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)

Various aspects of hormone treatment of tumor cells are reported; it is shown that following treatment with certain hormones, the cells are less susceptible to killing by antibody and complement. The diethylnitrosamine-induced guinea pig hepatoma, designated Line 1, is susceptible to killing by anti-Forssman immunoglobulin M (IgM) antibody and guinea pig complement (GPC) but not by specific antitumor antibody and GPC. The antigenetically distinct Line 10 hepatoma, when sensitized with either antibody, is susceptible to killing by human complement (HUC) but not by GPC. Strain 2 of Servall-Wright male guinea pigs were used. 2 antigenetically distinct diethylnitrosamine-induced hepatic tumors (ascites form), Lines 1 and 10, passed in Strain 2 guinea pigs, were collected and suspended in RPMI 1640-20% FCS. Toxicity assays were performed in VBS-gel. The hormones used were hydrocortisone sodium succinate, prednisolone sodium succinate, NSC9151, bovine insulin, L-epinephrine methyl ether HC1, DL-epinephrine, beta-estradiol, testosterone, pork insulin, chicken insulin, pork proinsulin, pork DAA insulin, and the A and B chains of pork insulin. Tumor cells were cultured in 10-ml volumes of RPMI 1640-20% FCS in plastic Petri dishes. After incubation, cell cultures were washed 5 times in VBS-gel and tested for their susceptibility to killing by antibody and complement. Rabbit antiserum to sheep Forssman antigen was prepared and stored at -20 degrees until used. Tumor specific rabbit Antilines 1 and 10 antisera were prepared and similarly stored. Results of tests show that Line 1 tumor cells incubated in a medium containing the polypeptide hormone, insulin, the catecholamine, L-epinephrine HCl, or the glucocorticoid steroids, hydrocortisone sodium succinate, or prednisolone sodium succinate were rendered resistant to killing byanti-Forssman IgM antibody and GPC. This effect was dependent on hormone concentration, temperature, and time. Effects were reversible. Similar results were obtianed with Line 10 cells under attack by specific antitumor and HUC or anti-Forssman antibodies. Less physiologically active analogs of the hormones did not have this effect. Tumor cells showed maximum resistance within 30-60 minutes of exposure to the hormones and reverted to the sensitive state within 4 hours. Resistance of the cells to killing was observed at 37 degrees but not at 0 degrees. It is concluded that the effect of hormone treatment was not due to a direct inactivation of bound or fluid-phase complement components by the hormones or to a decrease in the ability of the cells to bind complement-fixing antibody.
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PMID:Inhibition of antibody-complement-mediated killing of tumor cells by hormones. 18 62

Line 10 hepatoma cells were incubated with antiserum specific against line 10 cells (RaL10) and then tested for growth in syngeneic Wright strain 2 guinea pigs. Palpable tumors appeared in only 11 of 23 animals inoculated id with 10(5) RaL10-treated tumor cells, compared with an incidence of 21 of 23 for nonimmune rabbit serum (NRS)-treated cells and 23 of 23 for cells treated with syngeneic guinea pig serum. Animals inoculated with RaL10-treated tumor cells did not develop systemic tumor immunity. The long-term survival of guinea pigs receiving RaL10-treated tumor cells iv was 6 of 12 with a dose of 10(5) cells and 8 of 11 with 10(4) cells. None of the animals receiving 10(4) or 10(5) control tumor cells treated with NRS survived. RaL10 antiserum was not toxic to line 10 tumor cells in vitro, but mediated tumor-specific cytolytic reactions in the presence of fresh guinea pig serum or on the addition of peritoneal exudate cells from nonimmunized syngeneic guinea pigs.
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PMID:Suppression of tumor growth in strain 2 guinea pigs by xenogeneic antitumor antibody. 18 78

Mitotic cells from the H-4-IIE-C3 rat hepatoma tissue culture line showed a range of 45 to 53 chromosomes per cell with 75% of the cells displaying a chromosome mumber between 49 and 52. Analysis of Wright's-Giemsa banded karyotypes of 22 cells revealed considerable cell to cell variation. Twenty-one structurally abnormal chromosomes were identified in these cells; the origin of nine of the 21 chromosomes were identified in these cells; the origin of nine of the 21 chromosomes could be determined. Of the structurally abnormal chromosomes detected, only one (M-1) occurred with a sufficiently high frequency to be of general use as a marker for these cells. This marker appears to be a Robertsonian translocation involving chromosome number 2 and chromosome number 10.
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PMID:Banded karyotypes of H-4-IIE-C3 rat hepatoma cells grown in vitro. 18 53

The growth of line-10 hepatoma in male Sewall Wright strain 2 guinea pigs was totally suppressed when tumor cells were mixed with heat-killed Candida albicans. In a significant number of animals, injection of C. albicans into established tumors 10-12 mm in diameter caused complete, rapid tumor regression. Guinea pigs whose tumors regressed or were suppressed as a result of injection of C. albicans rejected subsequent challenges at distant sites with the line-10 hepatoma, which indicated the development of systemic immunity to the tumor. Untreated control guinea pigs had positive delayed hypersensitivity reactions to intradermally injected C. albicans, which suggested prior natural exposure of the animals to C. albicans antigens. Peritoneal macrophages from mice that had received ip injections of phosphate-buffered saline (PBS) or C. albicans were not cytocidal for mouse 3T12 tumor cells in vitro. However, macrophages from the mice given injections of C. albicans, unlike those from mice given PBS, were markedly tumoricidal in the presence of 1 ng or more endotoxin/ml in vitro. These results demonstrated that heat-killed C. albicans, when inoculated into the peritoneal cavity, increased the tumoricidal potential of peritoneal macrophages.
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PMID:Enhanced macrophage tumoricidal activity and tumor suppression or regression caused by heat-killed Candida albicans. 38 16

Resistance to line-10 hepatocarcinoma was studied in the newborn offspring of inbred strain-2 Sewall Wright guinea pigs that had recovered from this tumor after prior administration of subcellular components of Mycobacterium bovis strain BCG. These mothers gave birth to 15 offspring, 53% of which resisted repeated challenges with this tumor. Offspring of mothers who had been given only BCG components were similarly tested. Complete protection was observed in 23.5% of 17 babies and attenuation of disease in many others. All control offspring from normal, untreated mothers succumbed to this tumor. Resistance was associated with delayed cutaneous hypersensitivity reactions to tumor and mycobacterial antigens.
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PMID:Transmission of BCG-associated tumor resistance from maternal to newborn guinea pigs. 125 44

Hepatocellular carcinoma cells obtained from ascitic fluid after diethylnitrosamine treatment of Sewall Wright strain-2 guinea pigs produce solid (primary) tumors, lymph-node metastases and malignant ascites when reinjected into animals of the same strain. When brought into culture the cells settle, form multilayer cultures and can be maintained in passage. In addition to epithelium-specific cytokeratin intermediate filaments (IF), these latter cells, like most cultured cells, also contain vimentin. Hepatocellular carcinoma cells in solid tumors and in metastatic tumors retain their original keratin IF and in general do not have an additional vimentin-IF system. When the tumor cells are present in ascites they develop vimentin-IF in addition to cytokeratin filaments. Vimentin is gradually lost when these cells sediment onto the peritoneal surface and proliferate continuously to form papillary projections, or when they are detected as circumscribed metastases. It seems likely, therefore, that in this system the synthesis of an additional vimentin cytoskeleton is related to reduced cell-to-cell contact and to the ability of the cells to survive individually or as cell clusters in body fluids, without being part of a cohesive tissue.
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PMID:Changing intermediate-sized filament patterns in metastatic hepatocellular carcinoma cells of the guinea pig. 242 67

A Sewall Wright strain-2 guinea pig model producing malignant ascites after injection of a diethylnitrosamine-induced hepatocellular carcinoma cell suspension (Line-10) was used to demonstrate the multilayered settling of tumor cells on the peritoneal surface, frequently followed by the formation of papillary projections and the early invasion in a proliferating submesothelial tissue. At the border of tumor cells and the desmoplastic tissue the malignant cells changed their shape and generally two categories were recognized. Often multilayering, atypical flat cells covered the stromal tissue, while mostly rounded ones invaded using their branched penetration processes, being devoid of cationized ferritin, which was only present on the luminal sides of all cellular elements. Flattened malignant cells, penetrating processes and invading cells lost their microvillous surface pattern. The infiltrating cells were often only detectable with the monoclonal antibody 10 TL 40 and the anti-cytokeratin OV TL 12-5, demonstrating the need for immunohistochemistry in diagnosing solitary invading malignant cells in light microscopy. It appeared that still numerous mesothelial cells were found scattered deeply within the desmoplastic tissue. These former lining cells were identified by their junctions and the presence of remnants of basal lamina as well as by their microvillous 5'-nucleotidase activity.
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PMID:Tumor cell settling and early invasion of the peritoneum. 246 62

Hepatocellular carcinoma cells (Line-10), obtained from ascitic fluid after diethylnitrosamine treatment of Sewall Wright strain-2 guinea pigs, produce solid (primary) tumours, lymph-node and lung metastases and malignant ascites when reinjected into animals of the same strain. Monoclonal antibodies were raised against the tumour cells by immunizing BALB/c mice with viable ascitic hepatocellular Line-10 tumour cells. Three hybridomas producing anti-Line-10 monoclonal antibodies were selected for further studies (10TL1, 10TL40 and 10TL43) and compared with monoclonal antibodies against intermediate filament keratins. The anti-Line-10 monoclonal antibodies did not cross react with Line-1 hepatocellular carcinoma cells, nor with normal guinea pig hepatocytes. When ascitic Line-10 cells form high papillary projections on the peritoneal surface, they significantly reduced their antigen expression of 10TL40 and of 10TL43 defined antigens, while the expression of 10TL1 defined antigens remained unaltered. Invading Line-10 cells in the deep submesothelial stromal tissue, however, lost reactivity with MoAb 10TL43 but not with the MoAb's 10TL40 and 10TL1. The antigens on lung- and lymphnode metastases remained largely unaffected. The reactivity with MoAb's 10TL40 and with 10TL43 was also lost upon prolonged culturing of Line-10 cells. The reactivity of Line-10 and Line-1 cells with all monoclonal antibodies against keratin filaments remained unaltered. Line-1 cells could be distinguished from Line-10 cells by the absence of any reactivity with the MoAb's 10TL1, -40, -43, but also by the fact that 100% of the Line-1 cells were positive with antibodies against keratins 5/8, 18, and 7.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Changing tumour antigen expression in metastatic hepatocellular carcinoma cells of the guinea pig. 246 49

U6 RNA is an abundant, capped small nuclear RNA (snRNA) associated with hnRNP particles (Reddy, R., and Busch, H. (1983) Prog. Nucleic Acid Res. Mol. Biol. 30, 127-162). Small nuclear ribonucleoprotein particles containing U4 and U6 RNAs are required components for splicing of pre-mRNAs (Berget and Robberson, 1986; Black and Steitz, 1986). In this study the Drosophila U6 RNA genes have been isolated and characterized. The Drosophila genome contains three U6 snRNA genes which are clustered in a 2-kilobase-pairs long DNA fragment. The U6 RNA coding regions are 100% homologous in all three genes, but the flanking sequences diverged significantly from each other. A possible secondary structure model for the Drosophila U4/U6 RNA complex is presented. Consistent with our previous observation that U6 RNA is a RNA polymerase III product (Reddy, R., Henning, D., Das, G., Harless, M., and Wright, D. (1987) J. Biol. Chem. 262, 75-81), all three genes contained a region homologous to the consensus intragenic regulatory region and a cluster of T residues on the 3'-end, characteristic of genes transcribed by RNA polymerase III. A TATA box was found between nucleotides -23 and -31, and a stretch of 28 nucleotides from -43 to -71 was conserved in the 5'-flanking region of all three U6 RNA genes. The Drosophila U6 RNA genes were transcribed in vitro by Drosophila nuclear extracts but were not transcribed by Novikoff hepatoma or HeLa cell extracts. Similarly, a mouse U6 RNA gene was transcribed in Novikoff hepatoma or HeLa cell extracts but not in Drosophila nuclear extracts. These results suggest that species-specific factor(s) are involved in the transcription of U6 snRNA genes.
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PMID:Structure, organization, and transcription of Drosophila U6 small nuclear RNA genes. 302 83

Several aspects of adoptive transfer of tumor immunity were studied in the line 10 hepatocarcinoma in the syngeneic Sewall-Wright strain 2 guinea pig. In particular, the need for cooperation between donor and recipient T-cells was investigated. Donor immune spleen cells remained immunologically capable of inducing tumor rejection for at least 160 days after adoptive transfer. Irradiated (1,000 rad) or mitomycin-treated immune spleen cells lacked tumor-rejection activity, which is indicative of the necessity for in vivo proliferation after adoptive transfer of immunity. Furthermore, adoptive transfer of tumor immunity was abrogated after treatment of the line 10 immune spleen cells with rabbit anti-guinea pig-thymocyte serum (ATS) plus complement. The role of recipient T-cells was investigated in strain 2 guinea pigs which were T-cell depleted by thymectomy, irradiation, and bone marrow reconstitution (T-XBM animals). Severe suppression of T-cell activity was present at 2 and 6 weeks after irradiation and bone marrow reconstitution. At 10 weeks nonspecific T-cell activity was partially restored. The induction of antigen-specific responses, measured by delayed-type hypersensitivity skin testing in vivo and antigenic stimulation in vitro, was suppressed at 2 weeks after irradiation and bone marrow reconstitution. Additional in vivo treatment of T-XBM animals with a rabbit ATS improved the T-cell depletion only moderately. Tumor growth and tumor rejection after adoptive transfer of immunity were equal in normal and T-cell-deprived recipient animals, thus indicating that recipient T-cells are not needed for tumor rejection after adoptive transfer of line 10 tumor immunity.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:T-cell involvement in adoptive transfer of line 10 tumor immunity in strain 2 guinea pigs. 387 51


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