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Query: UMLS:C0019204 (hepatocellular carcinoma)
 71,386 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The growth in the colon wall of a diethylnitrosamine-induced hepatocarcinoma was suppressed by BCG. Injection of BCG into established colon-wall tumors caused tumor regression. Successful therapy required a limited tumor burden. Guinea pigs in which growth of the neoplasm was suppressed at the site of BCG infection developed systemic tumor transplantation immunity.
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PMID:Suppression and regression of a transplanted tumor in the guinea pig colon mediated by Mycobacterium bovis, strain BCG. 23 37

A transplantable fibrosarcoma induced in inbred JY-1 guinea pig strain by 3-methylcholanthrene (MCA) and designated J4, an allotransplantable subline of J4 (JH4) which was obtained by the transplantation of J4 into the inbred Hartley/F guinea pig strain and maintained by passages in this strain, and a syngeneic liposarcoma H10 induced in a Hartley/F guinea pig by MCA were tested for their immunotherapeutic response with BCG. The growth of J4 and H10 tumors was suppressed in most of the animals when tumor cells were mixed with BCG before being injected sc into BCG-immune or BCG-nonimmune recipients. The growth of the JH4 tumor was suppressed at the sites of injection with a mixture of tumor cells and BCG in BCG-immune recipients but not in nonimmune animals. All guinea pigs surviving the injection of a tumor cell-BCG mixture resisted a second tumor cell challenge. When subcutaneous sarcomas grew to about 8-15 mm in diameter, BCG was injected into the tumors. The growth of JH4 tumor was not influenced by the injection in either BCG-immune or BCG-nonimmune animals, while the regression of the established J4 transplants was produced in 2 of 3 nonimmune recipients. The growth of the H10 tumor was not inhibited with an intratumor injection into nonimmune guinea pigs, while the H10 tumor regressed in BCG-immune animals for 4-5 weeks after intratumor injection and thereafter grew progressively. Skin reactions in animals that received repeated intradermal injections of the tumor cells and BCG were tested with 10(6) viable tumor cells as eliciting antigens. Typical delayed-type hypersensitivity reactions that were specific to the homologous antigens were observed. The possible reasons for the different responses to BCG among the guinea pig tumors, including line-10 hepatocarcinoma in strain-2 guinea pigs, were discussed.
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PMID:Responses of tumors induced in inbred guinea pig strain JY=1 and strain Hartley/F to BCG. 32 Mar 48

BCG cell wall skeletons (SK) derived from BCG cell walls (CW) by treatment with proteolytic enzymes and organic solvents were tested for their potency to cause regression of a transplanted guinea pig hepatoma. On a weight basic, SK were as effective as CW in causing tumor regression, and they, as well as purified protein derivative of mycobacteria, provoked delayed cutaneous hypersensitivity reactions in animals immunized with CW or with SK. On a weight basis, CW were more active than SK in eliciting delayed cutaneous hypersensitivity in sensitized guinea pigs whether the animals were immunized with CW or with SK. In unimmunized animals the inflammatory response to intradermally administered CW was greater than that evoked by SK. CW and SK provoked delayed cutaneous hypersensitivity reactions of similar strength in animals immunized with living BCG. This study provided no compelling reasons for using SK instead of CW in clinical trials of cancer treatment by mycobacterial vaccines.
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PMID:Immunotherapy of a guinea pig hepatoma with mycobacterial vaccines: comparison of BCG cell walls and cell wall skeletons. 36 72

The serum of athymic nude mice bearing rat tumour xenografts has been examined for tumour-specific antigen. With a sarcoma and a hepatoma, tumour-specific antigen expression continued in xenograft growths, and sera of tumour-bearing mice contained free antigen, assayed by its ability to neutralise reactivity of tumour-immune rat sera against tumour target cells in an indirect membrane-immunofluorescence test. In contrast, no anti-rat antibody was detectable in sera of mice bearing the xenografts, or rejecting cells injected in admixture with BCG.
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PMID:Serological aspects of rat tumour xenograft growth in athymic nude mice. 37 82

Heat-killed whole BCG cells (KC) and BCG cell walls (CW) were each tested in emulsified form for their potency to cause regression of a transplanted guinea pig hepatoma. On a weight basis, KC were at least as effective as CW in causing tumor regression and elimination of microscopic lymph node metastasis, and they, as well as purified protein derivative of mycobacteria, provoked delayed cutaneous hypersensitivity reactions in animals immunized with CW or with KC. On a weight basis, KC were as active as CW in eliciting delayed cutaneous hypersensitivity in sensitized guinea pigs whether the animals were immunized with CW or with KC. In unimmunized animals the inflammatory response to intradermally administered KC was similar to that induced by CW. Because KC are easier to prepare than CW, it is suggested that whole killed BCG might be used instead of CW in clinical trials of cancer treatment requiring administration of nonliving mycobacteria.
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PMID:Immunotherapy of guinea pigs with a transplanted hepatoma: comparison of intralesionally administered killed BCG cells and BCG cell walls. 38 92

Efficacy of oral administration of BCG on the growth of various tumors in mice and guinea pigs was studied. The growth-inhibitory effect varied depending on the tumor systems and the experimental conditions. Weekly oral administrations with 5-mg doses of BCG to mice or 80-mg doses of BCG to guinea pigs were ineffective on syngeneic mouse melanoma B16 or syngeneic guinea pig hepatocarcinoma line-10 but effective on syngeneic mouse carcinoma IMC and syngeneic guinea-pig fibrosarcoma H9A. Oral BCG seemed effective also on allogeneic mouse carcinoma Ehrlich, developed with a relatively small size of tumor cell inoculum, and on guinea-pig syngeneic liposarcoma H10. On Ehrlich tumors, oral BCG given once a week seemed to have better effects than did oral BCG given twice a week or subcutaneously once or repeatedly; heat-killed BCG given orally showed no effect. However, it seems premature to draw a definite conclusion on the efficacy of oral BCG on Ehrlich and H10 tumors, because some of these tumors regressed spontaneously even in nontreated control animals. The host responses to oral BCG were studied with the following results. Weekly oral administration with 80-mg doses of BCG to guinea pigs elicited positive skin reactions to 25 TU PPD in about 65 days after the first BCG, while a single sc injection of 8 mg of BCG did so within 10 days. Orally administered BCG organisms were recovered largely from Peyer's patches, a little from the mesenteric lymph nodes, and very little from the liver and the spleen. The BCG distributive pattern was in reverse order when BCG was given subcutaneously. Histologic examinations of Peyer's patches indicated enlargement of germinal centers, in which primitive reticular cells proliferated prominently and the macrophages with tingible bodies scattered frequently.
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PMID:Immunotherapeutic trials of murine and guinea-pig solid tumors by oral administration of BCG. 47 Feb 20

The ability of cord factor (trehalose-6, 6'-dimycolate) and a range of shorter carbon chain fatty acid trehalose diesters to suppress growth of an ascitic rat hepatoma has been examined and compared with that of whole, living BCG organisms. Aqueous suspensions of BCG, and cord factor in 0.4% arachis oil:Triton emulsion, injected intraperitoneally, retarded growth of up to 10(5) ascites tumour cells. Trehalose-6, 6'-dibehenate was also tumour-suppressive, but only against lower challenge inocula (10(4) cells). Trehalose-6, 6'-dipalmitate and 6,6'-di-0-2-tetradecyl -3-hydroxyoctadecanoyl alpha, alpha trehalose (designated C76) were virtually ineffective and 6,6' -di-0-2-eicosyl-3-hydroxy-tetracosanoyl alpha, alpha trehalose (designated C100) gave small and variable effects only against low challenge inocula. However, improved responses were seen with light mineral oil in place of arachis oil in the emulsions.
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PMID:Immunotherapy of an ascitic rat hepatoma with cord factor (trehalose-6, 6'-dimycolate) and synthetic analogues. 54 31

Bilateral axillary lymph node metastases occurred after intradermal (id) injection of line 10 hepatocellular carcinoma cells over the thoracic spine of inbred guinea pigs. Excision of the dermal tumor 7 days after injection of tumor cells did not prevent the development of metastases. Injection of BCG into dermal tumors without surgery led to their regression and prevented the growth of microscopic metastases in both right and left superficial distal axillary lymph nodes. Bilateral id injection of BCG between the dermal transplant and each of the regional lymph nodes followed by excision of the dermal tumor also prevented progression of metastases. Unilateral id injection of BCG before excision of dermal tumors failed to retard metastases in contralateral superficial distal axillary lymph nodes. These results suggested that elimination of microscopic lymph node metastases required delivery of adjuvant to or near each metastatic site. Systemic tumor immunity alone may be inadequate to eradicate lymph node metastases.
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PMID:Immunotherapy of bilateral lymph node metastases in guinea pigs by intralesional or paralesional injection of Mycobacterium bovis (BCG). 64 33

Incorporation of 3H-TdR into EL4 leukemic cells in vitro was inhibited by peritoneal exudate cells (PEC) harvested from syngeneic C57BL/6J mice given an intraperitoneal (i.p.) injection of 1x10(7) viable Mycobacterium smegmatis ATCC 607 (Smeg) 4 days before. This phenomenon was also observed in the following five systems of PEC from animals and syngeneic tumor cells: C57BL/6J mice and B16 melanoma; DBA/2 mice and P815 mastocytoma; SWM/Ms mice and K5 fibrosarcoma; BALB/c, nu/nu mice and KKN-1 fibrosarcoma; and strain 2 guinea pigs and line-10 hepatoma. The in vitro cytotoxicity of the PEC activated by viable Smeg was much higher than those activated by dead-Smeg, viable BCG or proteose peptone. The activity of the adherent fraction of the PEC was stronger than that of the nonadherent one, and not influenced by either anti-theta or anti-mouse lymphocyte rabbit sera. The PEC induced with Smeg 4 days before contained a large population of mononuclear cells (88.9%) and a significant level of polymorphonuclear cells (PMN) (3.2%), and showed a much higher cytotoxicity than the PEC induced with Smeg 3 hr before, which contained a much larger population of PMN (71.9%), suggesting that PMN were not the effector cells in this system. In vitro and in vivo treatment with macrophage-inhibitors such as carrageenan, trypan blue and cytochalacin B, reduced the activity of the PEC. All of these facts suggested macrophages as the effector. Viable macrophages were required for the growth inhibition of EL4 in vitro: gamma-ray irradiated or freeze-thawed macrophages were ineffective. Kinetic studies revealed that inhibition of 3H-TdR incorporation into EL4 cells started within 3 hr of incubation together with the activated macrophages at an effector to target (E/T) ratio of 5, and the incorporation decreased gradually with the lapse of incubation time. On the other hand, 51Cr release from labelled EL4 was undetected when the E/T ratio was 5 but detected at on E/T of 10 or more. Even at the higher E/T ratio, at least 10 hr were needed until the release of 51Cr, suggesting that the activated macrophages produced growth inhibition of tumor cells followed by cell destruction.
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PMID:In vitro cytotoxicity of peritoneal macrophages activated with Mycobacterium smegmatis. 66 26

The adjuvant activity of the cell-wall skeletons prepared from eight species (ten strains) of Nocardia was determined by Brunner's method using allogeneic cell-mediated cytotoxicity test. The antitumor activity of the cell-wall skeleton of N. rubra, which showed the most potent adjuvant activity, was examined using EL-4 leukemia and MH-134 hepatoma cells in syngeneic mice. Its results suggest that the cell-wall skeleton of N. rubra is more potent than BCG cell-wall skeleton as the immunotherapeutic agent for cancer immunotherapy in man. The chemical properties of the cell-wall skeleton of N. rubra were also described.
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PMID:Adjuvant and antitumor activities of Nocardia cell-wall skeletons. 79 26


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