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)

This study was undertaken to investigate the antigenic relationships between human malignant melanoma cells and Mycobacterium bovis (BCG). Rabbits were immunized with sonicates of BCG or with malignant melanoma cells from different patients and the resulting antisera were tested for their capacity to bind radiolabeled soluble extracts prepared from BCG and melanoma cells. The binding of antibodies to radiolabeled antigens was studied by precipitation of radiolabeled antigen-antibody complexes by anti-rabbit immunoglobulin. Antibodies in sera from rabbits immunized with either BCG (anti-BCG) or melanoma cells (anti-melanoma) bound both the labeled BCG and melanoma antigens. Control antisera, from rabbits immunized with human acute or chronic lymphatic leukemia cells or with normal human spleen cells, did not bind significant amounts of radiolabeled BCG. Antibodies in sera from rabbits immunized with normal spleen cells bound small but significant amounts of radiolabeled melanoma antigens. Binding by anti-BCG and anti-melanoma to the radiolabeled antigens was studied before and after absorption of antisera with cells from human melanoma, leukemia, guinea pig hepatoma, and normal human spleen cells. Inhibition studies using unlabeled BCG extracts also were carried out. The absorption and inhibition studies confirmed that the binding reactions were specific and that antigens from five melanoma patients shared antigenic determinants with BCG.
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PMID:Shared antigens between human malignant melanoma cells and Mycobacterium bovis (BCG). 5 33

Agarose microdroplet leukocyte migration inhibition (LMI) assays were performed to measure reactivity against line 10 hepatocarcinoma antigens and purified protein derivative (PPD) with the use of peripheral blood leukocytes from line 10 and/or BCG-sensitized syngeneic guinea pigs. The assay was quite sensitive and detected leukocyte migration inhibition with concentrations as low as 12.6 ng protein/ml of the crude sonicate of the line 10 tumor and 0.1 pg PPD. Specificity was shown by lack of reactivity in leukocytes of line 10 and/or BCG-sensitized animals with antigen preparations of L2C leukemia cells or normal syngeneic liver. Furthermore, leukocytes from normal control guinea pigs failed to react with any antigen. The results also suggested antigen cross-reactivity between line 10 tumor and BCG. Leukocytes from guinea pigs sensitized to only BCG became LMI reactive to the line 10 sonicate as well as PPD. No reactivity was observed with leukocytes of the animals in simultaneous tests with a sonicate of guinea pig L2C leukemia cells. The results demonstrated the usefulness of this microassay in detection of LMI reactivity with low antigen concentrations and small volumes of whole blood.
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PMID:Leukocyte migration inhibition of tumor antigen and purified protein derivative reactivity in guinea pigs sensitized to line 10 hepatocarcinoma and BCG. 7 70

Glycolipid A1 isolated from Mycobacterium bovis BCG, when dissolved in olive oil and injected together with Line 10 transplantable hepatoma cells, is able to elicit a host response which results in the abrogation or retardation of tumor growth in syngeneic guinea pigs. Glycolipid A1 does not have adjuvant activity for delayed type hypersensitivity, and antibodies to A1 have not been detected in the sera of guinea pigs during or after the tumor abrogation induced by A1 injection Glycolipid A1 does not share antigenic determinants with Line 10 cell lipid fractions. The possible role of the granuloma response elicited by A1 in controlling tumor growth is discussed.
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PMID:Antitumor activity of mycobacterial glycolipid A1. 8 9

Growth of a guinea pig hepatoma was suppressed when tumor cells were mixed with viable Listeria monocytogenes (LM) before intradermal (id) injection into syngeneic recipients. Heat-killed LM were less effective than viable organisms in suppressing tumor growth. A vaccine containing oil droplets and LM cell walls lacked antitumor activity. Intratumor injection of viable LM on the 7th day after id injection of tumor cells prolonged survival of guinea pigs that did not succumb to LM infection. After intratumor injection of 0.6 times 10-8-1.0 times 10-8 LM, 5 of 22 guinea pigs died from acute infection (23 percent). In the 17 survivors, 3 tumors regressed completely (18 percent). Animals surviving injections of LM and tumor cells were immune to a second challenge with tumor cells. Immunization ofguinea pigs with an intravenous injection of LM decreased the mortality from intratumor injection of LM, but the intratumor injection of LM failed to cure a significant fraction of LM-immune animals bearing 7-day hepatoma transplants. BCG was more effective than LM in producing tumor regression. Synergism between LM and BCG was not observed, and simultaneous intratumor injection of BCG and LM was no more effective than intratumor injection of BCG alone in the treatment of 12-day tumor transplants.
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PMID:Antitumor activity of bacterial infection. II. effect of Listeria monocytogenes on growth of a guinea pig hepatoma. 16 68

Growth of intrapleurally injected cells of immunogenic methylcholanthrene-induced rat sarcomas was suppressed by intrapleural injection of viable or 1 times 10-6 R radiation-sterilized BCG vaccine. As little as 10 mug moist weight of organisms was effective, and treatment could be given several days before or after tumour challenge. Pleural effusion growth of a moderately immunogenic ascitic hepatoma was also controlled by intrapleurally administered BCG. In contrast, BCG injected intravenously, subcutaneously or intraperitoneally was without influence on pleural tumour growths. Similarly, intraperitoneal growth of these tumours was suppressed only by intraperitoneal injection of BCG. With two other transplanted tumours, a chemically induced mammary carcinoma and a spontaneous sarcoma, both of which lack significant immunogenicity, BCG treatment of pleural and peritoneal growths was less successful and more variable. Nevertheless, these studies indicate the potential of this type of treatment of thoracic and peritoneal tumour deposits for possible clinical application in the treatment of malignant mesothelioma.
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PMID:BCG therapy of pleural and peritoneal growth of transplanted rat tumours. 16 55

Subcutaneous growth of immunogenic chemically induced rat sarcomata and a hepatoma was restricted when cells were injected into syngeneic animals in admixture with MER. Rats rejecting mixed inocula were immune to further challenge with the same tumour. Growth of a chemically induced mammary carcinoma which lacks detectable immunogenicity was suppressed when low cell inocula were injected in admixture with MER or intact BCG organisms, although animals were not immune to re-challenge. These studies indicate that clinically MER may be a suitable alternative to BCG for contact suppression of tumour growth or incorporation into tumour cell:adjuvant vaccines for active immunotherapy.
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PMID:Methanol extraction residue of BCG in the treatment of transplanted rat tumours. 16 61

Rabbit antibody to fibrin fragment E (FFE) was used in an immunotherapy model for the treatment of the line-10 ascites variant of a diethylnitrosamine-induced hepatoma in strain 2 guinea pigs. When 0.75 or 1.0 mg of an IgG preparation containing anti-FFE antibody was injected s.c. 6 and 16 days after the injection of a uniformly lethal dose of line-10 tumor cells, complete regression of the i.d. growing tumor was observed in all 18 strain 2 guinea pigs treated. Thus, this therapy appears to be more effective than any BCG or other immunotherapeutic regimen thus far reported for this tumor. No significant anti-tumor effect was noted when normal rabbit IgG or smaller doses (0.25 or 0.50 mg) of the anti-FFE IgG preparation were used. The injection sites exhibited an inflammatory response for 7 to 10 days characterized by erythema and hemorrhage. Since all animals were treated after the metastatic progression of the tumor is known to frequently occur, the long-term tumor-free survival of these animals as well as their resistance to subsequent tumor challenge indicate that the anti-FFE antibody therapy led to systemic tumor immunity.
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PMID:Complete local tumor regression with antibody to fibrin Fragment E. 17 Mar 40

The lymphocyte distribution into the tumor-draining node was studied with AH-130 hepatoma cells and Donryu strain rats in relation to the adjuvant activity of the oil-attached BCG whole cell wall. The mixed inoculation of the oil-attached BCG cell wall with tumor cells resulted initially in further augmentation of increased distribution of 51Cr-labeled lymphocytes into the draining-node induced by inoculation of the tumor cells alone, and secondarily in the systemic stimulation of response of the lymph node lymphocytes to phytohemagglutinin. Suppression of the inoculated tumor growth and lymph node metastasis was finally observed. These results were discussed in connection with the therapeutic effect of BCG and its cell wall fraction.
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PMID:Effect of oil-attached BCG cell wall on the kinetics of lymphocytes in the tumor-draining node. 17 Nov 93

A transplantable hepatocarcinoma of guinea pigs was used as an experimental model for immunotherapy of cancer. Earlier work showed that complete regression of 6- to 7-day-old tumors could be obtained in about 60% of cases by inoculation of the tumors with live BCG or certain fractions of BCG attached to minute oil droplets and suspended in Tween-saline. One of the most essential fractions was P3, a nonsensitizing, nonantigenic trehalose mycolate related to, but not identical with, cord factor. We now report that oil-droplet preparations containing P3 and bacterial endotoxin (ET) produced cure rates of up to 90% in the same system. In addition, regression was faster than with BCG, and older tumors could be treated successfully. The most effective ET's were from rough strains of salmonellae, known as Re mutants, which could not synthesize and attach the polysaccharide portion of endotoxin.
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PMID:Tumor regression caused by endotoxins and mycobacterial fractions. 17 65

The levels of tumour-specific antigen, antibody and specific immune complexes in the sera of rats bearing lung nodules of a chemically induced rat hepatoma, produced by intravenous inoculation of viable tumour cells, have been examined and compared with the levels of serum factors in animals actively immunized by intravenous inoculation of mixed tumour cells and BCG. Animals inoculated with cells alone developed multiple lung nodules which slowly grew, until on day 24 the remaining animals had to be killed due to respiratory distress. In contrast, the animals receiving a mixed inoculum of BCG and tumour cells developed no visible lung nodules and were capable of rejecting a further challenge of tumour cells. Tumour-specific antigen could be detected in the sera of both groups of rats at different times. In actively immunized animals free antigen could be detected from day 3 to day 10 after inoculation of cells BCG whereas in animals receiving cells alone, free antigen could not be detected until day 14 and persisted until the termination of the experiment. Free tumour-specific antibody, however, was found in the sera of rats actively immunized with tumour cells and BCG from day 10 onwards, although in the other group of animals it could not be detected. Conversely, immune complexes of tumour-specific antigen and antibody could be detected from day 10 in rats receiving cells alone and only at day 10 in actively immunized rats. The relevance of these findings in relation to what is known about serum factor levels during tumour growth and regression is discussed.
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PMID:Serum factor levels during the growth of rat hepatoma nodules in the lungs. 17 30


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