bluuebunny/crossref_metadata_2025_split huggingface dataset:
Cancer cell traffic from the lungs to the liver: An example of metastatic inefficiency
Authors: Weiss Leonard 
Published: February 2007

AbstractIt is probable that metastasis is an inefficient process in terms of cancer cells. One cause of this inefficiency may be that cancer cells temporarily arrested in one organ are «processed» by it, so that they die before or shortly after arrival in another organ. In the present experiments, the lung‐to‐liver traffic of [125I]dUrd‐labelled W‐256 cancer cells is examined over the course of 27 h in tumor‐bearing and non‐tumor‐bearing rats, following injection into, and sampling from, various points in the cardiovascular system. Following tail‐vein injections, W‐256 are temporarily arrested in the lungs and slowly released; some of the released cells are then temporarily arrested in the liver. Two percent of the cells detected in the lungs are non‐viable compared with approximately half of those in the liver; these measurements of viability correlate with a higher (10:I) incidence of lung transplants over liver transplants, and with the observation that extrapulmonary metastases are uncommon with this tumor. Direct injections of cancer cells into the liver indicate that the reduced viability of cancer cells at this site is not due to an inherently hostile hepatic environment. Injections into and sampling from, other sites indicate that only small proportions of cells were killed on their way to the lungs, during their arrest in the pulmonary capillaries and arterioles, or between the left ventricle, aorta, hepatic artery and liver. Pretreatment of W‐256 cells with neuraminidase, which is expected to make them more deformable, did not affect the viability of cells in the liver, thereby arguing against «processing» occurring during transit in the pulmonary circulation distal to the initial arrest sites. By a process of elimination it is concluded that a significant amount of trauma resulting in cancer cell death occurs during the events culminating in their release from temporary arrest sites at the pulmonary vascular endothelium. As the lungs are commonly the first organ encountered by circulating tumor cells, it is suggested that the low viability of cells released from the lungs contributes to metatastic inefficiency.
Natural killer cell activity associated with reticulum cell neoplasms
Authors: Chang Kenneth S. S. , Log T. 
Published: February 2007

AbstractA marked increase in natural killer (NK) activity is observed with lymphoid cells prepared from SJL/J mouse spleen and lymph nodes, in which a transplantable reticulum‐cell neoplasm (RCN) is growing. The killer cells are non‐adherent, non‐phagocytic, relatively resistant to X‐ray, and scarcely or only partially inactivated by treatment with anti‐Thy 1.2 serum and complement. The killer activity is directed against a wide variety of tumor target cells, not requiring homology in histocompatibility, but is selective and not indiscriminate. Kinetics of in vivo development on NK activity, competitive inhibition of in vitro cytotoxicity by target cells and their membrane extracts are described. The NK activity appears to increase in parallel with the infiltration and growth of RCN in these organs. No such augmented NK activity was observed with other types of tumors that grew in these organs of SJL/J mice. (C57BL/6 × SJL/J)F1 mice pretreated with silica to abrogate Hh restriction and subsequently injected with RCN of SJL/J (H‐2s) origin supported the growth of transplanted RCN. The high NK activity associated with this RCN was markedly reduced by in vitro treatment with anti‐H‐2b serum plus complement, indicating the host origin of NK cells. However, the close association of RCN growth with elevated NK activity may indicate a special function of RCN in promoting NK activity by an unknown mechanism(s) of cellular interactions.
Differential inhibition of epstein‐barr virus induction by the amino acid analogue, L‐canavanine
Authors: Yamamoto Naoki , Mueller‐Lantzsch Nikolaus , Hausen Harald Zur 
Published: February 2007

AbstractThe effect of an amino acid analogue, L‐canavanine, on the synthesis of Epstein‐Barr virus (EBV) antigens was investigated in lymphoblastoid cells. The analysis revealed that after infection of BJAB and NC‐37 cells with P3HR‐I EBV synthesis of early antigen (EA) was not affected by canavanine in concentrations up to 8.4 mM. The synthesis of EBV‐determined nuclear antigen (EBNA) and of viral capsid antigen (VCA) was significantly inhibited at concentrations higher than 2.8 mM. Spontaneous induction of EA in P3HR‐I cells was not affected by canavanine. On the other hand, EA induction by the tumor promoter TPA, by iododeoxyuridine (IdUrd), by antiserum to human IgM and by n‐butyric acid was clearly inhibited by this treatment. Application of 0.3 mM canavanine resulted in more than 95% inhibition of EA induction by TPA. Under these conditions cell growth and incorporation of radiolabelled amino acids into an acid‐insoluble fraction was significantly impaired. Differential treatment of the cells with canavanine established that EA induction was completely suppressed when the cells were treated concomitantly with canavanine and TPA. Subsequent treatment with canavanine after prior exposure to TPA resulted in some viral antigen induction depending on the time period of TPA exposure. Pretreatment of the cells overnight with canavanine followed by washing and addition of the tumor promoter did not suppress EA induction by TPA. These data support the concept that EA induction by superinfection follows a different pathway from antigen induction by chemical inducers.
Humoral immune response in glioma patients: A solubilized glioma‐associated membrane antigen as a tool for detecting circulating antibodies
Authors: Birkmayer Georg D. , Stass H.‐P. 
Published: February 2007

AbstractPlasma membranes from normal and neoplastic human brain tissue were isolated and compared morphologically, biochemically and immunologically. Their ultrastructure was identical, electrophoresis on polyacrylamide gel revealed at least 24 protein components, four of which were absent from membranes of normal tissue, whereas one was missing in the tumor pattern. The tumor‐associated components could be solubilized by the non‐ionic detergent Triton‐X100 and were used as an antigen source for the immunological characterization of glioma membranes. By means of a rabbit antiserum immunologically identical components could be detected in the Triton extract of the membranes from all the 20 human gliomas tested so far, but not in normal or fetal brain, nor in liver, kidney or spleen tissue. These data indicate that the solubilized membrane components contain common glioma‐associated membrane antigens which might be used in the detection of circulating antibodies in the sera of glioma patients. Of the 24 samples of sera tested so far, 19 (79%) contained precipitating antibodies against these membrane components as revealed by countercurrent electrophoresis.
Differential expression of trophoblast‐specific membrane antigens by normal and abnormal human placentae and by neoplasms of trophoblastic and non‐trophoblastic origin
Authors: Loke Y. W. , Whyte A. , Davies S. P. 
Published: February 2007

AbstractUsing a specific antiserum to human syncytial trophoblast plasma membrane (TrPM), we have investigated the expression of these antigens on a variety of trophoblastic and non‐trophoblastic tissues by a standard peroxidase/anti‐peroxidase staining method. Normal placenta (first‐trimester as well as full‐term), placenta from tubal pregnancy and placenta accreta were all found to express TrPM antigens. However, malignant change in trophoblast neoplasms appeared to be accompanied by a loss of these antigens, with 7 out of 10 specimens of hydatidiform mole staining positively while 3 specimens of invasive mole and 7 specimens of choriocarcinoma were all negative. In contrast, a number of malignant tumours of non‐trophoblastic origin such as carcinomas of the colon, cervix, bladder and hepatomas were found to express TrPM antigens. The possible significance of the reversal to a trophoblast phenotype by malignant neoplasms of non‐trophoblastic origin is discussed.
Humoral immune responses to human lymphoma cell heterotransplants in the central nervous system of athymic, nude mice
Authors: Adelman Daniel C. , Miller Richard A. , Kaplan Henry S. 
Published: February 2007

AbstractHuman malignant lymphoma cells may be readily heterotransplanted into the brains of athymic nude mice. We have examined humoral immune responses to these lymphoma cells and have found a primary cytotoxic IgM and a late cytotoxic IgG response. Nude mice with tumors growing intracerebrally were injected intravenously with fractionated IgM or IgG anti‐lymphoma cell antibody obtained from heterozygous immunocompetent animals. Frozen brain sections from these mice stained with fluoresceinated antibodies to mouse IgG and IgM revealed the presence of IgG but no IgM. Thus, IgM could not cross the blood‐brain barrier to react with the heterotransplanted lymphoma cells. It is proposed that xenogeneic tumor cells grow readily within the brains of nude mice because these cells are protected from a primary host cytotoxic IgM response by the blood‐brain barrier. The blood‐brain barrier renders the brain an immune sanctuary within which the impaired cell‐mediated immune responses of nude mice are further compromised by the exclusion of a major component of the humoral immune response.
In vivo natural reactivity of mice against tumor cells
Authors: Riccardi C. , Santoni A. , Barlozzari T. , Puccetti P. , Herberman R. B. 
Published: February 2007

AbstractA rapid in vivo clearance of tumor cells was found in normal mice following intravenous inoculation of [125l]dUrd‐labelled YAC‐1 and RBL‐5 cultured cell lines derived from lymphomas. The ability of mice to eliminate tumor cells from spleen, liver and lungs during the first 4 h, as evaluated by the recovery of radioactivity in these organs, was found to correlate with the level of natural killer (NK) cell reactivity in their spleen and lungs, as measured simultaneously in vitro in a shortterm 51Cr release assay (CRA). Lower recovery of radioactivity was found in mouse strains with high spontaneous levels of NK activity. The degree of clearance was also found to be age‐dependent and older mice of several strains, whose NK activity had declined to low levels, were less effective in eliminating tumor cells. In vivo treatment with interferon and interferon inducers (poly I:C, pyran copolymer, Corynebacterium parvum, murine sarcoma virus) increased the levels of NK activity in the spleen and lungs and also augmented the in vivo clearance of tumor cells from the lungs and liver. Immunopharmacological treatments with antimacrophage agents (silica, iota‐carrageenan, Seakem‐carrageenan), antineoplastic drugs (dexamethasone, cyclophosphamide, 5‐(3,‐3′dimethyl‐I‐triazeno)‐imidazole‐4‐carboxamide, 4‐amino‐L‐D‐arabinofuranosyl‐2‐(IH)‐pyrimidone, adriamycin) or irradiation (850 R γ‐ray) had comparable effects on both in vitro cytolytic activity and in vivo clearance of tumor cells. When the susceptibility to in vitro and in vivocytotoxicity by several other tumors was examined, the lines with detectable sensitivity to lysis by NK cells were found to be cleared in vivo to a greater degree in a high NK strain (CBA) than in a low NK strain (SJL). In contrast, NK‐resistant lines were cleared at approximately the same rate in both strains. However, the actual levels of in vivo clearance and the degree of difference between the strains for the various NK‐sensitive lines did not correlate well with their relative sensitivities to lysis in vitro. In the various situations in which the in vivo recovery of a particular NK‐sensitive line was studied relative to the levels of NK reactivity in the recipients, the best correlations were seen with clearance from the lungs. In several instances, clearance from the spleen did not correlate well with splenic NK activity. These data indicate that rapid in vivo clearance of radiolabelled NK‐sensitive tumor cell lines is appreciably influenced by levels of NK reactivity, but that other factors are probably also involved.
Effector and enhancing lymphoid cells in plasmacytoma‐bearing mice. I. Methodological studies on the winn assay
Authors: Wang K. C. , Berczi I. , Sehon A. H. 
Published: February 2007

AbstractSome parameters of the Winn assay for the detection of tumor‐suppressing (“effector”) and tumor‐enhancing lymphoid cells were studied in BALB/c mice. Spleen cells of mice that were preimmunized with mitomycin‐C‐treated MOPC‐104E plasmacytoma cells were inhibitory in this test system for both the MOPC‐104E and the HOPC‐1 plasmacytomas, thus indicating cross‐reactivity. Spleen cells taken from mice 6 days after the surgical removal of 15‐day‐old MOPC‐104E tumors inhibited the growth of lethal doses of MOPC‐104E cells in normal recipients, but no inhibition was observed 2 days after the removal of 18‐day‐old tumors. Spleen cells from mice bearing MOPC‐104E for 13 days enhanced tumor growth. This enhancement was not influenced significantly by the wide dose range (from 105 to 3 × 107) of MOPC‐104E cells used to initiate tumors in the lymphoid cell donors, although a tendency for stronger enhancing potential occurred after low tumor doses. When spleen cells from donors bearing MOPC‐104E for 10 days were injected at the constant tumor‐lymphocyte ratio of 1:30 with increasing numbers of tumor cells (from 5 × 105 to 2 × 106), tumor inhibition occurred at the lowest dose only, while no significant effect was observed at higher tumor cell doses. When a constant dose (5 × 105) of tumor cells was injected with spleen cells from 10‐day tumor‐bearers at tumor/lymphocyte ratios of 1:10, 1:40 and 1:160, a significant tumor inhibition occurred only at the ratio of 1:40. The relevance of the Winn test to the study of immune mechanisms in tumor‐bearing hosts is discussed.
Effector and enhancing lymphoid cells in plasmacytoma‐bearing mice. II. Dynamic changes during tumor progression
Authors: Wang K. C. , Berczi I. , Hoffmann E. G. , Sehon A. H. 
Published: February 2007

AbstractThe Winn assay was used for the study of effector (tumor‐inhibiting) and enhancing (tumor‐promoting) lymphoid cells in BALB/c mice bearing MOPC‐104E plasmacytomas. Kinetic studies with thymus, lymphnode, spleen and bone‐marrow cells revealed that spleen, lymph node and to a lesser extent bone‐marrow cells from 7‐ and 10‐day tumor‐bearers inhibited MOPC‐104E growth, while at day 13 all three cell populations enhanced tumor growth. However, at day 16 strong tumor inhibition was observed again by spleen cells and to a lesser extent by lymph‐node cells and thymocytes. Peritoneal cells from normal and tumor‐bearing (7 and 10 days) animals enhanced tumor growth significantly. Separation of spleen cells on nylon wool columns showed that at 10 days the effector cells were T lymphocytes, but at a later stage (35 days) a different effector mechanism was present in the spleen. Treatment of MOPC‐104E recipients with carrageenan or silica had little influence on tumor growth, but marked tumor inhibition occurred after lethal irradiation and bone‐marrow reconstitution. This latter observation, together with the finding that bone‐marrow, lymph node and peritoneal cells from normal donors enhanced tumor growth inseveral experiments, suggests that this plasmacytoma, like hormone‐dependent tumors, requires lymphocyte‐derived growth factors.
Spontaneous immune response of bovine leukemia‐virusinfected cattle against five different viral proteins
Authors: Deshayes Laurence , Levy Daniel , Parodi André L. , Levy Jean‐Paul 
Published: February 2007

AbstractThe sera from cattle exposed to bovine leukemia virus (BLV) have been studied by the radioimmunoprecipitation assay (RIPA) of disrupted virus proteins. All sera of animals with the adult form of lymphosarcoma precipitated four different viral proteins: gp51, gp35, p24 and p12. In contrast, the sera of five animals with the juvenile or thymic forms of bovine lymphosarcoma were completely devoid of precipitating activity against BLV proteins, confirming the absence of relationship between these rare malignant diseases and BLV infection. The sera of non‐leukemic cattle from areas of high risk of exposure to BLV were either negative or positive to a lower degree than the sera of lymphosarcomatous cows. When positive they precipitated gp51, p24 and p12. Only one serum precipitated gp35. The difference was probably quantitative, the sera of leukemic animals having higher levels of precipitating activity against all the viral proteins. The anti‐gp51 reactivity was in most cases the strongest, whatever the origin of the serum. In the rare sera which were positive in the classical antigp51 radioimmunoassay (RIA) but negative in the antip24 RIA, an anti‐p24 activity was, however, detected by the RIPA. These results suggest that BLV‐infected cows regularly produce antibodies reacting with four different viral proteins including minor viral components. In three cases with no other special features a low level of activity was detected against a fifth component: p15. There was no apparent correlation, however, between the antibody response and an hypothetical protection against BLV‐induced disease.
Human cell line (COLO 357) of metastatic pancreatic adenocarcinoma
Authors: Morgan R. T. , Woods L. K. , Moore G. E. , Quinn L. A. , McGavran L. , Gordon S. G. 
Published: February 2007

AbstractA continuous human cell line, COLO 357, with exceptional characteristics was derived from a metastasis of a pancreatic adenocarcinoma. COLO 357 grew as an adhering monolayer with a cell doubling time of 21 h and grew with 10% clonal efficiency in soft agar. COLO 357 cells had numerous lamellar inclusions. The cells elaborated the pancreatic enzymes trypsin, elastase and chymotrypsin. COLO 357 also secreted appreciable amounts of carcinoembryonic antigen and human chorionic gonadotropin. COLO 357 had a chromosome mode of 53 with 20 identifiable Giemsa‐banded marker chromosomes. Nine nucleolar organizing regions were found by silver‐stained metaphase preparations. COLO 357 has been “fingerprinted” for seven allelic isozymes. This cell line has been maintained in active culture for over 2 years, is preserved in a cell bank, and is available to other investigators.
Distribution and characterization of alpha hCG in the serum and tumor cytosol of patients with breast cancer
Authors: Shindelman Jeffrey E. , Ortmeyer Ann E. , Wada H. Garrett , Stockdale Frank , Sussman Howard H. 
Published: February 2007

AbstractSerum and tumor tissue from breast cancer patients were evaluated for the presence of alpha subunit of hCG, by means of the specific radioimmunoassay. Elevated serum levels occurred in 0/50 (0%) of normal female controls, 1/17 (6%) of patients with benign breast disease, 3/53 (6%) of patients with primary breast cancer, and 12/84 (14%) of patients with metastatic breast cancer. Cytosols from 10/56 (18%) primary tumors and 10/37 (28%) metastatic tumors were found to contain the alpha subunit. Comparison of serum and tumor cytosol levels in nine patients with metastatic disease showed a correspondence between elevated cytosol levels and elevated serum levels. No similar correspondence in 25 patients with primary disease was observed. Alpha subunit was isolated from one tumor cytosol and was characterized with respect to its immunochemical cross‐reactivity and molecular weight as compared with native alpha subunit from hCG. For both parameters, the native and ectopic alpha subunit were found to be identical.
Multiple antigenic specificities within primary 3‐methylcholanthrene‐induced rat sarcomas and metastases
Authors: Pimm M. V. , Embleton M. J. , Baldwin R. W. 
Published: February 2007

AbstractSarcomas were induced in WAB/Not rats by subcutaneous injection of 10, 5 or 1 mg 3‐methylcholanthrene (MCA) but not by 0.1 mg. Although tumours appeared earlier in rats given 10 mg MCA, compared with 1 mg, the majority of transplant lines from primary tumours were immunogenic and there was no correlation between the inducing dose of carcinogen and the growth characteristics or immunogenicities of the transplant lines. Most importantly sublines established from opposite poles of primary sarcomas were antigenically distinct in a substantial portion of cases, indicating that the primary tumours consisted of antigenically heterogeneous populations of cells. Furthermore, with one rat, renal and pulmonary metastases were antigenically distinct from a peritoneal secondary and the primary growth. These findings indicate that primary carcinogen‐induced tumours may be polyclonal in origin and this has implications for both the understanding of the carcinogenic process, and for the immunotherapy of malignant disease.
Inhibition of effector cell functions in natural killer cell activity (NK) and antibody‐dependent cellular cytotoxicity (ADCC) in mice by normal and cancer sera
Authors: Nair P. N. M. , Fernandes G. , Onoé K. , Day N. K. , Good R. A. 
Published: February 2007

AbstractEffector cells mediating natural killer (NK) cell activity and antibody‐dependent cellular cytotoxicity (ADCC) have been receiving considerable interest recently as they may represent an additional cellular defense mechanism against maglinancy. Spleen cells from normal young C3H (MTV+) female mice were found to have relatively high natural killer (NK) activities toward RL 1 and YAC‐1 tumor cell lines and high antibody‐dependent cell‐mediated cytotoxicity (ADCC) activities toward chicken RBC and SB tumor targets. Serum inhibition of NK and ADCC activities was either not demonstrable or only seen at low levels in the young mice. Following injection of a transplantable mammary adenocarcinoma that grew progressively in these mice, both NK and ADCC activities decreased and serummediated inhibition of both NK and ADCC increased as the tumors grew. NK and ADCC activities declined with age in C3H (MTV+) mice, and the serum inhibition of NK and ADCC activities of young mice increased with age. Aging mice, however, which had developed spontaneous mammary adenocarcinoma, although having increased levels of inhibitor against both NK and ADCC activities and decreased NK and ADCC activities of their spleen cells as compared to young normal mice, did not have different levels from those of aging mice which had not developed the mammary tumor. Correlation was poor between the amount of serum inhibitor(s) on NK and ADCC activities. NK versus RL 1 and ADCC for chicken RBC were not correlated, but NK versus YAC‐1 and ADCC for the tumor cell line SB appeared to be correlated. Decreasing NK and ADCC and increasing serum inhibitory activity toward these functions appeared to correlate with tumor progression. Sera from transplantable tumor‐bearing young C3H mice contained increased amounts of circulating immune complexes, but the amount of circulating immune complexes was only weakly correlated with the serum inhibition of NK activity of spleen cells from young animals by sera from tumor‐bearing young mice. These findings indicate that a serum blocking factor(s) that can inhibit natural cell‐mediated cytotoxicity or antibody‐mediated cytotoxicity in vitro must be considered in analyzing host resistance to tumor growth.
Liver and kidney tumors induced by N‐nitroso‐dimethylamine in Xenopus borealis (Parker)
Authors: Khudoley V. V. , Picard J. J. 
Published: February 2007

AbstractN‐nitroso‐dimethylamine dissolved in aquarium water at a concentration of 400 ppm (1/4 of the LD 50/30d) induced malignant tumors in 39 (54.2%) out of 72 young adult animals of the amphibian species Xenopus borealis. The first tumor was detected at 11 weeks, and the average latency was 35.1 weeks. Tumors were located in the liver (32 cholangiocarcinomas and 13 hepatocellular cancers) and the kidney (9 adenocarcinomas and 2 anaplastic cancers). Thirteen animals bore two or more types of tumors. These results demonstrate that a high percentage of tumors can be induced in amphibians by chemical carcinogens if appropriate methods are used.