bluuebunny/crossref_metadata_2025_split huggingface dataset:
Epstein‐Barr virus‐induced membrane antigens: Immunochemical characterization of triton X‐100 solubilized viral membrane antigens from EBV‐superinfected raji cells
Authors: Qualtiere Louis F. , Pearson Gary R. 
Published: February 2007

AbstractIn an attempt to qualitatively identify the membrane antigen (MA) complex induced by Epstein‐Barr virus (EBV) infection of lymphoblastoid cells, superinfected Raji cells were surface labelled with 125I by the lactoperoxidase method and solubilized with Triton X‐100, then the 125(‐labelled membrane proteins were precipitated by sera containing high antibody titers to MA. Analysis of these immune precipitates on sodium dodecyl sulfate polyacrylamide gel electrophoresis identified four major EBV‐specific membrane proteins with molecular weights (mol. wt) of 280,000, 250,000, 170,000 and 90,000. Sera from patients with Burkitt's lymphoma (BL), nasopharyngeal carcinoma (NPC) and infectious mononucleosis (IM) and from EBV‐infected disease‐free individuals showed differential patterns of reactivity to these antigens with some sera only recognizing three or less of the antigens. The results from investigations with these sera also indicated that these major proteins were not related to EBV‐induced viral capsid antigens (VCA) or the virus‐associated early antigen (EA) complexes as defined by immunofluorescence. Metabolic labelling of EBV‐infected Raji cells with [14C]glucosamine, followed by Triton X‐100 solubilization and radioimmune precipitation, identified the 280,000, 250,000 and 90,000 components as glycoproteins. The lactoperoxidase‐labelled 170,000 molecular weight component was not significantly glycosylated and, therefore, could not be categorized as a glycoprotein on the basis of this study. In addition, a glycoprotein with a mol. wt of 130,000 was identified by this approach which also appeared to be specified by EBV. The results from these investigations, therefore, indicated that the EBV‐induced MA complex was composed of four major glycoproteins and one non‐glycosylated high mol. wt protein.
Tumour antigens and alloantigens. I. Relation of a rat tumour‐specific antigen with normal alloantigens of the host strain
Authors: Bowen J. Gareth , Baldwin R. W. 
Published: February 2007

AbstractIt has been shown that tumour‐specific antigen from a chemically‐induced rat hepatoma is capable of binding to immunoadsorbent columns made from the Ig fractions of antisera raised in allogeneic animals against a variety of normal tissues. This reactivity is observed with antisera directed against normal syngeneic liver, spleen and lymph‐node cells but it is not detected in normal sera, F, hybrid sera or an antiserum directed against syngeneic erythrocytes. This phenomenon is specific since soluble extracts of normal syngeneic liver, but not of normal altogeneic liver, are capable of inhibiting the binding of hepatoma‐specific antigen to an immunoadsorbent column of Ig from an allogeneic anti‐normal‐liver antiserum. Syngeneic and allogeneic rats were immunized with immune complexes made from xenogeneic sera, alloantisera or syngeneic immune serum and soluble extracts of normal tissue and affinity‐chromatography‐purified hepatoma‐specific antigen. The resulting sera were examined by means of the membrane immunofluorescence test for reactivity against a panel of syngeneic and allogeneic cells. Xeno‐antisera directed against normal syngeneic tissue precipitated with purified hepatoma antigen and this material generated tumour‐specific antibody following immunization into syngeneic rats. The phenomenon of cross‐reactivity of one chemically‐induced rat hepatoma‐specific antigen with normal syngeneic alloantigens is not a unique phenomenon as preliminary results indicate that two other immunologically distinct hepatomas show similar characteristics.
Tumour antigens and alloantigens. II. Lack of association of rat hepatoma‐D23‐specific antigen with β2 microglobulin
Authors: Bowen J. Gareth , Baldwin R. W. 
Published: February 2007

AbstractIt has previously been shown that the tumourspecific antigen of the chemically‐induced rat hepatoma D23 has determinants recognised by alloantisera raised against normal syngeneic liver and spleen. However, no reactions were observed with alloantisera raised against syngeneic erythrocytes suggesting that the alloantigenic determinant responsible for this cross‐reactivity is not a major serologically‐defined histocompatibility antigen. This concept has been further examined using a defined turkey anti‐rat β2 microglobulin antiserum. This antiserum failed to block the binding of syngeneic antihepatoma D23 sera to hepatoma D23 target cells as assessed using membrane immunofluorescence and complement‐dependant 51Cr release tests. Furthermore, immune precipitates formed from soluble tumour extracts containing hepatoma D23 specific antigen with turkey anti‐rat β2 microglobulin failed to generate a tumour‐specific antibody response in syngeneic rats although a cross‐reactive antiserum was produced following immunization of allogeneic rats with the immune precipitate.
Sites of integration of herpes simplex virus type‐2 thymidine kinase gene in human chromosomes
Authors: Kit Saul , Teitz Yael , Hazen Marion , Qavi Hamida 
Published: February 2007

AbstractIsozyme analyses have been carried out to investigate the sites of integration of the herpes simplex type 2 (HSV‐2) thymidine kinase (TK) gene in biochemically transformed human [HeLa(BU25)/HSV‐2–6 Cl 4] cells. Extracts were prepared from He La (BU25)/HSV‐2–6 Cl 4 cells and from human—mouse somatic cell hybrids, which were obtained by fusing the biochemically transformed human cells with TK‐deficient mouse [LM(TK−)] cells, and were assayed for 26 isozymes representing markers for 20 human chromosomes. The isozyme analyses were generally consistent with previous karyotype studies, which revealed that the HSV‐2 TK gene was associated with an isochromosome, designated M13, formed from the short arm of human X chromosome in human—mouse hybrid lines HL/2 to HL/7, but with human chromosome 17 containing a trans‐location on the short arm in hybrid line HL/1 and its TK‐positive subclones. The isozyme analyses also indicated that the translocation on the short arm of human chromosome 17 in hybrid line HL/1 was probably derived from human chromosome 21. Hybrid line HL/1 and its TK‐positive subclones expressed a human—mouse heteropolymeric form of superoxide dismutase, a marker for human chromosome 21, but bromodeoxyuridine‐resistant, TK‐negative subclones of HL/1, and hybrid lines HL/3 to HL/6, which did not contain the modified chromosome 17, failed to express the human—mouse heteropolymeric form of superoxide dismutase. The human galactokinase isozyme, which is coded by a gene mapping close to the cytosol TK gene on human chromosome 17, was detected in extracts of TK‐positive HeLa S3, TK‐deficient HeLa(BU25), and biochemically transformed HeLa(BU25)/HSV‐2–6 Cl 4 cells, but not in extracts prepared from human—mouse hybrid line HL/1 and its subclones. These observations suggest that the gene for human galactokinase was either deleted or inactivated in HL/1 and its subclones, perhaps as a result of the translocation to chromosome 17.
Milky spots (taches laiteuses) as structures which trap asbestos in mesothelial layers and their significance in the pathogenesis of mesothelial neoplasia
Authors: Kanazawa Kyotaro , Roe Francis J. C. , Yamamoto Tadashi 
Published: February 2007

AbstractThe UICC standard sample of asbestos, crocidolite, was injected subcutaneously into the flanks of CBA/lac mice. Asbestos fibres were found in milky spots in the serosal cavities more than 442 days after the injection, in the form of either naked fibres or asbestos bodies. Milky spots were the only structure in which asbestos fibres were observed in the mesothelial layer. The fact that asbestos fibres were found in the liver, spleen, kidney, brain, etc., in addition to milky spots, suggested that they were transported by the blood stream throughout the body. This assumption was confirmed by the similar distribution of asbestos after intravenous administration. The vascular and cellular structure of milky spots is such that they are particularly likely to trap blood‐borne asbestos fibres. Hyperplastic changes were observed in milky spots after both subcutaneous and intravenous administration of asbestos in mice. The possible involvement of milky spots in the genesis of tumours of the mesothelium following exposure of animals to asbestos is discussed.
Enhancement by asbestos of oncogenesis by moloney murine sarcoma virus in CBA mice
Authors: Kanazawa Kyotaro , Yamamoto Tadashi , Yuasa Yasuhito 
Published: February 2007

AbstractFive μg of finely ground crocidolite asbestos (UICC standard sample) were Injected intraper‐ itoneally into 3‐week‐old CBA mice, together with 105 FFU of Moloney murine sarcoma virus. Altogether 44 out of 61 mice (72.1%) so treated developed palpable intraperitoneal tumours, and half of these died of such tumours within 100 days. The same amount of quartr and carbon similarly administered gave lower tumour incidences, namely, 19.4% (3.2% fatal) and 11.9% (1.5% fatal) respectively. Only 1 out of 59 mice inoculated with the virus alone developed a palpable intraperitoneal tumour, and this regressed spontaneously within 10 days of its first appearance. No tumours were encountered in mice treated with either asbestos, quartz or carbon alone. All the neoplasms had the appearance, under the light microscope, of anaplastic sarcomas. Most of them were confined to the serosal surface of the abdominal cavity, although invasion of underlying tissues was observed in some of the animals that died. Electron microscopical examination of tumours revealed the presence of C‐type particles budding off from cellular surface. Some neoplastic cells showed characteristic features of mesothelial lining cells. The role of milky spots (taches laiteuses) in oncogenesis by asbestos and virus, especially in the induction of mesothelioma, is discussed.
Circulating levels and tissue localization of placental protein five (PP5) in pregnancy and tropho‐blastic disease: Absence of PP5 expression in the malignant trophoblast
Authors: Seppälä M. , Wahlström T. , Bohn H. 
Published: February 2007

AbstractPlacental protein five (PP5) was studied by radio‐immunoassay in 360 serum samples from 334 pregnant women, 96 serum samples from eight patients with trophoblastic disease, and 80 samples from apparently healthy women. PP5 was not found in the serum of healthy controls. It became detectable in maternal serum 8 weeks after the last menstrual period, and the levels progressively increased as pregnancy advanced. The highest levels (mean 26–29 ng/ml) were seen between weeks 37–39 of gestation. PP5 was rarely found in the serum of patients with trophoblastic disease. The first pretreatment samples of two patients with hydatidiform mole had PP5 levels of 0.6 and 2 ng/ml when the concentrations of human chorionic gonadotrophin (hCG) and pregnancy‐specific beta‐1‐glycoprotein (PSBG) were high, whereas the subsequent 17 samples were PP5‐negative. All seven samples from a patient with invasive mole and 70 samples from five patients with choriocarcinoma were PP5‐negative including those with high hCG and PSBG concentrations. Even a patient whose choriocarcinoma followed term pregnancy had no detectable PP5 in the serum. The occurrence of PP5 in tissue was studied by the three‐layer bridge immunoperoxidase method. PP5 was localized in the syncytiotrophoblast between 6 and 42 weeks of gestation, but the cytotrophoblast was PP5‐negative. The staining for PP5 was positive in all hydatidiform moles tested and in one of 10 cases of invasive mole. Choriocarcinomas were constantly PP5‐negative (6 cases). In the light of the biological role of PP5 as trypsin and plasmin inactivator its presence in normal and absence from malignant trophoblast suggests that PP5 may be involved in the regulation of trophoblastic invasiveness. The absence of PP5 expression in malignant trophoblastic disease makes it possible to use the serum PP5 measurement for the differential diagnosis of trophoblastic disease and normal pregnancy: in normal pregnancy the placental proteins PP5, hCG and PSBG are all present in serum 10 weeks after the last menstrual period, whereas in malignant trophoblastic disease hCG and PSBG are expressed in the absence of PP5.
Indirect leukocyte migration assay in patients with malignant melanoma
Authors: Morrison Lindsay J. , Cochran Alistair J. , Mackie Rona M. , Ross Catherine E. , Todd Gaye , Claire  , Garland G. 
Published: February 2007

AbstractLeukocytes from 72 melanoma patients and 75 control donors were examined in a two‐stage (indirect) leukocyte migration assay, using formalin‐fixed melanoma cells (FMC) and control, normal or non‐melanoma tumour cells (FCC) as the source of antigen. Inhibitory supernatants were produced significantly more often by cultures of melanoma leukocytes and FMC than by melanoma leukocytes and FCC or control leukocytes and FMC or FCC. Reactive leukocytes were most frequently derived from stage II patients (65%), followed by stage I patients with tumour present (58%), stage III patients (29%) and stage I patients without detectable tumour (20%). The likelihood that a melanoma patient's leukocytes would react increased progressively with the number of different FMC preparations tested. A similar, though less steep increase in reactivity was seen with control donor leukocytes and different FMC preparations. No significant increase in reaction frequency was seen with melanoma or control leukocytes exposed to increasing numbers of different FCC preparations. Significant discrimination between melanoma patients' and control donors' leukocytes was achieved with FMC from both primary and metastatic tumours. Concordance of positivity or negativity was seen in 60% of concurrent one‐stage and two‐stage leukocyte migration assays.
Reciprocal 8;14 translocation in EBV‐negative B‐cell acute lymphocytic leukemia with burkitt‐type cells
Authors: Mitelman F. , Andersson‐Anvret M. , Brandt L. , Catovsky D. , Klein G. , Manolov G. , Manolova Y. , Mark‐Vendel E. , Nilsson P. G. 
Published: February 2007

AbstractA cytogenetic study, including prophase‐prometaphase chromosome analysis, of a patient with EBV‐genome‐negative acute lymphocytic leukemia of B‐cell type with Burkitt‐type cells is presented. All bone‐marrow mitoses examined had a 14q + marker chromosome which was identified as a reciprocal 8;14 translocation of exactly the same type as in Burkitt's lymphoma.
Cell lines with spontaneous secretion of pregnancy‐associated α2‐globulin
Authors: Lundgren E. , Damber M. G. , Roos G. , von Schoultz B. , Stigbrand T. , Nilsson K. , Alexander J. J. 
Published: February 2007

AbstractPregnancy‐associated α2‐globulin (PA α2G) was quantitated by radioimmunoassay in culture media from 34 exponentially growing human cell lines. Only 8/34 cell lines produced PA α2G. The highest secretion was found in cell lines of histiocytic lymphoma origin while it was low in some carcinoma‐derived lines. The results may support an assumption that PAα2G is a normal cell product of B‐lymphoid, monocytic and epithelial cells but may also simply indicate that ectopic PAα2G production is especially common in tumors derived from such cells. The availability of PAα2G‐producing cell lines should facilitate studies of the immunoregulatory role of this protein.
Enhancement of carcinoembryonic antigen expression by interferon
Authors: Attallah Abdelfattah M. , Needy Charles F. , Noguchi Philip D. , Elisberg Bennett L. 
Published: February 2007

AbstractHuman interferon decreased DNA but not RNA synthesis in a human colon carcinoma cell line, WiDr; in addition, there was a two‐ to three‐fold increase in the expression of a tumor‐associated antigen, carcinoembryonic antigen. In contrast, interferon had no effect on a normal human diploid cell line, WI‐38. Thus, in addition to its anti‐cellular effect against tumor cells, interferon can also modulate tumor antigenicity.
Early detection of the CH1 murine lymphoma by tumor‐associated idiotype in the serum
Authors: Lanier Lewis L. , Babcock George F. , Lynes Michael A. , Haughton Geoffrey 
Published: February 2007

AbstractIn this report, we describe a sensitive C‐dependent2 51Cr release inhibition assay using anti‐idiotype antiserum which allows early detection of the CH1 murine B‐cell lymphoma by the presence of 19S tumor‐associated immunoglobulin in the serum. The assay is based on the finding that sera from mice bearing the CH1 lymphoma specifically inhibit C‐dependent 51Cr release from labelled CH1 cells in the presence of A‐Id serum. Groups of mice were injected ip with 102, 103, or 104 CH1 cells and serum samples were collected every other day until host death. Tumor‐specific idiotype was detectable as early as 8 days after a 104 CH1 tumor cell challenge and by 12–14 days in mice inoculated with 103 or 102 CH1 cells. The amount of idiotype increased in parallel with tumor burden and reached a peak titer just before host death In all cases, tumor‐associated idiotype was present in the serum time significantly prior to observation of a visible tumor mass (ca. day 20–28). In subsequent experiments, mice were inoculated with 104 CH1 cells and treated 16 days later with a single dose of melphalan (10 mg/kg), vincristine sulfate (0.75 mg/kg), or cyclophosphamide (100 mg/kg). Serum samples were taken from these animals and the level of serum idiotype was monitored. After M or VS drug therapy, the level of idiotype decreased in all mice, however host survival was not significantly prolonged. By contrast, mice treated with Cy survived significantly longer than untreated controls, and the serum idiotype titer in these mice decreased to undetectable levels from day 20–28. By day 37, idiotype was detectable again in the serum and all mice died of ascites tumor by day 44. The results of these experiments suggest that the presence of idiotype in the serum of a lymphoma‐bearing host may provide a marker which will allow early detection of tumor growth during periods of tumor remission induced by conventional chemotherapy.
Revertants of adenovirus type‐12‐transformed hamster cells have lost part of the viral genomes
Authors: Groneberg J. , Doerfler W. 
Published: February 2007

AbstractThe cell line T637 was derived from BHK21 cells (subline B3) by transformation with adenovirus type 12. The T637 cells contain multiple copies of the viral DNA, with different parts of the viral genomes being represented in unequal amounts. The persisting viral DNA has been shown in previous work to be covalently linked to cellular DNA. In the present report, the isolation and characterization of 18 morphological revertants of the T637 line are described. The T637 cells are round and epithelioid, the revertants are fibroblasts. The revertants arose spontaneously and could be enriched by letting the T637 culture grow to very high density; the T637 cells detached from the plastic surface, whereas the revertants stayed attached and could then be cloned. The morphological revertants of T637 cells differed from both the B3 and the T637 lines in a number of biological properties, such as saturation density, growth rate, agglutinability by plant lectins and uptake of low‐molecular‐weight compounds. The revertants were all T‐antigen negative, but reacted with anti‐LETS serum (antiserum against the large external transformation‐sensitive protein). The B3 and T637 cells were LETS‐negative. The revertants exhibited a pseudodiploid karyotype. All of the 18 revertants could be transplanted into 4‐week‐old Syrian hamsters, although most of the revertants grew less rapidly than the B3 cells. The patterns of integration of adenovirus type‐12 DNA were investigated using the DNA‐DNA hybridization technique of Southern. Some of the revertant lines (TR3, TR7, TR16, and F10) appeared to have lost almost all viral DNA sequences; the other revertant lines lacked several of the viral DNA sequences present in the T637 line. Upon superinfection of the T637 line and all of the revertants with adenovirus type 2 (Ad2), Ad2 replication was inhibited in T637 cells. In the revertants, however, Ad2 grew as efficiently or even more so than in the B3 line.
Growth of diploid, epstein‐barr virus‐carrying human lymphoblastoid cell lines heterotransplanted into nude mice under immunologically privileged conditions
Authors: Giovanella Beppino , Nilsson Kenneth , Zech Lore , Yim Ock , Klein George , Stehlin John S. 
Published: February 2007

AbstractHuman Epstein‐Barr virus‐carrying lymphoid cell lines which have been classified on the basis of studies on clonality and morphological, chromosomal and functional parameters as lymphoblastoid cell lines (LCL) of presumed non‐neoplastic origin were inoculated intracerebrally into nude mice. All eighteen of them grew, killing the host mice within 7 to 25 days, except for 2 which grew more slowly. At autopsy, the brain of the nudes was found to be invaded by infiltrating lymphomas. Sixteen of these lymphomas, when recultured in vitro, gave rise to cell lines with growth properties and morphology indistinguishable from those of the inoculated LCL. Chromosomal examinations showed that 3/7 cell lines injected, which grew as lymphomas in the brain, were still normal diploid on reexplantation whereas the remaining four had become aneuploid. Four lines derived from intracerebral lymphomas (2 diploid, 1 aneuploid and 1 untested) were inoculated subcutaneously into adult nude mice. None of them grew. When the corresponding four original LCL lines were inoculated subcutaneously into newborn nude mice, they grew rapidly, but failed to do so in newborn normal mice or intracerebrally in adult normal mice. One such line, U‐1450, was inoculated subcutaneously into adult nude mice treated with anti‐lymphocyte serum (ALS). Small nodules developed at the site of inoculation. From one nodule a cell line was cultured, 1450 ALSAD. It was morphologically indistinguishable from the line of origin. The lines obtained from nude mice inoculated with polyclonal LCL seem to have a restricted clonal representation, but were not monoclonal, as evidenced by analyses of their pattern of immunoglobulin synthesis.
Establishment, characterization and virus expression of cell lines derived from radiation‐ and virus‐induced lymphomas of C57BL/Ka mice
Authors: Lieberman Miriam , Decléve Alain , Ricciardi‐Castagnoli Paola , Boniver Jacques , Finn Olivera J. , Kaplan Henry S. 
Published: February 2007

AbstractPermanent cell lines have been established in vitro from lymphoid tumors induced in C57BL/Ka mice by fractionated X‐irradiation or by inoculation of the radiation leukemia virus (RadLV). The cultured cells are lymphoblastic, replicate rapidly in vitro, and are tumorigenic in vivo. The cell surface markers Thy 1, Ly 1, Ly 2,3 and Gix are expressed by the lymphoid tumor cells in the mouse and persist in the corresponding cell lines; expression of the H‐2 and TL antigens is greatly reduced during in vitro passage, but is restored on in vivo transplantation. The cell lines derived from RadLV‐induced tumors (BL/VL lines) produce a virus population (RadLV/LTC) with the thymotropic and leukemogenic attributes of RadLV. Those derived from radiation‐induced, virus‐negative lymphomas (BL/RL lines) are initially devoid of MuLV expression, but frequently become spontaneous virus producers during in vitro cultivation.