bluuebunny/crossref_metadata_2025 huggingface dataset:
Cytostasis of lymphoma cells in suspension: Probable non‐thymic origin of the cytostatic lymphoid cells in mice bearing MSV‐induced tumors
Authors: Senik A. , De Giorgi L. , Gomard E. , Levy J. P.
Published: February 2007

Lymphoid cell suspensions of MSV‐tumor‐bearing mice were studied in the cytostasis assay (CA) against syngeneic lymphoma cells in suspension. Pretreatment by anti‐θ serum and complement, carbonyl iron and a magnet, or filtration through antiimmunoglobulin‐coated glass bead columns shows that macrophages are probably the main effector cells of the cytostatic anti‐tumor effect demonstrated by the CA, which further illustrates the diversity of the anti‐tumor immune response in the MSV system.
Embroynic antigens associated with chemically induced colon carcinomas in rats
Authors: Steele Glenn , Sjögren H. O.
Published: February 2007

Blood lymphocytes of multiparous, pregnant Wistar/Furth rats were cytotoxic to plated cells derived from chemically induced rat colon carcinomas as well as to fetal kidney, fetal liver and fetal colon cells, but not to normal adult rat colon mucosa cells. Blood lymphocytes and lymph‐node cells from rats bearing colon carcinomas induced by two different chemical carcinogens were consistently cytotoxic to fetal colon cells but never cytotoxic to fetal kidney, fetal liver, or normal adult rat colon mucosa cells. Sera from multiparous, pregnant rats always (4/4 experiments) blocked the cytotoxicity of lymphocytes from colon‐carcinoma‐bearing rats against fetal colon target cells, but less frequently (2/4 tests) inhibited the cytotoxicity of these lymphocytes against colon carcinoma target cells. Sera from colon carcinoma bearers blocked the cytotoxicity of lymphocytes from colon tumor bearers on either colon carcinoma or fetal colon target cells. When assayed with colon carcinoma target cells exposed to lymph‐node cells from colon‐tumor‐bearing rats, the blocking activity of sera from multiparous, pregnant rats could be absorbed out by treatment with colon carcinoma and fetal gut cells, but not by polyoma‐virus‐induced sarcoma, normal colon mucosa, fetal kidney, or whole embryo cells. Blocking activity could be recovered from low pH eluates of the colon carcinoma and fetal gut cells. In 2/3 absorption experiments the ability of sera from multiparous, pregnant rats to block cytotoxicity of lymphocytes from colon tumor bearers incubated with fetal colon target cells was abolished by absorption of the sera with colon carcinoma, fetal gut, fetal kidney and whole embryo cells, but not by absorption with polyoma‐virusinduced sarcoma cells or with normal colon mucosa cells. These results indicate that (1) embryonic antigensgare immunogenic in multiparous, pregnant rats; (2) chemically induced colon carcinomas in rats share at least a partial antigenic identity with a wide spectrum of fetal tissues; and (3) a more particular antigenic cross‐reactivity exists between the colon carcinomas and fetal gut, reflecting the presence of fetal organ‐specific antigens.
Friend lymphatic leukemia virus‐induced autoimmune hemolytic anemia with glomerulpnephritis in the rat
Authors: Kuzumaki Noboru , Kodama Takao , Takeichi Noritoshi , Kobayashi Hiroshi
Published: February 2007

WKA/Mk rats injected with Friend lymphatic leukemia virus at birth developed a runt ing syndrome which was associated with a high incidence of hemolytic anemia. The anemia was characterized by the presence of incomplete anti‐erythrocyte autoantibodies detected by the direct antiglobulin test and the indirect enzyme‐augmented hemagglutination assay, and, in some cases, was followed by glomerulonephritis. This system in the rat may represent a new model of autoimmune hemolytic anemia in man.
Immunoprophylaxis and immunotherapy for a murine fibrosarcoma with C. Granulosum and C. Parvum
Authors: Milas Luka , Gutterman Jordan U. , Bašić Ivan , Hunter Nancy , Mavligit Giora M. , Hersh Evan M. , Withers H. Rodney
Published: February 2007

Prophylactic and therapeutic effectiveness of killed C. granulosum and C. parvum bacteria was investigated against a methylcholanthrene‐induced fibrosarcoma in syngeneic C3Hf/Bu mice. Subcutaneous or intravenous treatment of mice with 0.25 mg of these bacteria greatly reduced the number of tumor nodules (metastases, colonies) in the lung generated by 105 or 106 fibrosarcoma cells inoculated intravenously 7 days later. The treatment also prolonged the survival of tumor‐cell recipients, and to some mice afforded complete protection against tumor growth. Number of lung metastases and survival of the recipients were more affected by intravenous than by subcutaneous treatment with the bacteria. Given intravenously to mice 3 days after intravenous inoculation of 2×105 fibrosarcoma cells, these non‐specific immunostimulants significantly reduced the number of pulmonary colonies and prolonged survival of mice. In contrast, subcutaneous application of the bacteria was only slightly effective. Both C. granulosum and C. parvum administered intravenously to mice 3 days following subcutaneous injection of 4×105 fibrosarcoma cells did not affect the development of subcutaneous tumors. However, when the tumors had grown to 25‐17 mm in diameter 67% and 80% of them underwent complete and lasting regressions in mice treated with C. granulosum and C. parvum, respectively. C. granulosum and C. parvum were approximately equally effective against both intravenously and subcutaneously injected tumor cells.
Cytotoxicity with antibody‐glucose oxidase conjugates specific for a human colonic cancer and carcinoembryonic antigen
Authors: Shearer William T. , Turnbaugh Thomas R. , Coleman William E. , Aach Richard D. , Philpott Gordon W. , Parker Charles W.
Published: February 2007

Rabbit or goat antibodies to a human colonic cancer cell line (HT‐29) and to carcinoembryonic antigen (CEA) were studied with respect to their ability to cause complement‐mediated and enzyme‐mediated cytotoxicity. IgG fractions of normal sera and antisera to CEA and HT‐29 were prepared and conjugated to glucose oxidase, an enzyme which permits specific iodination of cell membranes in the presence of glucose, iodide, and lactoperoxidase. Cytotoxicity was evaluated with several established tumor‐cell lines in vitro by measuring the uptake of 125 I‐iododeoxyuridine after 24 h in tissue culture. Specific iodination and cytotoxicity were observed with both enzyme‐antibody conjugates, but the enzyme‐antibody conjugate specific for CEA was much less effective than that for HT‐29. Complement‐mediated cytotoxicity was obtained with both antibodies, but with anti‐CEA antibody effects were obtained only at high antibody concentrations. The attachment of enzyme to antibody produced manifold enhancement of the inherent cytotoxicity of the antibody.
Distinctive properties of thymidine kinase isozymes induced by human and avian herpesviruses
Authors: Kit Saul , Leung Wai‐Choi , Jorgensen George N. , Dubbs Del Rose
Published: February 2007

Biochemical and immunological experiments have been performed to learn whether human and avion herpesvirus‐induced dT kinases could be distinguished from the cytosol and mitochondrial dT kinase isozymes of uninfected cells. The dT kinases induced by human herpes simplex virus types 1 and 2 (HSV‐1 and HSV‐2) and by avian infectious laryngotracheitis virus (ILTV) and herpesvirus of turkeys (HVT) were used. The present experiments extend previous investigations and demonstrate that: (1) human and avian herpesvirus‐induced dT kinases differ from cytosol dT kinases of uninfected cells with respect to electrophoretic mobility, isoelectric point and phosphate donor specificity; (2) human and avian herpesvirus‐induced dT kinases differ from mitochondrial dT kinases of uninfected cells with respect to sedimentation coefficients and sensitivity to dCTP inhibition; and (3) HSV‐1‐ and HSV‐2‐induced dT kinases differ from human cytosol and mitochondrial dT kinases in thermal lability and antigenic determinants. The cellular and the viral‐induced dT kinase isozymes were all inhibited by the end product inhibitor, dTTP. Immunoglobulin (Ig) from sera of rabbits immunized with the HSV‐1‐induced dT kinase inhibited the homologous enzyme and some anti‐type 1 Ig preparations partially inhibited the HSV‐2 dT kinase, but the anti‐type 1 Ig inhibited neither cytosol and mitochondrial dT kinases from human, mouse, and monkey cells, nor the dT kinases induced by ILTV, HVT, or vaccinia virus. Anti‐type 2 Ig inhibited the homologous HSV‐2 dT kinase, but not HSV‐1 or human mitochondrial dT kinase.
The lymphocyte response to primary moloney sarcoma virus tumors: Definition of a non‐specific component of the in vitro cellular hyporeactivity of tumor‐bearing hosts
Authors: Kiessling Rolf , Bataillon Georges , Lamon E. W. , Klein Eva
Published: February 2007

Adult CBA mice injected with Moloney Sarcoma Virus (MSV) developed tumors within 5 to 8 days which usually completely regressed within 1 month. Maximal tumor size was variable, occurring between 10 and 15 days. Lymphocytes from these animals were examined for activity against syngeneic target cells bearing the Moloney Leukemia Virus (MLV) ‐associate dcell‐surface antigen. As previously found with BALB/c mice, the lymphocytes were found to be active in microcytotoxicity tests against these target cells; however, the animals which were bearing tumors at the time of testing were found to have the least active lymphocytes. These animals were also immunized against H‐2d antigens 10 to 13 days prior to testing and their lymphocytes tested for cytotoxicity against H‐2d target cells in 51Cr release assays. It was found that the tumor‐bearing animals, by day 10‐16 after MSV infection, had lymphocytes which were significantly less active against the H‐2d antigens than those of animals tested prior to the development of tumor or those in which the tumors had regressed. It was thus concluded that a component of the cellular hyporeactivity, as measured by in vitro cytotoxicity in these primary MSV tumor bearing hosts, is non‐specific.
Treatment of Kaposi's sarcoma by combination of actinomycin‐D, vincristine and imidazole carboxamide (NSC‐45388): Results of a randomized clinical trial
Authors: Olweny Charles L. M. , Toya Tom , Katongole‐Mbidde Edward , Lwanga Stephen K. , Owor Raphael , Kyalwazi Sebastian , Vogel Charles L.
Published: February 2007

Previous trials at our Institute revealed the effectiveness of actinomycin‐D and vincristine in the treatment of Kaposi's Sarcoma. We herein report the results of a further randomized trial designed to test the efficacy of the three‐drug combination consisting of actinomycin‐D, vincristine and imidazole carboxamide and to compare the results with those obtained by combining actinomycin‐D and vincristine only for all forms of Kaposi's Sarcoma. Of the 40 patients treated with two drugs, 22 (55%) achieved complete tumour regression, 13 (32.5%) had partial response and 5 (12.5%) did not respond. On the other hand, 30 out of 32(94%) of those receiving three drugs had complete tumour regression, one had partial and one had no response. There is a significantly higher complete response rate (p<0.002) in the group receiving three drugs than in that receiving two drugs. The side effects encountered were comparable.
Absence of RSV production in enucleated RSV‐transformed virogenic mammalian cells fused with chick embryo fibroblasts
Authors: Donner L. , Turek L. , Svoboda J.
Published: February 2007

Cells of an RSV‐transformed virogenic Chinese hamster line, RSCH, were enucleated by combining the actions of high g forces and cytochalasin B, and fused with RIF‐free chick embryo fibroblasts using beta‐propiolactone‐inactivated Sendai virus. Contrary to nucleate RSCH cells, enucleated RSCH cells did not produce RSV after fusion. This finding supports the view that proviral RSV DNA is not fully transcribed in a virogenic cell.
Rejection of tumors and metastases in fischer 344 rats following intratumor administration of killed corynebacterium parvum
Authors: Likhite Vilas V.
Published: February 2007

Killed Corynebacterium parvum vaccine was infiltrated into growing subcutaneous tumors (two antigenically different types) syngeneic to the Fischer 344 rats. In all these animals decrease in tumor size was followed by total and lasting disappearance. The protective response conferred as a result of intratumor C. parvum appeared to prevent progressive growth of potentially lethal pulmonary and visceral metastases. Animals which rejected their tumors showed an increased protection that was tumorspecific. Histological examination of tumors from rats exhibiting C. parvum‐mediated rejection revealed an intense non‐specific infiltration consisting mainly of macrophages with some lymphocytes. Of the groups of rats treated with surgical removal of the growing tumor, 30‐60% died with growing tumors and metastases. Suppressed rates of tumor growth and prolonged survival were observed in the group of rats treated with killed C. parvum subcutaneously 1 cm around and away from the growing tumors.
Influence of exogenous interferon on the peripheral white blood cell count in mice
Authors: Degré Miklos
Published: February 2007

The effect of interferon (IF) injected intraperitoneally on the peripheral white blood‐cell (WBC) count in mice was studied. Mouse serum or brain IF produced in vivo in different mouse strains by injecting various viral inducers depressed the lymphocyte count from 3 to 24 h after the injection. The effect was correlated to the antiviral titer of the preparations. The inhibitory factor exhibited physico‐chemical properties of IF. Crude IF preparations obtained from mouse cell cultures, human IF and mock preparations devoid of anti‐viral activity exerted no lymphocytopenic effect.
Cytogenetic studies on human lymphoblastoid cell lines from burkitt's lymphomas and other sources
Authors: Jarvis J. E. , Ball G. , Rickinson A. B. , Epstein M. A.
Published: February 2007

The occurrence and incidence of a characteristic banding abnormality in a No. 14 chromosome has been studied in Burkitt‐lymphoma‐derived and certain other EB virus‐associated lymphoblastoid cell lines. The abnormality was readily detected in 7 out of 7 Burkitt lines, and when present could be seen in 100% of cells with recognizable No. 14 chromosomes. In contrast, the abnormality was not observed in 775 cells from 31 infectious mononucleosis‐derived lines nor in 450 cells from 18 lines obtained from cord blood lymphocytes experimentally transformed by EB virus in vitro. The significance of the abnormality as an indication of cells transformed by the virus in vivo is discussed, and the importance of this considered in relation to a possible oncogenic role for EB virus in man.
Isolation of a primate type‐C virus from a lymphomatous baboon
Authors: Goldberg Robert J. , Scolnick Edward M. , Parks Wade P. , Yakovleva L. A. , Lapin B. A.
Published: February 2007

A type‐C RNA virus has been isolated from various tissues of a lymphomatous baboon (sp. P. hamadryas). Virus isolations were made by co‐cultivating baboon cells from the inguinal and mesenteric lymph nodes, testes, kidneys and spleen with cells of canine or human origin. The isolated virus grew in canine, bat, rhesus and human cells but not in cells of mouse, rat, cat or rabbit origin. The baboon isolate resembled a type‐C virus when infected cells were examined by thin section in the electron microscope. In addition, the virus was capable of providing helper function by rescuing and transmitting the Moloney and Kirsten sarcoma virus genome from non‐productively transformed cells. Antibody directed against the RD114 virus reverse transcriptase was very effective in inhibiting the baboon virus polymerase while anti‐mouse and woolly type‐C virus polymerase antibodies had no significant inhibitory activity. Further analysis by immunodiffusion and competitive radioimmune assay revealed a close immunological relationship between this virus, RD114 and another type‐C virus isolated from the placenta of a different species of baboon. Finally, three different classes of interspecies antigenic determinants have been demonstrated in mammalian type‐C viruses.
Evaluation of epstein‐barr virus‐associated nuclear antigen with various human cell lines
Authors: Suzuki Masahiro , Hinuma Yorio
Published: February 2007

Critical evaluation of the anti‐complement immunofluorescence (ACIF) test for Epstein‐Barr virus‐associated nuclear antigen (EBNA) in known EBV‐associated cell lines was carried out. The ACIF procedure, in which the cell smears were thoroughly air‐dried and fixed with carbon tetrachloride (for 15 min at room temperature), provided reproducible staining results with minimum variations. The fixed smears could be stored for at least 5 weeks at −8° C without loss of reactivity. On the basis of the above evaluation, a total of 59 human cell lines, which had unknown or uncertain association with EBV, were examined for the presence or absence of EBNA by the ACIF procedure. All of the cell lines tested could be judged positive or negative for EBNA. All of 21 lines growing as monolayer or in a mixed state of monolayer and suspension, were negative. Of 38 lines grown in suspension, 36 lymphoblastoid lines were positive but the remaining 2 lines (seemingly not lymphoblastoid) were negative.
Actinomycin‐D‐resistant in vitro mouse cell line derived from a methylcholanthrene‐induced sarcoma: Decrease of malignancy and antigenic characteristics
Authors: Belehradek J. , Biedler J. L. , Thonier M. , Barski G.
Published: February 2007

The tumorigenic EPO clonal cell line, derived from a methylcholanthrene‐induced murine sarcoma, was exposed to increasing concentrations of actinomycin D and gave rise to a subline, resistant to 0.02 μg of actinomycin D per ml of medium, which was designated EPO/ADj. Drug resistance was accompanied by a striking decrease of tumorigenic capacity as determined by the tumor take incidence and tumor growth rate in syngeneic C57BL/6 mice (normal and X‐irradiated), as well as by tumor take incidence in the cheek pouch of cortisone‐treated weanling Syrian hamsters. One of the tumors obtained after inoculation of EPO/ADj cells into syngeneic mice was reexplanted in culture and developed as the EPO/ADj/T subline. It was found to be relatively resistant to actinomycin D as compared to the parental EPO cells. The morphology of cells changed with actinomycin‐D‐resistance: EPO/ADj cells were more spread and flattened and less overlapping than the original fibroblast‐like EPO cells. EPO/ADj/T cells, however, had an aspect similar to that of EPO cells. No major differences were seen between the karyotypes of EPO, EPO/ADj and EPO/ADj/T cells. Tumor‐specific antigen(s), characteristic of the drug‐sensitive, parental EPO line, was expressed in the resistant EPO/ADj and EPO/ADj/T lines, as shown by: (a) transplantation resistance to challenge with EPO cells in syngeneic mice pretreated with EPO/ADj cells; and (b) cross‐reactivity in indirect immunofluorescence tests performed with sera from syngeneic animals hyperimmunized with EPO or EPO/ADj cells. Furthermore, an additional surface antigen (s), absent from EPO cells, was demonstrated in EPO/ADj and EPO/ADj/T cells by means of immunofluorescence tests performed with specific anti‐EPO/ADj syngeneic sera previously absorbed on EPO or EPO/ADj cells.
Genetic control of the regulation of cell susceptibility to carcinogenic polycyclic hydrocarbons by cyclic AMP
Authors: Huberman Eliezer , Yamasaki Hiroshi , Sachs Leo
Published: February 2007

The metabolism of benzo (a) pyrene (BP) in normal golden hamster and BHK cells in culture was increased by treating the cells with dibutyryl cyclic AMP (dcAMP), prostaglandin E1, theohylline or aminophylline. The largest increase, 6‐fold for the normal cells and 20‐fold for the BHK cells, was obtained by treatment with both dcAMP and aminophylline. Treatment with aminophylline also stimulated the metabolism of 20‐methylcholanthrene and 7,12‐dimethylbenz (a) anthracene. The increased metabolism of these three carcinogenic polycyclic hydrocarbons was associated with an increased cytotoxicity. Treatment with aminophylline increased the cytotoxicity of five other potent and weak carcinogenic polycyclic hydrocarbons, but not of two non‐carcinogenic polycyclic hydrocarbons. The amount of BP metabolism in 27 different cell types from various mammals, including humans, ranged from less than 0.1 μg to 2.3 μg metabolized BP per 106 cells. Treatment of these different cell types with aminophylline gave either an increase in BP metabolism, an induction of metabolism in cells that did not metabolize without aminophylline, or no induction after treatment with aminophylline and dcAMP. The existence of responding and non‐responding cell lines indicates that the regulation of the level of polycyclic hydrocarbon metabolism by dcAMP is genetically controlled. The induction of metabolism in cells that did not metabolize without aminophylline resulted in the conversion of cell resistance to cell susceptibility to the cytotoxic effect of BP. Treatment with dcAMP and aminophylline can therefore be used to increase the sensitivity of screening tests for chemical carcinogens.
Properties of reticulum‐cell sarcomas in SJL/J mice. I. Proliferative response to tumor cells of T‐derived lymphoid cells from normal mice
Authors: Lerman Stephen P. , Chapman Judith M. , Carswell Elizabeth A. , Thorbecke G. Jeanette
Published: February 2007

Cells from reticulum‐cell sarcomas (RCS), tumors with a probable B‐cell origin in the SJL/J mouse strain, induced a high degree of proliferation in 6‐bearing syngeneic lymph‐node and thymus cells obtained from young non‐tumorous mice. Although of considerably lower magnitude, a proliferation of SJL/J thymus cells to syngeneic normal lymph‐node cells was also noted. Sera from normal syngeneic mice did not block either of these proliferative responses. Stimulation by RCS cells also occurred with normal lymph‐node cells from F1 hybrids, SJL/J × C57Bl/6, and SJL/J × ASW and from the H‐2S identical ASW mouse strain. It is suggested that these results are due either to the presence of viral antigens on the surface of RCS cells or to an exaggerated form of the normal syngeneic response of T to B lymphocytes. Another tumor of B‐cell origin, the PU5 tumor of BALB/c mice, failed to induce proliferation in normal syngeneic lymph‐node or thymus cells.
Activity of uridine kinase in different lines of AKR leukemic mice and its relation to chemotherapy with 5‐azacytidine
Authors: Veselý J.
Published: February 2007

The sensitivity of different wild‐type and 5‐azacytidine‐resistant lines of AKR leukemic mice to 5‐azacytidine varies in relation to the activity of uridine kinase isolated from corresponding leukemic livers. The enhancement of liver uridine kinase activity observed in leukemic mice following the administration of a single large dose of 5‐azacytidine is accounted for by the presence of hepatocytes in infiltrated leukemic livers. The optimal schedule for the treatment of AKR leukemic mice with 5‐azacytidine requires equally divided doses administered daily and not an initial high dose followed by low doses.
Non‐producer human cells induced by murine sarcoma virus
Authors: Rhim John S. , Cho Han Y. , Huebner Robert J.
Published: February 2007

Non‐producer (NP) human cells were isolated from transformed foci induced by the Kirsten mouse sarcoma virus. These morphologically altered NP cells produced neither infectious virus nor complement‐fixing antigens of the murine sarcoma‐leukemia virus complex. However, the sarcoma virus genome could be rescued from these NF cells by co‐cultivation with cells carrying „helper”︁ Kirsten mouse leukemia virus or Woolly Monkey leukemia virus. The possible usefulness of these cells in efforts designed to detect covert or repressed RNA tumor viruses in various animal and human tissues is discussed.
Epstein‐barr virus‐induced transformation of human leukocytes after cell fractionation
Authors: Schneider Ulrich , Hausen Harald Zur
Published: February 2007

The efficiency of transformation of human lymphocytes after infection with Epstein‐Barr virus (EBV) was determined in fractionated and non‐fractionated preparations derived from 16 human cord blood samples and two blood samples from adult donors. The transformation efficiency of macrophage‐depleted leukocytes was consistently lower as compared to non‐fractionated leukocytes. Additional depletion of B‐cells resulted in a further decrease. Reduction of T‐cells, however, did not influence significantly the transformation rate. In non‐fractionated leukocyte cultures, as well as in macrophage‐depleted and B‐cell enriched cultures, colonies of transformed cells were regularly observed within the first week of cultivation. All cell lines established after EBV‐infection revealed membrane‐bound immunoglobulin. Reconstitution of macrophage‐depleted, B‐cell enriched or B‐cell depleted cultures with autologous macrophages resulted in an increase of the transformation efficiency up to the values of non‐fractionated leukocyte preparations. Addition of heterologous human embryonic lung fibroblasts resulted in a similar increase. The results support the interpretation that EBV transforms only those cells of the hematopoetic system which are derived from the bone‐marrow entity. The transformation efficiency is considerably increased by co‐cultivation of lymphocytes with macrophages and heterologous human fibroblasts which seem to exert a feeder‐layer effect by enhancing survival of lymphocytes in vitro.
Type‐c virus‐specific nucleic acid sequences in cultured rat cells
Authors: Tsuchida Nobuo , Gilden Raymond V. , Hatanaka Masakazu , Freeman Aaron E. , Huebner Robert J.
Published: February 2007

Single‐stranded DNA transcripts of rat type‐C viruses prepared in the presence of actinomycin D, hybridized specifically to DNA of several rat cell cultures with no obvious qualitative or quantitative differences. Similar products prepared from a pseudo‐type sarcoma virus with contributions from rat and mouse type‐C viruses hybridized to both rat and mouse cellular DNA, while mouse viral transcripts did not hybridize to rat cell DNA. Viral RNA was detected in all rat cells by means of the rat viral DNA transcripts, with some differences between untreated low‐passage cells and sister cultures treated with bromodeoxyuridine or bromodeoxyuridine and methylchol‐anthrene. Cells treated with both compounds were previously shown to be transformed and tumorigenic, and these were distinguishable by kinetic analysis from the control cells.
In vitro immunological studies on east african cancer patients. II. Increased sensitivity of blood lymphocytes from untreated burkitt lymphoma patients to inhibition of spontaneous rosette formation
Authors: Gross R. L. , Levin A. G. , Steel C. M. , Singh S. , Brubaker G. , Peers F. G.
Published: February 2007

Frozen aliquots of peripheral blood mononuclear cells from patients with Burkitt's lymphoma (BL) at various stages of the disease have been compared with samples from East African children who were healthy or who suffered from non‐malignant disorders. Using the sheep‐cell rosette test (which is believed to identify T‐lymphocytes), we found a significant reduction in the proportion of rosette‐forming cells (RFC) in the samples from untreated BL patients. After induction of remission the difference between BL patients and controls was abolished. Rosette formation was more readily inhibited by anti‐lymphocyte globulin (ALG) in samples from untreated BL patients than in controls. On induction of remission the rosette inhibition curve shifted towards the control values. The findings are compatible with the presence, in untreated BL, of a circulating factor which impairs the capacity of T‐lymphocytes to form rosettes with sheep erythrocytes. It remains to be established whether the functional capacity of T‐cells to protect the host against tumour proliferation is also impaired.
In vitro immunological studies on east african cancer patients. III. Spontaneous rosette formation by cells from burkitt lymphoma biopsies
Authors: Gross R. L. , Steel C. M. , Levin A. G. , Singh S. , Brubaker G.
Published: February 2007

Spontaneous rosette formation was observed in eight out of nine Burkitt lymphoma biopsies. These were examined fresh and/or after culture in vitro for up to 48 h. The percentage of rosettes varied from 3.7% to 38%. There was a tendency for the percentage of rosettes to increase with time in tissue culture. It is suggested that the rosette‐forming cells are T‐lymphocytes infiltrating the tumour and functioning as a host defence mechanism against the proliferating tumour cells.
Transformation of horse skin cells by type‐c sarcoma viruses
Authors: Rhim Johng S. , Ro H. S. , Kim E. B. , Gilden R. V. , Huebner R. J.
Published: February 2007

A horse skin cell line (E. Derm, NBL‐6, CCL‐57) was susceptible to focus formation by the Kirsten mouse sarcoma virus, feline sarcoma virus (ST strain) and the MSV pseudotypes with woolly monkey, gibbon monkey, RD‐114, AT‐124, baboon placenta and murine xenotropic (BALB/c 3T3 and C57L/JD) type‐C viruses. Foci were detected within 5 days after infection and the transformed cells continued to produce infectious virus and group‐specific antigen of their respective type‐C leukemia viruses. The transformation efficiency of various type‐C sarcoma viruses in horse cells was also very high.
Immunological mechanisms in the pathogenesis of virus‐induced murine leukemia. II. Characterization of autoreactive thymocytes
Authors: Proffitt Max R. , Hirsch Martin S. , McKenzie Ian F. C. , Gheridian Beatriz , Black Paul H.
Published: February 2007

The nature of the reaction and the type of effector cells involved in the reactivity of thymocytes from Moloney murine leukemia virus (MuLV‐M)‐carrier mice against normal syngeneic target cells has been further characterized. The reaction is mediated by viable MuLV‐infected thymocytes. Lysates of carrier thymocytes are not more effective in causing target cell reduction than are lysates of normal thymus cells. Soluble mediators do not appear to be involved in the reaction. The thymocytes mediating the reaction are non‐adherent cells positive for the theta‐C3H and H‐2k alloantigens, but are negative for detectable murine IgG determinants. Their resistance to corticosteroid treatment further identifies them as functionally mature immunocytes.
Tumor‐induced angiogenesis: Lack of inhibition by irradiation
Authors: Auerbach Robert , Arensman Robert , Kubai Louis , Folkman Judah
Published: February 2007

The effect of irradiation of tumors on their ability to induce vascular responses (angiogenesis) was studied. Rat Walker carcino‐sarcoma 256, rabbit V2 carcinoma, mouse (C57Bl) melanoma and mouse (129) teratoma (OTT 6050, 100K) were irradiated with up to 5000R, then grafted either to the chicken chorioallantoic membrane or intracorneally into adult rabbits to assess competence to provoke angiogenesis. For all tumors and both assay systems the results were similar: irradiation did not interfere with tumor‐induced vascular responses.
Changes in the surface membrane of lymphocytes from patients with chronic lymphocytic leukemia and hodgkin's disease
Authors: Mintz Uri , Sachs Leo
Published: February 2007

Lymphocytes were isolated from the peripheral blood of 15 normal persons, 15 patients with chronic lymphocytic leukemia (CLL), 10 patients with Hodgkin's disease and 3 patients with CLL in remission. The cells were studied for cap formation and agglutinability by concanavalin A, and for cell attachment to the surface of a Petri dish. The percentages of lymphocytes with a cap were 25–34% for normal persons, 5–9% for CLL patients whether under treatment or not, 1–3% for untreated patients with Hodgkin's disease and about a normal percentage for CLL in remission. Vinblastine in all cases induced only about a 1.5‐ to 2‐fold increase in the percentage of cells with a cap. Agglutinability by concanavalin A was low for normal persons and high for all the patients including those with CLL in remission. Cell attachment to the Petri dish was low for normal persons and Hodgkin's disease patients, intermediate for CLL in remission and high for patients with CLL. Similar results for normal persons were obtained with peripheral blood lymphocytes that were predominantly T cells and with isolated normal B cells. Compared to lymphocytes from normal persons, lymphocytes from CLL patients were therefore different in cap formation, agglutinability and cell attachment; those from Hodgkin's disease in cap formation and agglutinability; and those from CLL in remission in agglutinability and cell attachment. These results indicate that there are different surface membrane changes in lymphocytes from patients with CLL, Hodgkin's disease and CLL in remission. It is suggested that these membrane changes may be useful as an aid in diagnosis.
Bcg therapy of pleural and peritoneal growth of transplanted rat tumours
Authors: Pimm M. V. , Baldwin R. W.
Published: February 2007

Growth of intrapleurally injected cells of immunogenic methylcholanthrene‐induced rat sarcomas was suppressed by intrapleural injection of viable or 1 × 106 R radiationsterilized BCG vaccine. As little as 10 μg 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.
Oncogenesis by interspecific interaction of malignant murine and non‐malignant hamster cells in vitro
Authors: Goldenberg David M. , Pavia Rose A.
Published: February 2007

A clone of Cloudman S91 murine melanoma 1 was fused in vitro with non‐malignant hamster cheek pouch cells by means of lysolecithin, and the putative hybrid progeny cells, HCP‐MM, were found to be highly malignant in hamsters, but not in appropriate mice. A malignant clone of HCP‐MM cells was shown to have hamster species‐specific surface antigens (as demonstrated by immunofluorescence and the cytotoxic antibody) and hamster‐like lactate dehydrogenase and NAD‐dependent malate dehydrogenase isoenzyme profiles. Nevertheless, chromosomes similar to those of both murine and hamster parental cells could be distinguished in cells of this malignant clone and in hamster tumor grafts by the method of trypsin‐Giemsa banding. A majority of the murine chromosomes, however, appeared to be lost. This study indicates that a murine melanoma previously found untransplantable in hamsters could produce a highly malignant and lethal tumor for hamsters after being mixed in vitro with non‐malignant hamster cells, in the presence of a fusing chemical. It is not as yet certain whether the production of transformed cells in vitro and of highly malignant tumors in the hamster (both with predominantly hamster properties) required heterosynkarion formation between the murine melanoma and hamster cheek pouch cells. Nevertheless, our results suggest that the presence of the murine melanoma, and possibly the interaction of its genome with non‐malignant hamster cells, was implicated in this process.
Cell‐mediated cytotoxicity to human pulmonary neoplasms
Authors: Vose B. M. , Moore M. , Jack G. D.
Published: February 2007

Peripheral blood leukocytes from patients with confirmed pulmonary neoplasia were tested for cytotoxicity against cultured cells derived from lung tumours of various histological types, foetal and normal adult lung tissue and tumours arising in organs other than the lung. Leukocytes from 73% of patients were cytotoxic for lung‐tumour derived cells compared with age‐ and sex‐matched normal donors, while the frequencies of reactivity against normal adult lung‐derived cells and cells from unrelated tumours (e.g. bladder, colon, breast) were 42% and 18% respectively. Leukocytes from lung cancer patients were also cytotoxic for cells derived from foetal lung but susceptibility to cytolysis was variable, cells from 13‐ and 14‐week embryos revealing greatest reactivity (88%). Leukocytes from patients with a variety of tumours of non‐pulmonary origin or with non‐malignant conditions (including respiratory disorders) were also reactive with lung‐tumour‐derived target cells but with a lower overall frequency (35%) than those from lung‐cancer patients. The significance of these cytotoxicity data for the existence of tumour‐specific host immunoreactivity in lung neoplasia is discussed.
Cell‐mediated cytotoxicity to moloney sarcoma in syngeneic and allogeneic rats
Authors: Veit B. C. , Feldman J. D.
Published: February 2007

Cell‐mediated cytotoxicity in the primary immune response to Moloney sarcoma tumor (MST) in allogeneic and syngeneic rats was found to be predominantly T‐cell‐dependent. A minor non‐T‐cell cytotoxic activity may also have been detected. CMC was presumably directed against tumor and viral related antigens in the syngeneic host and primarily against alloantigens in the allogeneic host. CMC was more vigorous in the allogeneic recipient than in the syngeneic host. This may be due to differences in quantities or immunogenicities of the various antigens involved. Two peaks of T‐cells in effector populations were observed during a 20‐day post‐inoculation period. The first peak corresponded to peak T‐cell‐mediated cytotoxicity on day 8 and the second peak occurred on days 13 or 14 when CMC was minimal or undetectable.
Regression of spontaneous mammary tumors in dogs after injection of neuraminidase‐treated tumor cells
Authors: Sedlacek H. H. , Meesmann H. , Seiler F. R.
Published: February 2007

The effect on tumor progression produced by the injection of VCN‐treated tumor cells in dogs with spontaneous mammary tumors was investigated. Untreated dogs of different races and different ages with at least two palpable spontaneous mammary tumors were selected. One of the tumors was left in the animal for further clinical examination whereas the other tumor (s) was (were) excised for preparation of a single‐cell suspension by mechanical disintegration and enzymatic digestion with collagenase and trypsin. (1) In the first group, each animal was injected with 2 × 107 similarly prepared autologous, mitomycin‐treated tumor cells: in 8 out of 12 dogs of this group the tumors progressed while so far 1 dog has died of metastasis. (2) In the second group, each animal received the same number of 2 × 107 tumor cells, which were mitomycin‐ and VCN‐treated: 13 out of 15 dogs had a significant regression of their tumors to less than 10% of the original volume; in 1 dog the tumor remained unchanged and in 1 dog it progressed. (3) In the third group, 8 dogs received 1 × 108 mitomycin‐ and VCN‐treated tumor cells: the application of this cell dose resulted in an accelerated tumor progression in all 8 dogs, 3 of which have already died of metastasis. The significance of these findings, with respect to potentiation and abrogation of the immunological response and with regard to immunotherapy in man, is discussed.
Human, rat and mouse liver‐mediated mutagenicity of vinyl chloride in S. typhimurium strains
Authors: Bartsch H. , Malaveille C. , Montesano R.
Published: February 2007

Exposure of S. typhimurium strains TA 1530, TA 1535 and G‐46 to vinyl chloride increased the number of His+ revertants/plate 16, 12 or 5 times over the spontaneous mutation rate. After 6 h of exposure to vinyl chloride, the mutagenic response for TA 1530 strain was enhanced 7‐, 4‐ or 5‐fold when fortified postmitochondrial liver fractions from humans, rats or mice were added. The enzyme‐mediated vinyl chloride mutagenicity was dependent on an NADPH generating system and the enzyme activity was localized in a liver microsomal fraction; 9,000 × g liver supernatant was three times more active than microsomes, while liver cytosol or alcohol dehydrogenase did not affect the mutagenicity. Phenobarbitone pretreatment of rats and mice increased the mutagenic response by up to 15–40% as compared to untreated controls. The relative mutagenic activities of VCM, taking the value from mouse liver as 100, for TA 1530 strain mediated by 9,000 × g tissue fractions were: rat liver, 80; mouse and rat kidney, 20 and 16; mouse and rat lung, less than 7; human liver (from four biopsy specimens), 170, 64, 70 and 46. Chloroacetaldehyde and chloroacetic acid, a urinary metabolite of VCM, showed toxic effects, while chloroethanol was weakly mutagenic for TA 1530 strain.
Tumor‐specific and forssman antigens of guinea‐pig hepatoma cells: Comparison of tumor cells grown in vivo and in vitro
Authors: Evans Charles H. , Ohanian Sarkis H. , Cooney Adele M.
Published: February 2007

Cloned tumor‐cell lines were derived from two antigenically distinct ascites variants of diethylnitrosamine‐induced guinea‐pig hepatomas (designated line 1 and line 10). Cell‐surface antigens on the ascites and in vitro‐grown tumor cells were analyzed with immunofluorescence, C1 fixation and transfer, and antibody‐complement‐mediated cytotoxicity tests. Tumor‐specific and Forssman antigens continued to be expressed during 3–6 months of in vitro cultivation. Differences between ascites and cultured cells were noted in the degree of antigen expression and sensitivity to antibody‐complement‐mediated cytotoxicity. Cells grown in vitro exhibited a greater number of Forssman and tumor‐specific antigen sites than in vivo grown cells as determined by the quantitative C1 fixation and transfer test. Immunofluorescent staining indicated that some cloned lines were considerably more homogeneous in terms of antigen expression than were the cultured, non‐cloned parent cells or ascites‐grown cells. Cloned lines were frequently more sensitive to the cytotoxic action of antibody and complement than were the in vivo grown and cultured non‐cloned parent tumor cells. Sensitivity to cytotoxicity did not necessarily correlate, however, with the degree of antigen expression. These results suggest that; (1) the expression of Forssman and tumor‐specific antigens does not diminish on cells cultivated in vitro and (2) ascites hepatoma cells in vivo are a heterogeneous population of cells differing in their degree of antigen expression and sensitivity to antibody‐complement‐mediated cytotoxicity.
The detection of the epstein‐barr virus (ebv) nuclear antigen (ebna) by anti‐complement immunofluorescence. Immunoglobulin class of antibodies and role of complement
Authors: Liabeuf A. , Nelson R. A. , Kourilsky F. M.
Published: February 2007

The Epstein‐Barr virus (EBV)‐associated nuclear antigen (EBNA) was detected by anti‐complement immunofluorescence (ACIF) in Raji lymphoblastoid cell line, and the mechanism of the reaction explored, using Ig fractions of anti‐EBNA sera and purified components of complement. Following fractionation of serum from 13 donors, anti‐EBNA antibodies were always found to be associated with IgG, but were also detectable in the IgM fraction of four sera. Sequential addition of functionally pure complement components in the ACIF reaction showed that the classical sequence of complement activation is involved. Anti‐EBNA antibody reactions in Raji cell nuclei can also be detected by anti‐Ig immunofluorescence with a low level of sensitivity. The same pattern of granular fluorescence was observed when C3 (β1A/β1C), or C4 or IgG anti‐EBNA antibodies were revealed with the corresponding fluorescein‐conjugated reagents. Blocking of the ACIF reaction was achieved with Fab'2 anti‐EBNA antibody fragments, which therefore provided an appropriate specificity control for the detection of EBNA.
Immunofluorescence and anti‐complement immunofluorescence absorption tests for quantitation of epstein‐barr virus‐associated antigens
Authors: Reedman Beverley M. , Hilgers J. , Hilgers F. , Klein G.
Published: February 2007

Immunofluorescence absorption methods are described which permit quantitative estimation and differentiation of Epstein‐Barr virus (EBV)‐associated antigens (virus capsid antigen, VCA, early antigen, EA and EBV‐determined nuclear antigen, EBNA) in cell extracts. EBNA was present in all cell lines (producer and non‐producer) which carried the EBV‐genome, while VCA and EA were present in producer lines only. All the antigens were absent from a lymphoid cell line (MOLT‐4) which lacked the EBV‐genome, as well as from leukemia cells from peripheral blood. The techniques demonstrated antigenic identity of the various antigens when prepared from different cell lines.
Leukaemogenesis and regeneration of lymphoid system in (C3H × AKR/tiald)F1 hybrids restored with parental bone marrow and thymic cells
Authors: Legrand E. , Duplan M. C. Kressmannet J. F.
Published: February 2007

Leukaemogenesis and repopulation of the lymphoid system have been studied in sub‐lethally irradiated (C3H × AKR/TIALD) F1 hybrids which have been restored with parental Bone Marrow (BM) cells with or without thymic cells. The metacentric marker of the TIALD sub‐strain made it possible to identify the host or donor origin of leukaemias. Leukaemias occur either in the thymus (lymphosarcomas) or in the other lymphoid tissues (extra‐thymic leukaemias). After irradiation, the percentage of lymphosarcomas increases from 5 to 95%. The rate of leukaemias in hybrids which have been restored only with BM cells is 55, 56 and 100% respectively depending on the origin of BM: syngenic, C3H and AKR. In this last group 75% of the lymphosarcomas originate from donor cells. The inhibitory efficiency of the three kinds of BM on leukaemogenesis seems to be related to their respective abilities to spontaneous malignant transformation. When AKR or C3H thymic cells are injected together with BM cells, leukaemogenesis is altered. The effect is indirect as these cells are not actually concerned by the malignant transformation. The percentage of LS is significantly reduced and the mean survival improved in hybrids restored with C3H thymic, mixed with AKR or C3H BM cells. AKR thymic cells are less efficient. In both cases, the percentage of extra thymic leukaemias increases at the expense of lymphosarcomas. Thymic cells do not change the kinetics of repopulation in thymus and lymph‐node by the BM cells, except when C3H thymic cells are mixed with TIALD BM cells; in this case, the lymph‐node repopulation is temporarily enhanced. Different hypotheses might explain the effect of thymic cells on leukaemogenesis: enhanced recovery of the post‐irradiation immunological deficiency, transfer of virus by the AKR thymic cells, and more probably influence of the thymic cells on the maturation or/and differentiation of the lymphoid cells.
Enhancement by drugs of metastatic lung nodule formation after intravenous tumour cell injection
Authors: Van Putten L. M. , Kram L. K. J. , Van Dierendonck H. H. C. , Smink T. , Füzy M.
Published: February 2007

In studies on a model of induced pulmonary metastasis in mice a tumour host system was analysed which was not affected by immunogenicity of the tumour for the host; neither intensive immunosuppression nor immunization caused a significant change in the quantity of pulmonary metastatic nodules. In contrast the application of cytostatic drugs and of Corynebacterium parvum could modify the pulmonary resistance to the formation of tumour nodules by a factor greater than 100 in either direction. This finding confirms the observation of others that major modification of the resistance to metastatic tumour formation can occur independently of classical immunological mechanisms. Special attention is drawn to the fact that cyclophosphamide enhances the formation of metastatic nodules in this model by factors of 100 to more than 1,000, whereas other cytostatic drugs including the cyclophosphamide congeners iphosphamide and trophosphamide are active only by factors between 2 and 12. The possible practical significance of these findings is discussed.