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 present study demonstrates the intratumoral infiltration of lymphocytes mediating anti-tumor delayed-type-hypersensitivity (DTH) responses as well as in vivo protective immunity. The surface phenotype and tumor specificity of these effector lymphocytes were determined. X5563 tumor-infiltrating lymphoid cells were obtained from the tumor mass of syngeneic C3H/HeN mice 2 weeks after the intradermal inoculation of 10(6) viable X5563 tumor cells. These lymphoid cells consisted of Thy-1-positive (29-35%), surface immunoglobulin-positive (16-29%), large granule-positive (15-25%) and esterase-staining-positive (10-20%) cells. They were tested for anti-X5563 DTH responses by utilizing a local adoptive transfer system and for tumor-neutralizing activity in a Winn assay. The results indicate that X5563 tumor-infiltrating lymphoid cells exhibited appreciable anti-X5563 DTH responses and conveyed complete protection against the tumor. Treatment of these lymphoid cells with anti-Thy-1.2 or anti-Lyt antibodies plus complement revealed that the in vivo anti-tumor immune responses were mediated predominantly by a Lyt-1+2- T cell subset. Such Lyt-1+2- T cell-mediated immunity was tumor-specific, since X5563-infiltrating and syngeneic MH134 hepatoma-infiltrating cells exhibited DTH response and tumor-neutralizing activity selectively against the respective tumor cell types. Thus, these results indicate that tumor-specific in vivo-protective Lyt-1+2- T cells infiltrate into the tumor mass. The results are discussed in the context of 1) the interrelation of DTH responses and the tumor protection mediated by the Lyt-1+2- T cell subset and 2) possible cellular interactions between Lyt-1+2- T cells and co-existing nonspecific tumoricidal effector cells such as macrophages.
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PMID:Demonstration of intratumoral infiltration of tumor-specific Lyt-1+2- T cells mediating delayed-type hypersensitivity response and in vivo protective immunity. 308 30

Transgenic mice carry cloned DNA fragments that have been introduced into the mouse genome, generally by microinjection into pronuclei. They can be used to determine the cis-acting DNA elements responsible for the tissue-specific expression of genes. For this purpose, transgenic mice were obtained carrying either the mouse albumin gene or the human insulin gene. In the first instance, it was shown that the regulatory sequences necessary for expression of the albumin gene transfected into differentiated hepatoma cells are not sufficient to induce its expression in transgenic mice. In contrast with the albumin gene, the short sequence upstream to the insulin gene necessary for its expression in transfected insulinoma cells is sufficient to allow expression in transgenic mice. Similar experiments were performed to study another crucial step in differentiation of lymphoid B cells, namely rearrangement of the immunoglobulin (Ig) genes. The chicken Ig lambda light chain gene in the germ line (unrearranged) form was introduced into the mouse genome, and the rearrangement observed in transgenic mouse lines is briefly described.
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PMID:Transgenic mice: a tool for the study of tissue-specific gene expression. 313 35

Glucocorticoid hormone is shown to markedly suppress DNA synthesis in a line of rat hepatoma cells in vitro. In the presence of 300 nM hydrocortisone or 30 nM dexamethasone the incorporation of radioactive thymidine falls to 50% of control levels by 36 hr, and at higher concentrations of hormone inhibition can be noted as early as 12 hr and is nearly complete by 24 hr. This inhibition of radioactive thymidine incorporation reflects a true suppression of DNA synthesis, is accompanied by a corresponding inhibition of cell proliferation, and is readily reversible upon subsequent removal of hormone. In contrast to previously described effects of the glucocorticoid hormones on various cells of lymphoid origin, the inhibition of DNA synthesis in these hepatoma cells is not accompanied by appreciable cell lysis or by degradation of preformed DNA, and even when [(3)H]thymidine incorporation into DNA is inhibited by 90% or more, incorporation of [(14)C]uridine into RNA proceeds with little change. These findings all parallel previous observations on the effects of glucocorticoid hormone on the livers of intact animals and suggest that studies on the mechanism of the inhibition of DNA synthesis in the present more isolated system may lead to a better understanding of the means by which these compounds inhibit liver growth in vivo. Despite the ready suppressibility of DNA synthesis in these hepatoma cells and in two other cell lines of liver origin, none of these cell lines was found to be inducible for tyrosine aminotransferase. The apparent dissociation between two "steroid-sensitive" phenomena is of interest and warrants further investigation.
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PMID:Suppression of DNA synthesis in hepatoma cells exposed to glucocorticoid hormone in vitro. 414 35

Immunofluorescent staining of HeLa cells with rabbit antiserum raised against isolated HeLa cell nucleoli showed bright nucleolar fluorescence. Immunoprecipitation of nuclear extracts obtained from HeLa cells labelled with 35S-methionine or 32P-orthophosphate followed by gel electrophoresis of the precipitate revealed a major band of 90 kd. This antigen, called pp90, was judged to be responsible for the nucleolar fluorescence. Serine residues were predominantly phosphorylated in pp90. Similar nucleolar fluorescence was observed commonly in human cells derived from malignant tumors including acute lymphatic leukemia, adult T-cell leukemia, hepatitis B virus-associated hepatoma, adenocarcinoma, and in 5 lymphoid cells derived from Burkitt lymphoma but not in normal human lymphocytes or liver cells. In immunoprecipitation, 32P-labelled pp90 was commonly detected as the major component in all of those cells which showed nucleolar fluorescence. Resting human embryo lung (HEL) cells were negative for both nucleolar fluorescence and pp90 in immunoprecipitation, but turned positive when stimulated to grow, suggesting the involvement of pp90 in cell growth. Antigen pp90 was also induced in human lymphocytes and HEL cells by infection with Epstein-Barr virus in human cytomegalovirus, respectively, which are known to induce cell DNA synthesis in early stages of infection. A cross-reacting nucleolar antigen was detected in 2 monkey cells but not in 3 rodent cells tested.
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PMID:A human nucleolar antigen (pp90) associated with cell growth and its induction by Epstein-Barr virus and human cytomegalovirus. 609 64

An experimental model is described for analysis of cellular and molecular mechanisms involved in the modulation of tumorigenicity by syngeneic lymphoid cells and oncofetal products in vivo. The effect of mouse amniotic fluid (AF) and alpha-fetoprotein (AFP) from this fluid and from serum, free or bound to estrogens, upon the growth of a syngeneic hepatoma was examined in mice transferred with syngeneic spleen cells from hepatoma-bearing donors. Intraperitoneal transfer of spleen cells from hepatoma-bearing into normal syngeneic mice, either tended to stimulate or to inhibit tumor growth in the latter depending on the length of time elapsed between tumor-transplantation in the spleen-cell donor and their sacrifice for spleen excision. For example, only the spleen cells obtained on day 14 and 21 following tumor transplantation protected the recipients from tumor growth. When these protective cells were mixed with hepatoma cells from a low incidence line, and the mixture injected subcutaneously, tumor incidence increased (tumor-promotion effect) rather than the contrary. AF was immunosuppressive inasmuch as it amplified the tumor-promotion effect of the spleen cells. On the other hand, purified AFP from sera of hepatoma bearing mice abolished this tumor-promotion effect.
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PMID:Modulation of tumor incidence by oncofetal products in a syngeneic hepatoma cell-spleen cell model. 618 67

Erythroblastopenia occurred in the course of chronic B cell lymphocytic leukemia. The failure of chlorambucil therapy prompted the decision of thymic irradiation. This was effective on the lymphoid proliferation but did not modify the erythroblastopenia. Progressive hepatomegaly led to the diagnosis of hepatoma.
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PMID:[Chronic lymphoid leukemia with erythroblastopenia and primary liver tumor]. 629 69

The morphology of liver cirrhosis and the incidence of hepatocellular carcinoma (HCC) in HBsAg-positive alcoholics (17 cases) were examined and compared with those of HBsAg-negative alcoholics (31 cases) and HBsAg-positive non-alcoholics (59 cases). These materials were obtained from our autopsy cases during the last 9 years. About 70% of the 17 showed macronodular cirrhosis, in which periportal and portal lymphoid cell infiltration and liver cell dysplasia were often present, as seen in HBsAg positive non-alcoholics. Furthermore, the liver weight and age distribution at autopsy in HBsAg-positive alcoholics were similar to those of HBsAg-positive non-alcoholics and different from those of HBsAg-negative alcoholics. The association rate of HCC was very high in HBsAg-positive alcoholics (64.7%), similar to that in HBsAg-positive non-alcoholics (67.8%), while the rate in HBsAg-negative alcoholics was low (22.6%). It therefore seems likely that in HBsAg-positive alcoholics concomitant HB virus infection has a major effect on the development of cirrhosis, especially a macronodular type, and on HCC formation.
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PMID:Morphology of cirrhosis and occurrence of hepatocellular carcinoma in alcoholics with and without HBsAg and in non-alcoholic HBsAg-positive patients. A comparative autopsy study. 632 10

It has been demonstrated that the renal graft survival was prolonged after blood transfusion. The immunological action of blood transfusion in the host is not clear yet. The effect of blood transfusion on transplanted tumor growth in mice was examined. Using C3H/He (H-2k), AKR (H-2k), C57BL/6 (H-2b), and (C57BL/6xDBA/2)F1 (H-2b,d)mice, mutually different transfusion combinations were prepared. MH134 cells (hepatoma) originated from C3H/He mice or Lewis lung carcinoma cells originated from C57BL/6 mice were grafted beneath the back skin of mice on the second week after transfusion, and size of the tumor was measured. The results showed that 1) blood transfusion among mice with the same H-2 systems had no enhancing effect on grafted tumor growth, 2) blood transfusion among mice with different H-2 systems markedly enhanced the tumor growth, although different in degrees, 3) In the experiments of component transfusions, transfusion of lymphoid cells also enhanced the tumor growth, but not erythrocytes. The results of these experiments clearly showed the differential effects of allogeneic or syngeneic blood transfusion on transplanted tumor growth in mice.
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PMID:[Enhancement by blood transfusions of transplanted tumor growth in mice]. 633 80

The effects of carrageenan and trypan blue on the expression of adoptive immunity to the syngeneic guinea pig line 10 hepatoma were investigated. Adoptive immunity was assessed by observing dermal tumor growth in recipients of immune cells and by bioassays in which tumor challenge sites were transplanted into secondary hosts. Carrageenan abrogated transferred immunity in treated animals as evidenced by dermal tumor growth and by development of fatal ascites tumors in peritoneal cavities of the secondary hosts. Trypan blue, on the other hand, did not abrogate transferred immunity in treated animals. However, the i.p. bioassay revealed the presence of line 10 cells in the tumor challenge sites 10 days after adoptive transfer. In vitro and in vivo exposure of immune spleen cells to carrageenan or trypan blue had no significant effect on the subsequent adoptive transfer, indicating that the inhibitory activity of these agents cannot be attributed to direct toxicity to immune lymphoid cells. Tumor challenge sites taken from carrageenan or trypan blue-treated animals 5 days after adoptive transfer failed to grow progressively when transplanted s.c. into secondary hosts. This observation suggests the presence of immune cells at tumor challenge sites. Thus, the inhibitory effects were unlikely due to interference with recirculation of the i.v.-transferred immune cells. Adoptive immunity was not influenced in guinea pigs that received a lethal dose of irradiation (500 rads). These results demonstrate that a recipient component(s) sensitive to carrageenan and trypan blue but resistant to radiation is essential to the expression of adoptive immunity.
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PMID:Mechanisms of immunological eradication of a syngeneic guinea pig tumor: participation of a component(s) of recipient origin in the expression of systemic adoptive immunity. 634 56

Immunization of strain 2 guinea pigs with 10(7) syngeneic Ia+ L2C leukemia cells in adjuvant leads to L2C tumor protection. After subsequent challenges with L2C tumor cells, the sera and spleens of the protected guinea pigs had detectable anti-L2C reactivity. The L2C antibody reactivity was preferentially associated with the IgG1 isotype fraction and bound equally well to Ia+ or Ia- L2C cells but failed to bind to normal guinea pig lymphoid cells or hepatocarcinoma tumor cells. The binding was inhibited appreciably with F(ab')2 fragments specific for the L2C surface IgM idiotypic determinants. By contrast, the same reagent failed to inhibit the specific cytolysis of L2C tumor cells by T lymphocytes present in the spleens of L2C protected guinea pigs. However, the T cell mediated cytolysis was inhibited to some extent by F(ab')2 fragments specific for the B.1 alloantigen on the L2C tumor cells. These results indicate that the specificity of the L2C T effector cells appears to differ from that of the L2C antibodies and that in the elicitation of a humoral response the IgM idiotypic determinants may function as a tumor-associated antigen.
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PMID:Immune response in strain 2 guinea pigs to the syngeneic L2C leukemia. 635 30


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