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 transplantable MC-29 virus-derived hepatoma is a suitable model for studying the influence of immune status on virus-derived hepatomas in chickens. It was found that both humoral and cellular immunologic reactions have a role in the pathogenesis of virus-derived hepatomas and that virus-derived hepatomas can be influenced by nonspecific immunostimulation. The lymphoid system was profoundly altered in hepatoma-bearing chickens; this cannot be neglected when studying correlations between immune reactions and carcinogenesis. Profound changes were also observed in protein synthesis and the steroid receptor system of hepatoma-bearing chickens compared to healthy birds; this also complicates the understanding of the role of immune mechanisms in carcinogenesis.
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PMID:Influence of immune status on virus-derived transplantable hepatoma in chickens. 3 44

The basic phenomena of cell fusion and hybrid cell formation are briefly described and the potential of somatic cell hybridization in studies on the expression of differentiated cellular functions is discussed. The technique of cell hybridization has been applied to two types of cellular responses to glucocorticoids. The induction of specific proteins has been investigated in hybrids of inducible cells with uninducible cells. Most studies dealt with the liver-specific enzyme tyrosine aminotransferase, whose inducibility was extinguished in the majority of the hybrids between hepatoma and nonliver cells. However, upon chromosome segregation, inducibility reappeared in some of these hybrid cells. The current ideas about cellular control of inducibility are discussed. The other major glucocorticoid-responsive system investigated in cell hybridization studies consists of lymphoid cells which are killed when exposed to the steroid. Such sensitive cells were hybridized with several types of glucocorticoid-resistant lymphoid lines, and sensitivity was found to be dominant over resistence. Hybrids between sensitive and resistant lymphoid cells, however, showed an increase in the frequency at which resistance occurred as compared to the rate observed with the wild-type parental cells. No complementation to steroid sensitivity was found in hybrids between different types of resistant cells with defects in the glucocorticoid-specific receptor system.
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PMID:Somatic cell fusion in the study of glucocorticoid action. 4 Jan 17

The line-1 guinea pig hepatoma was used to study in vitro tumor cytotoxicity. Cytotoxicity was determined by measurement of the loss of tritiated thymidine-labeled target cells from culture vessels. With this technique, we demonstrated that significant tumor cytotoxicity was caused by lymphoid cells from tumor-immune guinea pigs, by cells from guinea pigs immunized against an antigen urelated to the tumor target, and by cell-free supernatants rich in lymphocyte mediators. Addition of normal peritoneal exudate cells enhanced the cytotoxic potential of a small number of highly purified immune lymphocytes, which suggested that recruitment of normal cells is an additional mechanism of tumor cell death in this system.
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PMID:Multiple in vitro mechanisms of tumor cytotoxicity demonstrated in the line-1 guinea pig hepatoma model. 5 20

Lymphokine-containing supernatants derived from seven different human lymphoid cell lines and lymphokine-containing supernatants from concanavalin A-stimulated murine lymphocytes were found to be capable of reversibly inhibiting the migration of tumor cells in vitro. The tumor cell lines used in these studies were the P815 mastocytoma, Ehrlich ascites, Walker carcinosarcoma, Hepatoma 129, and Sarcoma 37. Preliminary physiochemical evidence suggests that the mediator, here termed TMIF, is distinct from MIF. In any case, these results suggest the possibility that lymphokines other than lymphotoxin or macrophage-activating factors may play a role in tumor immunity.
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PMID:Inhibition of migration of tumor cells in vitro by lymphokine-containing supernatants. 9 77

Mice fed a diet containing 0.3 or 0.03% triethanolamine developed malignant tumors. Females showed a high incidence of tumors in lymphoid tissues, while this type was absent in males. Tumors in other tissues were produced at a considerable rate in both sexes, but no hepatoma was found. Triethanolamine was not mutagenic to Bacillus subtilis by itself, but it became mutagenic after reacting with sodium nitrite under acidic conditions or when the mixture was heated. Although N-nitrosodiethanolamine, a known carcinogen and mutagen, was detected in the reaction mixture by thin-layer chromatography, it may not be the main mutagenic product, because the product was a stable and direct mutagen and its mutagenic activity was destroyed by liver enzymes, unlike N-nitrosodiethanolamine. The lethal and mutagenic DNA damages produced by this unidentified product were susceptible to some extent to the repair functions of the bacteria.
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PMID:Carcinogenicity of triethanolamine in mice and its mutagenicity after reaction with sodium nitrite in bacteria. 10 Feb 10

Ribonucleic acid extracts of lymphoid cells from immune hosts were used to transfer in vivo and in vitro cell-mediated immune reactivity to a variety of antigens. The in vivo immune responses transferred by RNA included the delayed cutaneous hypersensitivity reaction to fungal and chemically-defined antigens and the tumor-rejection reaction to guinea pig hepatoma antigens. The in vitro immune responses transferred by RNA included macrophage migration inhibition by fungal, chemically-defined, and tumor antigens. The transfer activity of RNA preparations was contained in the 8 s to 18 s species of RNA and was sensitive to RNase but not to DNase or trypsin. Antigen was not detectable in the RNA preparations and appeared to have no role in the transfer activity. Syngeneic, allogeneic, or xenogeneic sources of RNA could transfer immune reactivity. In each system tested, the transfer of cell-mediated reactivity by RNA was specific for the antigen used to sensitize the RNA donor. The potential use of RNA-mediated transfer of immunity is discussed.
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PMID:Some perspectives on the transfer of cell-mediated immunity by immune-RNA. 11 79

Syngeneic and xenogeneic RNA-rich extracts of lymphoid tissues were used in an immunotherapeutic regimen to treat strain 2 guinea pigs that were given intradermal injections of a uniformly lethal dose (1 x 10(6)) of line 10 diethylnitrosamine-induced transplantable hepatoma cells. When 1 X 10(7) syngeneic nonsensitive peritoneal exudate cells, 2.5 mg RNA from line 10-immune strain 2 guinea pigs or line 10-immune Rhesus monkeys, and 1.0 mg of a line-10 tumor-specific antigen preparation were injected s.c. under the tumor cells injected 5 days previously, complete local tumor regression in all treated animals was observed. If either nonsensitive peritoneal exudate cells, RNA, or line 10 tumor-specific antigen was omitted, or if Escherichia coli RNA or RNA from animals sensitized to a different tumor (line 1) was used, little or no tumor regression was observed, suggesting that the action of the RNA may have resulted in an antitumor response specific for the noplasm being treated. The long-term tumor-free survival of all treated animals indicates that the action of the RNA is systemic, since metastases are known to occur frequently by the time our therapeutic regimen was given. Also, in testing the biological activity of the "tumor-immune" RNA in the in vitro cell-migration-inhibition assay, both the syngeneic and xenogeneic RNA extracts could transfer tumor-specific immunological sensitivity, as demonstrated by the elaboration of migration-inhibitory factor by the RNA-treated nonsensitive peritonial exudate cells in the presence of the line 10 tumor-specific antigen.
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PMID:Complete and apparently specif local tumor regression using syngeneic or xenogeneic "tumor-immune" RNA extracts. 16 38

Thymocytes or lymphocytes of mesenteric lymph nodes were obtained from mice bearing subcutaneously mouse ascites hepatoma MH-134 for 5 to 40 days. These lymphoid cells were added into the cultures of MH-134 cells. Morphological changes of cells in the mixed cultures were observed by time-lapse cinemicrography for the period of 4 weeks. Lymphoid cells were phagocytosed by MH-134 cells, and, in most cases, the tumor cells did not undergo any damage due to the phagocytosis. The exceptional cases were as follows: When MH-134 cells were mixed with thymocytes from mice bearing MH-134 tumor for 5 days, MH-134 cells phagocytosed thymocytes but some of them died later. In the mixed cultures of MH-134 cells and thymocytes or mesenteric lymph node lymphocytes from mice bearing MH-134 for 14 or 15 days, MH-134 cells phagocytosed lymphoid cells but died later by the burst of cytoplasm. By the burst many lymphoid cells phagocytosed appeared from the broken cytoplasm of MH-134 cells and, in some cases, the lymphoid cells looked to be alive. These findings suggest the possibility that lymphoid cells attack tumor cells not only from the cell surface but also from the inside being phagocytosed by tumor cells.
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PMID:Interaction in culture between mouse ascites hepatoma (MH-134) cells and lymphoid cells of isologous mice. 17 64

The effects of two immunotherapy regimens on the development of an untreated, uniformly lethal transplantable line-10 hepatoma in strain 2 guinea pigs were monitored during treatment of an identical tumor 10 cm away. Line-10 cells were injected intradermally simultaneously at each of two sites. When one site was treated 6 and 16 days later with rabbit antibody against guinea pig fibrin fragment E, the complete regression of the treated tumor, a 25--30% depression in the development of the untreated tumor, and an increased survival time were observed. In another group of animals, when one site was treated 5 days after tumor challenge with syngeneic or xenogeneic "tumor-immune" RNA in a regimen including syngeneic nonsensitive lymphoid cells and tumor-specific antigen, all animals survived after complete and apparently specific regression of the tumors at both the treated and untreated sites. For the RNA regimen, we have shown that immunotherapy of an intradermally established line-10 tumor results in complete abrogation of both the treated and a distant untreated tumor; i.e., demonstrating a systemic effect.
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PMID:Tumor regression at an untreated site during immunotherapy of an identical distant tumor. 17 71

Wistar rats were sensitized to rat embryonic tissue by immunization with irradiated (5000 rad) rat embryo cells (2 X 10(6) s.c. + 1 X 10(6) i.p.) derived from embryos aged 14-15 days, or by implantation of irradiated (5000 rad) tissue grafts from these embryos. Three to five immunizations were given at weekly intervals, and the rats were then challenged subcutaneously 7-10 days after the final inoculum with minimal tumour-producing tumour cell doses. Immunization with irradiated rat embryo cells failed to influence the growth and development of tumour cells prepared from hepatoma D23 and D30, sarcoma Mc57, mammary carcinoma AAF57 or cells prepared from spontaneously arising mammary carcinomata Sp4 and Sp15. Using adoptive transfer techniques, lymphoid cells from embryo-sensitized rats, when used in a 3000 : 1 ratio (lymphoid cells : tumour cells), were shown effectively to retard the growth of hepatoma D23 in 3 out of 7 experiments performed. Similar adoptive transfer procedures proved ineffective in preventing the growth of mammary carcinoma AAF57. Using in vitro cytotoxicity tests, lymph node cells and spleen cells from embryo-immunized rats were shown to be cytotoxic for several rat tumour cell targets : hepatoma D23 (7/10 tests), sarcoma Mc7 (8/12 tests), mammary carcinoma AAF57 (2/2 tests) and Sp4 (3/4 tests), and for 14-15-day-old rat embryo cells (5/10 tests). In comparative tests lymphoid cells were relatively non-cytotoxic for 20-day-old rat embryo cells (1/6 tests) or cells prepared from adult rat lung or kidney (1/10 tests). The role of embryonic antigen(s) in tumour rejection is discussed.
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PMID:Tumour rejection in rats sensitized to embryonic tissue. I. Rejection of tumour cells implanted s.c. and detection of cytotoxic lymphoid cells. 18 Oct 40


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