bluuebunny/crossref_metadata_2025_split huggingface dataset:
Farming and mortality from non‐Hodgkin's lymphoma: A case‐control study
Authors: Cantor Kenneth P. 
Published: February 2007

AbstractA case‐control study of non‐Hodgkin's lymphoma (NHL) and its subtypes among males was conducted using computerized mortality listings from the State of Wisconsin for the years 1968‐1976. Age, year of death, race, county of usual residence, marital status, and usual occupation were abstracted for the 774 records of male deaths due to NHL and a matched series of deaths due to other causes. The frequency of farming occupation among NHL cases was compared to the frequency among controls, and odds ratios (OR) were calculated. Farming was more common among cases than among controls (OR=1.22). The association of NHL with farming occupation was greater among decedents under 65 years of age (ORequlas;1.7) than among those who were older. The younger decedents were at higher risk of reticulum‐cell sarcoma (ORequlas;2.7) than of other cell types. The strength of the association increased over the 9‐year study period. County levels of selected agricultural characteristics were used as surrogate measures of farming exposures in residence counties of farmers and were summarized by factor analysis. Major findings were of elevated risk among younger farmers for reticulum‐cell sarcoma in counties high in summary measures of general agricultural activity (ORequlas;3.2), of small grain acreage and acres treated with insecticides (ORequlas;6.6), and of wheat acreage (ORequlas;4.4). Given the limitations of the data, further investigation of non‐Hodgkin's lymphoma in farmers is warranted.
Prospective evaluation of the leukocyte adherence inhibition (lai) test in breast cancer using a panel of extracts from known and unknown primary tumors
Authors: Fritze D. , Fedra G. , Kaufmann M. 
Published: February 2007

AbstractThe antigen‐induced leukocyte adherence inhibition (LAI) test is an assay of cellular immune reactivity which was expected to offer a promising adjunct to currently available diagnostic and monitoring procedures in cancer patients. We have applied this assay to (1) 83 inpatients clinically suspected of having breast cancer, (2) 50 outpatients before mammography, and (3) 37 healthy women. In order to account for the known heterogenicity of breast cancer, we performed LAI assays with extracts from 15 primary tumors of known and 14 primary tumors of initially unknown histology. Thus, the problem of tumor specificity in the LAI assay was tackled in a doubleblind fashion. The results obtained clearly show that breast‐tissue‐specific rather than tumor‐specific responses were detected by LAI testing. The LAI assay failed to discriminate between high‐risk patients with and without cancer and between extracts from breast tumors with and without carcinoma. The results are discussed with regard to the many claims for the detection of specific tumor immunity in the literature.
A cell‐surface antigen which is present in the ganglioside fraction and shared by human melanomas
Authors: Yeh M.‐Y. , Hellström I. , Abe K. , Hakomori S. , Hellström K. E. 
Published: February 2007

AbstractWe have raised a hybridoma, 4.2, which forms an IgM antibody to an antigen expressed on cultivated cells from most human melanomas, more infrequently on cells from other human tumors, and very weakly on cultivated fibroblasts, T cells and B cells. The antigen can be detected in biopsy material of human melanoma and, in smaller amounts, in fresh samples of normal human lung and kidney. Preliminary biochemical characterization indicates that it is associated with the ganglioside fraction. We feel that the antigen (referred to as 4.2) has a sufficient degree of tumor specificity to be rated as a human melanoma‐associated antigen.
Modulation of protein phosphorylation in human colon adenocarcinoma cell membrane preparations by epidermal growth factor in vitro
Authors: Zenisek S. C. , Fernandez‐Pol J. A. 
Published: February 2007

AbstractIncubation of membranes prepared from the human colon adenocarcinoma cell line LoVo in vitro with [γ‐32P]ATP demonstrated numerous components whose phosphorylation was stimulated several fold by epidermal growth factor (EGF). One major component of Mn 170 K, which was either undetectable or very weakly phosphorylated in the absence of EGF, was primarily affected by exposure to EGF. The phosphorylation of the 170 K Mr membrane component required the presence of Mn2+; Mg2+ was ineffective. Although the phosphorylation of many LoVo membrane components was significantly modified by cAMP or dibutyryl‐cAMP, none of these cyclic nucleotides appeared to be involved in the phosphorylation of the 170 K membrane component in the presence or absence of EGF. The phosphorylation system of the LoVo membranes efficiently utilized (γ‐32P)GTP in both the basal and EGF‐stimulated reactions. All the membrane components phosphorylated in the absence or presence of EGF, except a band comigrating with the tracking dye front, were digested by trypsin. The possible glycoprotein nature of the 170 K dalton phosphoprotein was indicated by the fact that the 170 K dalton band comigrated with a periodic acid‐Schiff base‐stained band. These findings suggest that one of the biochemical steps in the mechanism of action of EGF in LoVo cells is enhanced phosphorylation of several membrane proteins, especially that of a glycoprotein of Mr 170 K, by a membrane‐bound cyclic nucleotide independent protein kinase.
Interferon‐independent, lectin‐induced augmentation of murine natural killer cell activity
Authors: Brunda Michael J. , Varesio Luigi , Herberman Ronald B. , Holden Howard T. 
Published: February 2007

AbstractThe ability of lectins to augment natural killer (NK) cell activity was demonstrated using splenic effector cells from athymic nude mice. The addition of Helix pomatia agglutinin to the assay or pretreatment of the effector cells with lectin resulted in increased cytotoxicity against the human cell line K562, a relatively poor target for spontaneous mouse NK activity. When additional lectins were tested, NK activity was increased markedly by some lectins while others had no effect. The augmentation of cytotoxicity was dependent on the concentration of lectin added. Nylon‐wool‐nonadherent, nu/nu splenic effector cells mediated the lectin‐induced cytotoxicity, and antiasialo GMI plus complement abolished activity, indicating that the cells mediating the cytotoxicity were NK cells and not mature T cells, B cells or macrophages. When spleen cells from mice having different levels of NK activity were evaluated in this system, the magnitude of the lectin‐induced cytotoxicity obtained correlated with the level of spontaneous NK activity and no increased cytotoxicity was found using cell populations that had low spontaneous NK activity. By testing a panel of target cells, we found that certain human, mouse and rat cell lines, which had low to moderate susceptibility to spontaneous murine NK activity, were sensitive to lectin‐induced NK‐cell‐mediated cytotoxicity while others were completely resistant; resistance or susceptibility to cytotoxicity was not directly correlated with the ability of lectins to bind to the target cell. The lectin‐induced cytotoxicity was independent of interferon (IFN) since detectable levels of IFN were not produced in the cultures of lectins and effector cells, cytotoxicity was not increased when exogenous IFN was added to the assay, and inhibitors of RNA and protein synthesis, which block the action of IFN, had no effect on the cytotoxicity. These results indicate that NK cells can mediate lectin‐induced cytotoxicity and the implications of lectin interaction with NK cells are discussed.
Modulation of natural killer sensitivity of murine trophoblast cells by tumor promoter and interferon
Authors: Tanaka Kenichi , Chang Kenneth S. S. 
Published: February 2007

AbstractThe in vitro established lines of murine placental trophoblast cells showed little membrane expression of H‐2 antigens and a high degree of sensitivity to natural killer (NK)‐cell‐mediated cytotoxicity. This NK‐sensitivity was decreased either by short‐term treatment of these cells with murine interferon (IFN) or by culture for more than 4 days in the presence of a tumor promotor, 12‐O‐tetradecanoylphorbol‐13‐acetate (TPA). This effect of TPA was reversible after removal of TPA from the culture medium. However, IFN treatment of trophoblast cells cultured previously in TPA medium resulted in restoration of NK‐sensitivity to the original level exhibited by cells untreated with IFN or TPA. The mechanism for this antagonistic effect is not clear. The decrease in NK‐sensitivity of IFN‐ or TPA‐treated trohphoblast cells was not due to the loss of NK‐recognition membrane structures, or to induction of prostaglandin which elevates cyclic‐AMP levels. Inhibition of protein synthesis by cycloheximide restored the NK‐sensitivity of TPA‐treated trophoblast cells, indicating the possible contribution of de novo synthesized protein(s) which could confer NK‐resistance. The TPA‐treated trophoblast cells became more tumorigenic, producing larger tumors and a higher mortality than the untreated controls when inoculated into mice. The possible roles of NK cells in trophoblastic diseases and feto‐maternal relationships are discussed.
Cross‐reactions between tumor cells and allogeneic normal tissues. inhibition of a syngeneic lymphoma outgrowth in h‐2 and non‐h‐2 alloimmune balb/c mice
Authors: Parmiani Giorgio , Luisa Sensi M. , Carbone Giusi , Colombo Mario , Pierotti Marco , Ballinari Dario , Hilgers Jo , Hilkens John 
Published: February 2007

AbstractTo test whether alloimmunization with H‐2 or/and non‐H‐2 different normal tissues may increase the immunity to syngeneic tumors, groups of BALB/c (H‐2d) mice were immunized with a series of allogeneic lymphoid cells and then challenged i.p. with syngeneic lymphoma cells. The outgrowth of otherwise lethal doses of the Moloney virus‐induced lymphoma YC8 and of its clones was inhibited in BALB/c mice immune to DBA/2 (H‐2d), C3Hf (H‐2k), C3H.SW (H‐2b), C3H.OH (H‐2o2) and to B10 background tissues but not in mice immunized to A/He, BALB.K (H‐2k) or BALB.B (H‐2b) normal tissues. Anti‐YC8 effect was also induced by immunizing BALB/c recipients with a pool of five different allogeneic cell lines which included C3Hf, C57BL/6J (H‐2b), N:NIH (H‐2q), B10.M (H‐2f), and DBA/2 lymphoid cells. No growth inhibition of other BALB/c lymphomas induced by Moloney virus (LSTRA), X‐rays (RL♂I) or urethane (UR‐I) was evident in alloimmune mice. In vivo transfer of growth inhibition of YC8 was obtained with BALB/c anti‐B10.D2 peritoneal exudate cells in a Winn assay. The ability of these alloimmune lymphoid cells to delay significantly the survival time of BALB/c mice injected with the mixture of immune cell and YC8 cells was abrogated by anti‐Thy 1.2 plus C' treatment. In addition, nu/nu BALB/c mice were unable to develop resistance to YC8 outgrowth after alloimmunization. The results of this study show that: (1) syngeneic growth of a lymphoma can be prevented by alloimmunization with normal cells; (2) this cross‐reaction involved non‐H‐2 antigens; (3) the phenomenon appeared to be mediated by T cells.
Induction of γ‐glutamyltranspeptidase‐positive altered hepatocytic lesions by combination of transplacental‐initiation and postnatal‐selection
Authors: Ogawa Katsuhiro , Yokokawa Kinya , Tomoyori Takashi , Onoé Tamenori 
Published: February 2007

AbstractThe purpose of this study was to induce in postnatal life the selective growth of altered hepatocytic populations which had been induced in utero by various chemicals. Pregnant rats of a Wistar strain were given a single dose of various chemical carcinogens on the 18th gestational day. From two months postpartum, both the mothers and offspring were given a diet containing 2‐acetylaminofluorene (2‐AAF) at a concentration of 0.02% for two weeks. Then, at the end of the first week after the 2‐AAF feeding, a two‐third partial hepatectomy was performed. All the animals were killed one week after the partial hepatectomy and were examined for the incidence of γ‐glutamyltranspeptidase (GGT)‐positive altered hepatocytic foci in the liver. The transplacental administration of not only a hepatic carcinogen, diethylnitrosamine (DEN) but also 7,12‐dimethylbenzanthracene (DMBA), which does not usually produce hepatocellular carcinomas in adult rats, induced GGT‐positive altered hepatocytes in the liver of the offspring. These hepatocytes grew into grossly visible hyperplastic nodules within a week after the two‐third partial hepatectomy. The possible applicability of the transplacental initiation‐postnatal selection model for the short‐term assay of transplacental carcinogenicity is discussed.
Anti‐tumor immunity in b‐lymphocyte‐deprived mice. iii. immunity to primary moloney sarcoma virus‐induced tumors
Authors: Gordon Julius , Holden Howard T. , Segal Shraga , Feldman Michael 
Published: February 2007

AbstractTumor induction and immunity to tumors were studied following the injection of Moloney sarcoma virus (MSV) into mice whose B‐lymphocyte functions had been suppressed by the chronic administration of anti‐IgM antibodies. Two preparations of MSV were used; one which gives rise to tumors which uniformly regress in normal adult mice, and another which elicits progressively growing tumors in the majority of recipients. The tumor incidence, mean tumor size, and tempo of regression were not modified by treatment with anti‐IgM. However, whereas tumors induced by the regressor virus were all rejected in 19 NRG‐treated and 29 untreated recipients, continued growth was obtained in 2 of 23 B‐lymphocytedeprived mice. Furthermore, in 9 additional mice from this group, apparent rejection was followed by tumor recurrence at the site of the initial tumor. Continued growth was accompanied by widespread metastasis. These tumors were freely transplantable to normal syngeneic recipients. Metastasis and transplantability were also detected in 7 of 24 anti‐IgM‐treated mice given progressor virus, but were not seen in the control animals. Recurrence and metastasis was obtained despite the presence of high levels of specific cytotoxic T lymphocytes in the spleen. It is concluded that B lymphocytes or their products play an essential role in host protection against MSV‐induced tumors.
Activation of an endogenous mouse type c virus by uv‐irradiated murine cytomegalovirus
Authors: Sergiescu Dina 
Published: February 2007

AbstractInfection of Kirsten sarcoma virus‐transformed non‐producer BALB‐3T3 mouse cells with UV‐irradiated mouse cytomegalovirus (MCMV) resulted in activation of a xenotropic type C virus detected by infectious center formation in permissive rat or mink cells. The levels of type C virus activated by MCMV were related to the UV dose applied. Unter optimal conditions the frequencies of activation varied from 3.0 to 8.0 × 10−4. The capacity of MCMV to activate type C virus was abolished by heat inactivation and by neutralization with specific antiserum against MCMV. Virus induction decreased under conditions of cell exposure to hydroxyurea or actinomycin D, inhibitors of DNA and RNA synthesis, respectively, with actinomycin D having a greater inhibitory effect. This suggests that both DNA and RNA synthesis are required for UV‐MCMV induction of murine xenotropic virus.
Tumor enhancing T lymphocytes in mice: Further studies on characteristics and mechanism of activity
Authors: Small Myra 
Published: February 2007

AbstractIn order to test the possibility that tumor‐enhancing T lymphocytes can suppress other lymphoid cells, such as those with anti‐tumor activity, their effect was tested in an allogeneic response of cell‐mediated lysis. Normal thy‐mocytes and spleen cells from mice with advanced tumors, two populations which enhance the growth of solid tumors, both suppressed the generation of CML. Since these results suggest that the mechanism of enhancement by T cells may resemble suppression in other immune responses, we looked for Fc receptors on the sensitized cells involved in tumor enhancement Cells expressing Fc receptors appeared to be necessary for enhancement of tumor growth to occur.
Effect of mouse interferon on cell transformation and virus production in rat cells exogenously infected with moloney murine sarcoma and leukemia viruses
Authors: Huleihel Mahmoud , Aboud Mordechai 
Published: February 2007

AbstractFoci of transformed cells, produced by MSV(124), appeared to result only from the primary infection, since this virus stock yielded a virus‐nonproducing infection. On the other hand, the majority of foci scored in MSV/MLV‐infected cultures, were generated by multiple secondary infections with the progenies of the primary infection. Mouse interferon (IF) was highly inhibitory for cell transformation by both virus stocks. However, this inhibition was apparent in MSV(124) infected cultures only if IF was added at least 12 h before infection, whereas in MSV/MLV‐infected cultures IF was highly effective even if added 24 h after infection. The inhibition of focus formation by MSV(124) was irreversible after removal of IF, suggesting that IF inhibited an early step before provirus integration into the host genome. By contrast, in MSV/MLV‐infected cultures focus formation was almost completely restored after recovery from the IF effect Nevertheless, examination of virus production after IF removal proved that in MSV/MLV infection, too IF exerted and inhibitory effect before provirus integration.
Cell‐surface antigens of a clonal human embryonal carcinoma cell line: Morphological and antigenic differentiation in culture
Authors: Andrews Peter W. , Goodfellow Peter N. , Shevinsky Lynne H. , Bronson David L. , Knowles Barbara B. 
Published: February 2007

AbstractA cloned human embryonal carcinoma (EC) cell line has been derived from a testicular teratocarcinoma, and reproducibly forms EC tumors when injected into athymc (nu/nu) mice. These human EC cells are characterized by a newly described stage‐specific embryonic antigen, SSEA‐3. Unlike murine EC cells, they express major histocompatibility antigens (HLA‐A, B, C and β2‐microglobulin) but do not express the embryonic antigen SSEA‐I. We also report that these cells appear to be capable of differentiation and that this can be induced by initiating cultures at low cell density. Differentiation is marked by the appearance of morphologically distinct cells and by the induction of SSEA‐I, whereas the expression of other antigens, including SSEA‐3, is initially diminished. This well‐characterized system of human EC cells provides a model for the future investigation of other human teratocarcinoma cell lines and for the analysis of cellular differentiation during early human development.
In vitro transformation by avian erythroblastosis virus recruits cells of erythroid lineage with varying degree of differentiation
Authors: Therwath Ahmedunny , Scherrer Klaus 
Published: February 2007

AbstractWe have previously shown that AEV infection of leukosis‐free chickens provokes an erythroleukemia in the infected birds, and that the target cell for virus transformation is most likely an early pro‐erythroblast comparable to the BFU‐E. The virus infection correlates with a block in differentiation which was studied at a specific cellular gene level, namely that of the globin genes. In live birds, the viral transformation has been found to affect the transcriptional activity of two out of three adult globin genes and the phenotypic expression of the third. Indeed, the αA gene that is transcribed is silent as well, since its transcription product is fully eliminated in the nucleus following an “abortive processing”. Chick bone marrow cells can also be transformed in vitro by AEV in which case the virus recruits, as targets, cells of the erythroid lineage belonging to a wider spectrum and hence in varying degrees of differentiation. In contrast to the results obtained with in vivo transformed cells, molecular hybridization with globin cDNA probes showed that in the erythroblasts transformed in vitro under tissue culture conditions all the three adult globin genes are transcriptionally active. In fact, low but detectable amounts of globin mRNA sequences are present in both the nuclear and cytoplasmic compartment of the cell prior to exposure to any chemical inducers of red cell differentiation. Judging from our present results, we may propose that AEV transformation in vitro does not shut off but only modulates the already functioning erythroid cell differentiation program.
Expression of a monoclonal antibody‐defined liver‐associated antigen in normal rat hepatocytes and hepatocellular carcinoma cells
Authors: Holmes C. H. , Gunn Barbara , Austin E. B. , Embleton M. J. , Baldwin R. W. 
Published: February 2007

AbstractIn order to examine changes in the expression of normal cellular antigens during hepatocarcinogenesis, we have developed and characterized a monoclonal antibody detecting an antigen which is particularly associated with adult rat hepatocytes. The antibody showed no reactivity with a range of freshly‐prepared normal syngeneic adult rat cell types, but showed strong reactivity with hepatocytes derived from several rat strains in antibody binding tests. Immunoperoxidase staining of sections of normal rat liver showed that the antigen was distributed throughout hepatocytes within the liver, but did not stain cells other than hepatocytes. The antigen detected by this monoclonal antibody was not detectable on a number of transplanted and primary dimethylaminoazobenzene‐induced hepatomas. Preliminary data indicated that this monoclonal antibody may be suitable for use in flow cytofluorimetric sorting of mixed populations of normal and tumour cells, allowing the investigation of cell phenotypes during hepatocarcinogenesis.
Augmentation of metastasis formation by thioglycollate‐elicited macrophages
Authors: Gorelik E. , Wiltrout R. H. , Brunda M. J. , Holden H. T. , Herberman R. B. 
Published: February 2007

AbstractInoculation of thioglycollate‐elicited peritoneal exudate cells (PEC) into C57BL/6 mice reduced the rate of lung clearance of several intravenously (i.v.) injected murine tumor cells, and increased by up to 100‐fold the number of artificially‐induced metastatic lung nodules produced by the i.v. injection of B16 melanoma or Lewis lung carcinoma (3LL) tumor cells. Maximum effects were observed when PEC were injected either before, or shortly after, tumor cells. Modulation of lung clearance or metastasis formation was observed only with PEC and not with a variety of other cells, such as splenocytes, thymocytes, P815 mastocytoma cells, or several macrophage‐like cell lines (PU5‐1.8 and IC‐21). Lysates of PEC were as efficient in reducing lung clearance and augmenting metastasis formation as were intact viable PEC. Lysates of other cell types, including P815 and the macrophage‐like cell lines, were unable to produce these effects. PEC populations, enriched for macrophages by adherence to plastic or by percoll density gradient sedimentation, also increased the number of B16‐induced artificial metastasis, implicating the macrophage as the cell responsible for these observations.
Tumorigenicity of human bk papovavirus plaque isolates, wild‐type and plaque morphology mutant, in hamsters
Authors: Watanabe Sumie , Kotake Setsuko , Nozawa Akemi , Uchida Seijiro , Muto Takeshi 
Published: February 2007

AbstractThe polyoncogenic prototype human papovavirus BKV (Gardner's strain) produced clear, small and large plaques. Two small‐plaque isolates (wt‐500 and wt‐502), as well as a large‐plaque‐forming isolate (wt‐501), induced frequent brain tumors and occasional osteosarcomas (but no insulinomas) in hamsters. The large‐plaque former (wt‐501) was more tumorigenic than the two small‐plaque isolates. One small (pm‐522) and one large turbid plaque mutant (pm‐525), which had been rescued from hamster tumor cell lines and have small deletion near the origin of DNA replication, induced frequent brain tumors and insulinomas. Mutant 522 was about five times more tumorigenic than wt‐501. These results support the hypothesis that the polyoncogenicity of prototype BKV is accounted for by the presence of BKV mutants.