatment was a potent inhibitor of DNA synthesis in hepatoma nuclei. There was no significant difference in the rate of entry of heparin or its subfractions into either liver or hepatoma nuclei. In both cases less than 15% of added polysaccharide entered the nuclei and only about 4.5% was found associated with the chromatin. The influence of the anionic polysaccharides on DNA synthesis was correlated with their ability to complex with histones as determined by relative light scattering in a laser nephelometer. The relative light scattered on mixing with histones (H1, H2A + H3, H4) was high for DNA synthesis stimulators (heparin, dextran sulfate); medium for DNA synthesis inhibitors (chondroitin 4- and 6-sulfates, heparan sulfate) and low for non-effectors (keratan sulfate, hyaluronic acid). Heparin and chondroitin sulfate H, which at low concentrations stimulate DNA synthesis in liver nuclei, inhibited DNA synthesis by calf thymus DNA polymerase alpha at all concentrations. This inhibition was not simply due to electrostatic interactions.
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PMID:Influences of anionic polysaccharides on DNA synthesis in isolated nuclei and by DNA polymerase alpha: correlation of observed effects with properties of the polysaccharides. 688 67

The yields of immediate DNA single-strand breaks in normal tumour tissues of irradiated animals were measured by a viscosimetric method of determination of high-polymer single-strand DNA molecular weight in alkaline nuclear lysates. It has been shown that in irradiated thymus, bone marrow leukocytes, Ehrlich ascitic carcinoma and Zaidel hepatoma cells (first group by tissues) in vivo the yields of DNA single-strand breaks were characterized by 80 to 130 eV per break. In in vivo irradiated liver, lymph node, spleen, and sarcoma 180 cells (second group of tissues) the yields of DNA single-strand breaks have been characterized by 30 to 40 eV per break. DNA single-strand breaks of the first group of tissues have rejoined 1 hour after the irradiation in vivo; DNA single-strand breaks of the second group have not done so.
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PMID:Viscosimetric analysis of the occurrence and repair of DNA single-strand breaks in irradiated animal tissues. 697 61

In rat livers and hepatomas, carbamoyl phosphate synthetase (glutamine-hydrolyzing) (EC 6.3.5.5) (synthetase II), the rate-limiting enzyme of de novo pyrimidine nucleotide biosynthesis, was separated from carbamoyl phosphate synthetase (ammonia) (EC 6.3.4.16) (synthetase I) ammonium sulfate and hydroxylapatite fractionations and gel filtration on Sephadex G-25. Both liver and hepatoma 3924A synthetase II activities were subject to feedback inhibition by UTP and to stimulation by 5-phosphoribosyl 1-pyrophosphate. UTP (0.5 mM) enhanced the apparent Km for MgATP from 2.3 to 7.6 mM, whereas 0.1 mM 5-phosphoribosyl 1-pyrophosphate reduced it to 0.5 mM. At 2 mM MgATP, 3 or 7 microM 5-phosphoribosyl 1-pyrophosphate yielded half-maximal activation (Ka) in the absence or presence of 0.5 mM UTP; UTP altered the stimulation kinetics from hyperbolic to sigmoidal. In the rat, synthetase II activities were highest in thymus, testis and spleen. In differentiating and regenerating rat livers, activities were 2.2- and 1.5-fold higher than in adult livers. In 17 hepatomas of different growth rates, synthetase II activity increased 1.3- to 9.5-fold over liver values; the rise correlated positively with tumor growth rates. Synthetase II activities also increased in a kidney tumor (5.0-fold) and in a sarcoma (18.1-fold) in the rat and in a human colon tumor (3.3-fold).
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PMID:Regulatory properties and behavior of activity of carbamoyl phosphate synthetase II (glutamine-hydrolyzing) in normal and proliferating tissues. 705 79

DNA polymerase beta was purified from various mammalian cells, i.e. mouse myeloma, rat liver, rat ascites hepatoma cells, rabbit liver, pig liver, and calf thymus cells. The apparent molecular weights of the polypeptides composing these enzymes were all about 40,000, as determined by sodium dodecyl sulfate polyacrylamide gel electrophoresis. Moreover, tryptic peptide maps of these enzymes after radioiodination with 125I indicated that the molecular structures of the enzymes were basically identical. No difference was detected in the peptide maps of the mouse and rabbit enzymes, and only a few of the 22 spots in the fingerprint of the mouse enzyme were not detected in that of the rat enzyme. Furthermore, the peptide maps of DNA polymerase beta's from normal and malignant rat cells differed in only one spot.
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PMID:Structural homology of DNA polymerase beta from various mammalian cells. 720 93

The rapidly growing mouse Gaelstein hepatomas 22 and 22a and rat Zajdela hepatoma are characterized both by a high thymidine kinase activity, increased TTP pool and intense 14C-thymidine incorporation into DNA. This is indicative of an intensive thymidylate biosynthesis via a short, "salvage" pathway. The predominance of this pathway for thymidylate is also characteristic for the spleens of normal animals. On the contrast, in rat and mouse thymus, where the TTP pool was the highest of all normal tissues studied, the thymidine kinase activity and thymidine incorporation into DNA were relatively low. The growth of the three hepatomas under study induces involution of tumour carrier thymus, manifested in a decrease of the TTP pool and the rate of labelled thymidine incorporation into DNA, as well as in a 4-fold decrease of the thymidine kinase activity of rat thymus. In the spleen of mice carrying ascite 22a and solid 22 hepatomas an entirely opposite response to the tumour growth was observed, i. e. in the former case the organ weight and all indices of DNA synthesis were sharply reduced, while in the latter case they were substantially enhanced. In the spleen of Zajdela hepatoma carriers the DNA synthesis is suppressed as can be evidenced from the decrease of labelled thymidine incorporation into DNA and of TTP pool; the weight of organ and the thymidine kinase activity, however, exceed the normal level more than 2-fold.
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PMID:[Thymidine kinase activity, intracellular TTP content and DNA synthesis in transplantable hepatomas and lymphoid tissue of the host]. 721 50

Electrophoretically slow H1 histone subfractions with mobilities identical to that of the subfraction found in the Kirkman-Robbins hamster hepatoma chromatin have been shown to be present in 12-day hamster embryos and in a sarcoma-type hamster tumor induced by SV40. No subfractions of such mobility were found in hamster liver, regenerating liver, thymus, spleen, and a fast-growing transplantable amelanotic hamster melanoma. A suggestion is made that some defective mechanisms of differentiation may affect the regulation of expression of the genes coding for the H1 histone subfractions. The same mechanisms may possibly but not necessarily be connected with the molecular events leading to neoplastic growth.
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PMID:Occurrence of the low-mobility H1 histones subfraction in embryonic, differentiated, and neoplastic tissues of the Syrian hamster. 723 42

The presence of natural anti-tumor antibodies (NAA) against fibrosarcoma- and glioma cells was revealed in the normal sera of 10 different strains of rats. By means of a direct cytotoxicity test using guinea-pig complement and an absorption tests, NAA in inbred WKA/Hok rats were observed to be cytotoxically reactive to all investigated syngeneic and allogeneic fibrosarcoma lines and one glioma line, but not to hepatoma, lymphoma, leukemia, and neurinoma lines. Moreover, NAA reactivity to fibrosarcoma cells was significantly absorbed with brain, lung, kidney, skin homogenates, and cultured normal fibroblasts of syngeneic rats, but not with liver homogenates, thymus, spleen, lymph node and red blood cells. NAA were identified as being predominantly IgM and were stables at 56 degree C for 30 min. With the exception of one strain, there were no strain or sex differences in NAA levels among any of the investigated strains of rats. The level of NAA correlated with the in vivo anti-tumor response: when NAA-reactive fibrosarcoma or glioma cells were implanted into syngeneic WKA/Hok rats, groups of rats with high NAA levels suppressed tumor growth and survived longer than groups of rats with low NAA levels, while there was no difference in length of survival days in NAA non-reactive hepatoma or lymphoma cells. When 3-methylcholanthrene was inoculated into these two groups of rats, the tumor incidence in the groups of rats with high NAA level was significantly suppressed as compared to the group of rats with low NAA level. We discuss the mechanism of the induction of NAA in relation to the anti-tumor immunity.
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PMID:[Cytotoxic natural anti-tumor antibodies against fibrosarcoma and glioma cells in rats (author's transl)]. 731 60

Xenogenic antibodies with reactivity for surface determinants of the guinea pig line-10 hepatocarcinoma were isolated by using cellular immunoadsorbents prepared by coupling formalin-treated line-10 cells to diethylaminoethyl cellulose. Antibodies prepared in this manner exhibited a high degree of reactivity for line-10 surface determinants. These antibodies also reacted with surface determinants of the syngeneic line-1 hepatocarcinoma. Further specificity of antibody reactivity to the line-10 hepatocarcinoma was accomplished by passage of the antibodies through cellular immunoadsorbents prepared with syngeneic line-1 hepatocarcinoma cells. By direct binding studies, these antibodies showed significantly reduced reactivity for line-1 cells and no reactivity for guinea pig spleen cells or for the unrelated murine EL-4 lymphoma. By a competitive radioimmunoassay, these antibodies reacted only with determinants expressed on the surfaces of line-10 cells and not on syngeneic line-1, L2C, spleen, thymus; or xenogeneic EL-4 cell surfaces. In a similar manner, line-10-associated antigens were detected in ascites fluid derived from line-10 tumor-bearing animals. The sequential use of immunoadsorbents made of antigenically distinct but syngeneic tumor cells made it possible to prepare antibodies with restricted reactivity for line-10-associated antigens and should be applicable to the isolation of "tumor-specific" antibodies in other systems.
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PMID:The use of cellular immunoadsorbents to prepare antibody that distinguishes between syngeneic surface antigens on two guinea pig hepatocarcinomas. 735 79

1. A systematic study is reported on the control of 1-phosphatidylinositol 4-kinase (PI kinase) and PI 4-phosphate 5-kinase (PIP kinase), enzymes of the phosphatidylinositol phosphorylation pathway which leads to the production of second messengers. IP3 and DAG. In liver of normal male, adult, fed Wistar rats the steady state activity of PI kinase was 0.5 +/- 0.01 and that of PIP kinase was 0.046 +/- 0.003 nmol/hr/mg protein. The concentration of IP3 was 1.8 +/- 0.1 pmol/mg protein. 2. That the two kinases have short half-lives was observed in starvation. where in the rat liver or bone marrow activities rapidly decreased and on refeeding were restored in a day. Injection to rats of the protein synthetic inhibitor, cycloheximide, yielded t1/2 = 80 min for the two enzymes in bone marrow and t1/2 = 80 min in liver. 3. Linkage of the signal transduction enzymes with proliferation was shown by the high activities as compared to liver of these enzymes in rat organs of high cell renewal capacity, e.g., thymus, bone marrow, spleen and testes. 4. Linkage with malignant proliferation was indicated by the observation that in rat hepatomas the enzyme activities increased 5- to 9-fold and were highest in rapidly growing hepatoma 3924A (29- and 45-fold). 5. In human primary ovarian carcinoma PI and PIP kinase activities were elevated 4.4 and 2.9-fold, respectively, and in OVCAR-5 cells, 32- and 11-fold, respectively. Similar increases were observed in MDA-MB-435 human breast carcinoma cells in comparison with normal breast parenchymal cells. 6. The linkage of signal transduction enzyme activities with malignant proliferation was also observed in experiments when human breast carcinoma cells were plated in flasks and expressed their proliferative capacity in the log phase. PI and PIP kinase activities steadily and coordinately increased to a peak 11-fold rise in mid-log phase. In late log and plateau phases the kinase activities gradually declined to the starting level. Similar observations were made for the two enzymes in human ovarian carcinoma OVCAR-5 cells and in rat hepatoma 3924A cells in tissue culture. 7. In animals injected with cycloheximide the bone marrow PI and PIP kinase activities exhibited t1/2 = 0.12 hr, the shortest decay rate in comparison with 8 enzymes of purine and pyrimidine biosynthesis with t1/2 = 0.6 to 4.3 hr. 8. Injection of tiazofurin decreased PI and PIP kinase activities in the bone marrow with t1/2 = 82 and 78 min, respectively.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Regulation of signal transduction. 757 37


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