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 in vivo effect of blocking sera (bs) on both tumor growth and subsequent in vitro cytolytic activity of regional lymph node cells was determined following injection of hepatoma cells suspended in normal sera (ns) or bs into the hind footpads of guinea pigs. Tumor growth was unaffected by bs but the primary response to tumor by LNC draining tumor/bs sites was significantly lower in 4/6 experiments as compared to cells from lymph nodes draining tumor/ns sites.
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PMID:Cytolytic activity in vitro of lymph node cells after exposure in vivo to tumor cells suspended in blocking sera. 22 Jan 79

The activity of hexokinase (HK), its isoenzymes, glucose-6-phosphatase and glucose-6-phosphate dehydrogenase, and the triiodothyronine (T3) effect on this activity in the liver tissue of mice bearing transplantable hepatoma 22a were studied in different periods of the tumor growtn. It was shown that alterations in the activity of the enzymes in the liver of tumor-bearing mice occurred already in the presence of a small tumor. More profound alterations in the activity of all enzymes studied, apart from those in the enzymatic pattern of HK, could be observed starting from day 21after the tumor transplantation. In the initial stages of the hepatoma growth the activity of the test enzymes in the liver was regulated by thyroid hormone. The effect of Ta on the activity of the enzymes in the host liver was gradually lost in the course of the tumor growth.
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PMID:[Carbohydrate metabolism enzymatic activity and its alteration under the influence of thyroid hormone during tumor growth]. 22 89

Immunization of CBAT6T6 mice with MC-29 hepatoma antigen did not change the take of Rous sarcoma virus, Schmidt-Ruppin strain [RSV(SR)] mouse tumors after sc transplantation. Immunization with MC-29 hepatoma antigen only slightly increased the average survival time of the mice and significantly decreased tumor growth only at the minimal lethal dose level. Immunization of mice with MC-29 hepatoma antigen and immunization with chicken Rous sarcoma gave similar results; both elicited much less transplantation resistance than immunization with irradiated RSV(SR) mouse tumor cells. The data indicate that there are common tumor-specific transplantation antigens of MC-29 hepatoma and Rouse sarcoma, but further in vitro experiments are needed to prove this.
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PMID:Comparative study of tumor-specific transplantation antigens of MC-29 chicken hepatoma and Rous sarcoma virus-induced sarcomas in mice. 22 8

Complement-dependent cytotoxic antibodies against the cells of mammary tumor MMTI appeared in the blood of C3H/He and C3Hf mice at the terminal stage of tumor growth; at the same time the mice of the above-mentioned substrains showed no difference in the degree of reaction. The level of natural cytotoxic antibodies against MMTI tumor cells detected in old C3H/He and C3Hf mice significantly exceeded their level in young mice affected with tumor; however, MMTI tumor cells grew equally fast in both old and young animals. The sera of mice affected with tumor had a weak cytolytic activity against the cells of hepatoma 22a and did not affect L cells and embryonal fibroblasts. The sera were partially exhasted by spleen and renal tissues, as well as the cells of spontaneous mammary tumor obtained from syngeneic animals and were not exhausted by allogenic cells infected with Rauscher murine leukemia virus.
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PMID:[Cytotoxic antibodies in the serum of C3H mice after inoculating them with spontaneous mammary gland tumor cells]. 22 96

Induction of tyrosine aminotransferase (TAT) (EC 2.6.1.5) by hydrocortisone was studied during cofactor (pyridoxal phosphate) depletion in hepatoma-bearing BUF strain female rats. Pairs of rats were matched for weight and age and one from each pair was fed ad libitum a diet lacking pyridoxine; the other (referred to as "pair-fed") was given the same diet supplemented with the vitamin, with the amount restricted to that consumed by the matched animal on the deficient diet. All animals were inoculated with Morris hepatoma no. 7777 cell after 21 days on the respective diets. TAT specific activity was determined weekly in host liver and hepatoma, in the presence and absence of cofactor, before and after the administration of hydrocortisone. Free and bound pyridoxal phosphate was estimated enzymatically. The average weight of hepatomas from pair-fed animals was 1.5-fold to twofold greater than that of hepatomas from animals on deficient diets. TAT activity of hepatomas was two times greater than that of host liver, and lack of dietary pyridoxine was without effect. Hormonal induction of enzymatic activity was maximal after the first week of tumor growth and subsequently reached minimal values. In pair-fed animals, tumor TAT was approximately 60% saturated with cofactor. In vitamin-deficient animals, only 6% of the tumor enzyme was saturated with the cofactor. The percent saturation of host liver TAT varied, with minimal values found in the vitamin-deficient animals. Hepatic and tumor pyridoxal phosphate content of pair-fed animals was unusually high (10 mug/g); in vitamin-deficient animals, only the coenzyme content of hepatomas was high (7.0 mug/g). The results showed that presence of the tumor altered the a) specific activity level of TAT and tissue content of cofactor, b) pattern of hormonal induction of the enzyme, and c) effects of the absence of dietary pyridoxine on TAT induction observed in animals without tumors.
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PMID:Hormonal induction of tyrosine aminotransferase activity in host liver and hepatoma no. 7777 of normal and cofactor-depleted animals. 24 64

After a suspension of tumor pieces was grafted into newborn and adult (CBA X C57BL/6J)F1 and BALB/c mice, the growth of Lewis lung adenocarcinoma and mammary gland adenocarcinoma was inhibited in newborn mice, whereas sarcoma of the rectum (SR-1-75) grew at the same rate in newborn and adult recipients. Neonatal thymectomy stimulated the growth of hepatoma (H-2-73) in newborns. The degree of tumor growth inhibition was age-dependent: The maximum inhibition was observed in 1- to 6-day-old recipients, but later it gradually decreased. The hepatoma (H-2-73) and ovarian carcinoma (OC-1-75) with inhibited growth in newborns and the tumor (SR-1-75) with uninhibited growth had equally low immunogenicity. The data suggested that newborns possess factors that inhibit tumor growth but these factors disappear with increased age of recipients.
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PMID:Nonimmune and immune surveillance. II. Effect of recipient's age, tumor immunogenicity, and neonatal thymectomy on tumor growth inhibition. 27 51

The lipid composition of Yoshida ascites hepatoma cells was analyzed together with that of ascitic plasma and of livers and blood plasma from host and normal rats. In comparison to normal livers, host livers showed no significant differences in the content of the various lipid classes, but contained a higher percentage of palmitic acid and a lower proportion of arachidonic acid in the major phospholipid classes. In addition, tumor growth induced a marked hypertriglyceridemia in host animals; changes in the concentration of other plasma lipid classes were not statistically significant. The ascitic plasma contained small amounts of lipids mainly constituted by cholesteryl esters and phospholipids. Yoshida hepatoma cells contained less phospholipids in comparison to both host and normal liver, while the increased level of triglycerides and the decrease of free fatty acids were not statistically significant. Hepatoma cells showed appreciable amounts of ether-linked lipids associated in part to neutral lipids (as glyceryl ether diesters) and, in part, to ethanolamine and choline phosphoglycerides. The alkyl groups in GEDE as well as in ethanolamine and choline phosphoglycerides were mainly constituted by C16:0 and C18:0 followed by C18:1. The alk-1-enyl groups in ethanolamine and choline phosphoglycerides were C16:0 and C18:0 with only a minor proportion of C18:1. In comparison to both host and normal liver, Yoshida hepatoma cells showed significant changes in the fatty acid composition of neutral lipids and phospholipids. Some of the major changes consisted of an increase of monoenoic acids associated with a decrease of arachidonic and docosahexaenoic acids in phosphatidylethanolamine, phosphatidylcholine, and phosphatidylinositol.
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PMID:Lipid composition of Yoshida ascites hepatoma and of livers and blood plasma from host and normal rats. 44 23

The effect of brain trauma on the formation of metastatic growth was examined by iv injection of 6 strains of rat ascites hepatoma. Three of the tumors (AH7974F, AH66F, and AH13) were in the single-cell state and three (AH272, AH7974, and AH601) contained cell aggregates. None of the tumors showed any tumor growth in the intact brain after injection into the tail vein. However, after traumatization of the brain tissue it was possible to observe tumor formation in the lesion, mainly by injection of the single-cell type tumors. The brain tissue was most susceptive to the tumor cells 10 min and 7 days after trauma. On the other hand, after the injection into the carotid artery of traumatized animals, the tumor formation in the brain was found in both tumor groups.
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PMID:Tumor formation of rat ascites hepatoma cells in the traumatized brain. 46 95

C3HA mice were inoculated with a mixture of syngeneic transplantable hepatoma 22a cells and syngeneic splenocytes of mice immunized with normal syngeneic tissues or subjected to partial hepatectomy. Control mice were inoculated with a mixture of tumor cells and splenocytes of intact or sham operated mice. A considerable inhibition of tumor growth was observed in the experimental series. Immunization of mice with normal syngeneic tissues as well as partial hepatectomy results in sensibilization of splenocytes not only to normal tissue antigens, but to the antigens of hepatoma 22a cells too. This was shown by the reaction of indirect inhibition of glass adherence of peritoneal cells. The data obtained are considered to be one more possible prove of a special form immune surveillance which controls the state of cytodifferentiation being active in the organism. The involvement of this form of immune surveillance in the genesis of antitumor resistance is discussed.
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PMID:The role of autosensibilization of lymphoid cells in genesis of antitumor resistance. 52 15

For inbred rats with Morris hepatoma 3924A, increases in tumor size were accompanied by increases in weight and DNA content of spleen, DNA content of tibial marrow, and peripheral white cell concentrations of blood. White blood cell concentrations of rats with tumors weighing more than 5 g were approximately two-fold greater than for rats without tumors. Neutrophils were primarily responsible for the increase in white cells. Local x-radiation of 3750R to the tumor when the tumor was small prevented tumor growth and the increases in spleen weight, incorporation of 3H-thymidine into spleen DNA, white blood cell count, and tibial marrow DNA content related to tumor growth. Surgical removal of large tumors resulted in a return of spleen weight and DNA content to near normal values within 1 week. Despite the evidence for increased cell proliferation in hematopoietic tissues of rats with hepatoma 3924A, no systematic relationship has been observed between tumor size and animal survival following treatment with the cell cycle specific agent 5-fluorouracil when tumors have varied in size from 0.5 g to 5 g at the time of drug treatment.
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PMID:Cell proliferation in organs of rats bearing hepatoma 3924A: effects of X-rays of surgery. 61 17


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