bluuebunny/crossref_metadata_2025_split huggingface dataset:
Avian retrovirus‐induced surface antigens and their cross‐reactivity with chemically‐transformed cells and primary embryonic cells of Japanese quails
Authors: Hayami Masanori , Ignjatovic Jagodina , Bauer Heinz 
Published: February 2007

AbstractBy testing spleen cells from avian leukosis (ALV) and avian sarcoma virus (ASV)‐injected Japanese quails in a microcytotoxicity assay against various target cells, we have demonstrated the existence of several target antigens. With non‐transformed ALV‐infected Japanese quail cells used as target cells, an avian retrovirus subgroup‐specific destruction was obtained when spleen cells from animals infected with either avaian sarcoma or leukosis virus of the same subgroup were employed. This reaction is probably due to the virus envelope glycoproteins (Ve‐gp) expressed on the cell surface. Apart from this subgroup‐specific reaction, avian retrovirus group‐specific destruction of ASV‐trans‐formed cells was demonstrated by means of effector cells immunized with ASV of a different subgroup. This reaction is restricted to transformed cells and not due to the virus envelope glycoprotein because the same effector cells are not cytotoxic to ALV‐infected non‐transformed cells but cytotoxic to sarcoma‐virus‐transformed cells which lack Ve‐gp. Quail methylcholanthrene‐tumor cells which show a transformation phenotype similar to that of ASV‐transformed cells but which are free of detectable endogenous and exogenous retrovirus were also destroyed by the spleen cells from ASV tumor bearing animals. The same effector cells also exerted a weak cytotoxic effect on uninfected primary embryo cells but not to embryo cells after several passages.
Immunity to MCA‐induced rat sarcomas: Analysis of in vivo and in vitro results
Authors: Harmon Richard C. , Clark Edward A. , Reddy A. Lakshma , Hildemann William H. , Mullen Yoko 
Published: February 2007

AbstractThree in vivo techniques were used to establish the specificity of tumor immunity induced after sensitization of F344 rats to syngeneic MCA‐induced sarcomas: (1) post‐excision resistance to tumor challenge, (2) passive tumor neutralization (the Winn test), and (3) concomitant immunity. In general, these assays revealed unique non‐crossreactive antigens associated with each of three sarcomas, FMF1, FMM2, and FMM3. However, spleen cells from tumor‐sensitized rats did not demonstrate cell‐mediated cytotoxicity in vitro corresponding to the specificity of tumor resistance in vivo. In the (3H)‐proline cytotoxicity assay, spleen cells from FMM3 tumor‐bearing rats or from FMM3 tumor‐immune rats were not selectively cytotoxic for cultured FMM3 target cells. Parallel analysis of spleen cells from normal or FMM3‐sensitized rats using the Winn assay and the (3H)‐proline assay revealed that (1) spleen cell cytotoxicity in vitro did not correlate with effective tumor protection in vivo; and (2) normal spleen cells were cytotoxic against cultured sarcoma target cells in vitro and inhibited tumor growth in vivo. Thus, passive tumor protection by normal spleen cells in vivo corresponded with the demonstration of natural cytotoxicity in vitro, but induced specific anti‐tumor reactivity was observed only in vivo.
Analysis of karyotype variation following carcinogen treatment of chinese hamster primary cell lines
Authors: Connell J. R. , Ockey C. H. 
Published: February 2007

AbstractChinese hamster primary fibroblasts derived from several embryos were treated with the carcinogens benzo(a)pyrene, 7,12‐dimethylbenz(a)anthracene or N‐methyl‐N'‐nitro‐N‐nitrosoguanidine. Karyotype analysis, sister chromatid exchange frequency, evidence of transformation by growth in agar, cell morphology and reaction to cytocholasin B were tested at regular intervals over many culture passages. Carcinogen treatment was found to shorten the time period before onset of permanent karyotypically changed stem and side lines and in vitro transformation. Chromosomes X, 6 and 10 were more frequently involved in all cultures in these karyotype changes which were usually preceded by a period of chromosome variation. Spontaneous chromatid aberrations and aneuploidy increased in frequency with time in culture and generally appeared prior to the expression of transformation. No specific chromosomes were involved with the different carcinogens. There was no correlation between in vitro transformation and karyotype evolution and the criteria for transformation were present independently of one another. It is suggested that the lack of correlation between the parameters tested indicates that the expression of in vitro transformation is a result of selection for growth advantage from a cell population expressing an increasing degree of genetic instability and variation with time in culture.
Virus expression in different tissues of normal and tumor‐bearing mice inoculated with a murine leukemia virus
Authors: Youn J. K. , Santillana M. , Hue G. , Barski G. 
Published: February 2007

AbstractEvolution of virus expression in different lymphoid organs as well as in solid syngeneic tumors of mice inoculated with an MuLV was studied with the aid of in vitro XC co‐culture technique. When normal adult mice of strain XLII were inoculated intraperitoneally with a cultured Rauscher virus (RC), the virus could be detected, 10 days after inoculation, only in bone marrow in small amounts and there‐after no virus could be found in any of the organs tested, including bone marrow, spleen, thymus, lymph node and kidney. However, when age‐ and sex‐matched parallel mice bearing syngeneic subcutaneous non‐viral tumors were inoculated similarly with the RC virus, the virus could be detected abundantly not only in bone marrow and spleen but also in tumors during the first 3 weeks and even 6 weeks after virus inoculation. Transitional decrease or disappearance of the virus was observed around the 25th‐31st day in organs and tumors of the inoculated mice. When the tumor mass was removed from these mice by surgery, the virus disappeared rapidly and definitely from all the organs tested. The virus recovered from in vitro explanted and cultured tumors, taken from mice inoculated with the virus, induced typical lymphoid leukemia in BALB/c mice inoculated as newborns. However, from certain aspects (hypertrophy of the thymus and lymph nodes), this virus was different from the original RC virus.
Increase in immunogenicity of a pulmonary squamous‐cell carcinoma, propagated in vitro
Authors: Jamasbi Roudabeh J , Nettesheim Paul 
Published: February 2007

AbstractThe chemically induced, non‐immunogenic lung squamous‐cell carcinoma (MSC‐10) propagated in vitro gradually loses tumorigenicity in immuno‐competent hosts with increasing in vitro passage. This was found to be related to an increase in antigenicity, since immunosuppressed hosts (thymectomy plus 600 rads whole body X‐irradiation) supported the growth of tumor cells, whereas immunocompetent recipients did not. The antigens involved in rejection are not heterologous serum proteins present in culture media since the cell line grown in isologous serum is also rejected. Immunization with the in vitro tumor line partially protected against the parental in vivo line, therefore the antigens involved must be present on both tumor lines. Inoculation of the cultured cell line into normal or immunosuppressed hosts produced tumors with the same histological characteristics as those of the in vivo tumor line. We concluded that by in vitro culture the weakly antigenic carcinoma becomes more immunogenic and thereby capable of inducing transplantation resistance. The cultured tumor cells retain their antigenic specificity and histologic characteristics while increasing their antigenic potency.
Mechanism of the establishment of epstein‐barr virus genome‐containing lymphoid cell lines from infectious mononucleosis patients: Studies with phosphonoacetate
Authors: Rickinson A. B. , Finerty S. , Epstein M. A. 
Published: February 2007

AbstractA concentration of disodium phosphonoacetate (PA) has been defined which will reduce the synthesis of infectious EB virus in a producer cell line to 1% of control values but which will not affect the growth of EB virus‐transformed cells in a 12‐week colony‐forming assay. When total mononuclear cells or T‐lymphocyte‐depleted mononuclear cells from the blood of acute IM patients were cultured in the presence of PA at the above concentration, the regular establishment of EB virus genome‐containing cell lines seen in control cultures was almost totally abolished. In further experiments, when T‐lymphocyte‐depleted IM mononuclear cells were co‐cultivated with foetal cells of the opposite sex in the presence and absence of PA, cell lines of mixed or of exclusively foetal origin were obtained not only from control co‐cultures but also on those rare occasions when transformed foci developed in PA‐treated co‐cultures. The results suggest that all cell lines derived from the blood of IM patients are initiated in culture by a two‐step process of virus release and secondary infection, and argue against the occurrence of any direct outgrowth of IM cells transformed by the virus in vivo.
Growth requirements of human mammary epithelial cells in culture
Authors: Taylor‐Papadimitriou J. , Shearer M. , Stoker M. G. P. 
Published: February 2007

AbstractColony‐forming epithelial cells can be separated from the non‐dividing “foam cells” in human milk by differential adhesion to glass and freezing. The growth of such partially purified mammary epithelial cells is stimulated by co‐culture with non‐dividing feeder cells. Foam cells, mitomycin‐treated mouse fibroblast lines and human mammary fibroblasts and calf lens epithelial cells are all effective in promoting mammary epithelial cell growth. Contact between epithelial cells and feeders is not required for the growth‐promoting effect. The mitogenic effect of epidermal growth factor on mammary epithelial cells also requires feeder cell activity.
Immunostimulation of chemical oncogenesis in the mouse
Authors: Prehn Richmond T. 
Published: February 2007

AbstractPast work has demonstrated, both in vivo and in vitro, that a weak immune reaction can stimulate rather than inhibit the growth of many transplantable tumors. It was therefore predicted that animals with a weak immunological capacity would be more susceptible to tumor induction than would those with either a minimal or a maximal capacity. X‐rayed, thymectomized mice were inoculated with various numbers of normal syngeneic spleen cells and were subsequently exposed to various degrees of oncogenic stimulus by 3‐methylchol‐anthrene in the form of subcutaneous wafers. As expected, it was found that among animals exposed to a high oncogenic stimulus, the sarcoma incidence was significantly higher among those animals that had received small numbers (104) of spleen cells than among those that had either received none (0) or the maximal number (107). In contrast, when the oncogenic stimulus was low, the tumor incidence was the same in all groups regardless of the numbers of spleen cells the animals had received. Since the average immunogenicity of sarcomas has been shown to be directly related to the concentration of the chemical oncogen and inversely to the tumor latency, it can be inferred that the higher tumor incidence associated with 104 spleen cells in the experiments with a high oncogenic stimulus probably depended upon the immunogenicities of the induced tumors and was therefore consistent with an immunostimulation of oncogenesis.
Detection of a nuclear, EBNA‐type antigen in apparently EBNA‐negative Herpesvirus papio (HVP)‐transformed lymphoid lines by the acid‐fixed nuclear binding technique
Authors: Ohno Shinsuke , Luka Janos , Falk Larry , Klein George 
Published: February 2007

AbstractIn agreement with the findings of previous authors, we could not detect a virally determined nuclear antigen in Herpesvirus papio (HVP)‐transformed baboon lymphoid lines by anticomplementary staining in situ, as for EBNA. However, by means of our recently developed acid‐fixed nuclear binding technique an EBNA‐like antigen could be readily demonstrated, after extraction from both producer and non‐producer lines. We propose to designate the antigen as HUPNA. It can be detected by a human anti‐EBNA antibody, suggesting cross‐reactivity, if not identity, between EBNA and HUPNA. HVP‐DNA carrying non‐producer lines, negative for in situ ACIF stainability but capable of yielding HUPNA by the nuclear binding technique, can be superinfected with EBV, with brilliant EBNA expression as the result, suggesting that the defective in situ staining is a property associated with the baboon HVP, rather than the baboon lymphoid cell per se.
The effect of chronic protozoan infection by Babesia rodhaini on leukemogenesis in mice
Authors: Hugoson G. , Lagerlöf B. , Thorell B. 
Published: February 2007

AbstractThe effect of chronic infection with the protozoan parasite Babesia rodhaini on the subsequent development of mouse leukemia was investigated in three different murine leukemia‐lymphoma model systems: congenital lymphoma (in AKR mice), irradiation‐induced lymphoma (in C57BL mice), and Rauscher‐virus‐induced leukemia in NMRI mice. Leukemia incidence was significantly greater than in controls in Babesia‐infected (NMRI strain) mice that had been infected with an adjusted dose of Rauscher leukemia virus.
Screening of human brain tumors for SV40‐related T antigen
Authors: Tabuchi Kazuo , Kirsch Wolff M. , Low Margaret , Gaskin Doris , van Buskirk John , Maa Shane 
Published: February 2007

AbstractA series of 39 human brain tumors has been screened for the presence or absence of SV40‐related T antigen by the direct and indirect immuno‐peroxidase methods. Two tumors of ependymal origin (malignant ependymoma, choroid plexus papilloma) revealed markedly positive nuclear staining for T antigen both in vivo and in vitro. The relationship of these tumors to their experimental counterparts inducible by recent human papova‐virus isolates is discussed.
Chemical transformation of human revertant cells induced by murine sarcoma virus
Authors: Cho Han Y. , Arnstein Paul , Rhim Johng S. 
Published: February 2007

AbstractA human revertant cell line, derived from non‐producer human osteosarcoma cells (NP/KHOS) induced by Kirsten murine sarcoma virus, was treated in vitro with various levels of polycyclic aromatic hydrocarbons (3‐methylcholanthrene, 7,12‐dimethylbenz(a)anthracene, and benzo(a)pyrene [BP] or dimethyl sulfoxide (control). Cells treated only with 3‐methylcholanthrene and 7,12‐dimethyl‐benz(a)anthracene underwent morphological alteration in vitro, and produced tumors when injected into NIH nude mice. These human revertant cells may be a useful in vitro tool in screening for the potentital chemical carcinogens in human cell systems.
Characterization of the human natural killer (NK) cell in blood and lymphoid organs
Authors: Eremin O. , Coombs R. R. A. , Plumb D. , Ashby J. 
Published: February 2007

AbstractThe human natural killer (NK) cell in peripheral blood is a non‐thymus‐dependent, (Fc+ C3−), Ig‐bearing lymphocyte and is probably identical to the human K cell, although not requiring the Fc receptor, in contrast to the K cell, for the lytic process. The human NK cell in tonsil and lymph node, on the other hand, is a non‐Ig‐ bearing T lymphocyte, lacking both Fc and C3 receptors.
Immunotherapy of murine leukemia. I. protection against friend leukemia virus‐induced disease by passive serum therapy
Authors: Collins Jeffrey J. , Sanfilippo Fred , Tsong‐Chou Lynn , Ishizaki Ryo , Metzgar Richard S. 
Published: February 2007

AbstractPassive serum therapy with chimpanzee anti‐serum raised against Friend leukemia virus (FLV) or the major viral envelope glycoprotein of FLV, gp71, has been shown to be effective in protecting mice against the development of virus‐induced disease. The heterologous serum was administered in four doses beginning 3 days after virus inoculation and the mice were followed for the development of splenomegaly, virus level, and the induction of a host anti‐viral immune response. The latter was measured by an in vitro humoral cytotoxicity assay using FLV‐releasing mouse cells as targets, as well as by direct radioimmunoassay for the presence of mouse antibodies capable of binding FLV gp71. The results indicate a close correlation between the development of anti‐viral humoral immunity and protection against splenomegaly, with both of these parameters being inversely related to serum and spleen infectious virus titers. Recognition of and response to the administered heterologous immunoglobulin in by the recipient animal does not appear to represent an integral part of the mechanism leading to protection, as determined by the absence of mouse antibodies capable of binding chimpanzee γ‐globulin, as well as by the equal efficacy of the passive serum transfer protocol in mice after induction of tolerance to chimpanzee γ‐globulin. It is suggested that passive serum therapy protection may function via a mechanism involving the reduction of the virus burden below a level which is immunosuppressive, allowing the development of a host anti‐viral immune response which is necessary for elimination of virus and/or infected cells leading to long‐term resistance.
Inhibition and promotion of tumor growth by BCG: Evidence for stimulation of humoral enhancing factors by BCG
Authors: Ishibashi Tsuneo , Yamada Hozumi , Harada Susumu , Harada Yasuko , Takamoto Masahiro , Sugiyama Kotaro 
Published: February 2007

AbstractEffects of pretreatment with BCG, strain Japan, on tumor growth were studied using a transplantable methylcholanthrene (MCA)‐induced fibro‐sarcoma in C3H/He mice. Injection of BCG 7 weeks before tumor inoculation at a site distant from the tumor caused a slight inhibition of tumor growth. A low dose of tumor cells did not grow at the BCG‐primed site when BCG was injected 7 and 11 weeks before the tumor. When a high dose was inoculated into the BCG‐primed site, inhibition of the primary tumor occurred in mice which had received BCG 7 weeks previously, but the number of distant metastases in the popliteal lymph node and the lungs was increased in mice pretreated with BCG at any time. Furthermore, post treatment with BCG at a site distant from the tumor caused promotion of tumor growth. Enhanced antibody formation and suppression of delayed type hypersensitivity(DTH) occurred in tumor‐bearing mice. BCG treatment of such mice caused a vigorously enhanced antibody formation and a marked suppression of DTH. The sera from tumor‐bearing mice enhanced tumor growth. Tumor growth was suppressed in splenectomized mice. These findings suggested that antibodies against tumor‐specific antigens enhanced tumor growth in this system and that BCG treatment of tumor‐bearing mice stimulated formation of antibodies probably acting as blocking factors.
In vitro and in vivo expression of original and foreign H‐2 antigens and of the tumor‐associated transplantation antigen of a murine fibrosarcoma
Authors: Carbone Giusi , Invernizzi Giovanni , Meschini Angela , Parmiani Giorgio 
Published: February 2007

AbstractWe have previously shown that the methyl‐cholanthrene‐induced BALB/c fibrosarcoma C‐1 syngeneically transplanted in vivo expressed, in addition to its original H‐2d and tumor‐associated transplantation antigens, also the foreign H‐2Kk 23, 1, 5, 11, 25 specificities. In the present study we have investigated the expression and the immunogenicity of these antigens on an in vitro line of C‐1 tumor. The binding of C57BL/6J or C3Hf anti‐BALB/c sera or that of monospecific alloantisera to H‐2d specificities on plated C‐1 cells (evaluated by the indirect isotopic 125I‐antiglobulin assay) showed that the expression of H‐2d antigens was very low or undetectable on the tumor kept in vitro. Absorption by the in vivo and in vitro maintained C‐1 cells of the complement‐dependent cytotoxicity on BALB/c normal lymphoid cells of the C75BL/6J anti‐BALB/c serum confirmed the lower expression of H‐2d antigens on C‐1 kept in vitro as compared to the in vivo transplanted tumor. The H‐2k antigens found on C‐1 were also examined by the above methods using BALB/c anti‐C3Hf, anti‐AKR, anti‐C57BL/6J polyspecific sera and also monospecific alloantisera directed to H‐2k antigens. The C‐1 cultured cells displayed a significant reduction of H‐2k antigens as compared to the in vivo C‐1 tumor, the antigen 5 being undetectable on the in vitro cells. Allogeneic and syngeneic sera raised against in vitro or in vivo C‐1 cells were tested on either BALB/c or C3Hf normal lymph‐node cells by the complement‐dependent cytotoxicity assay. A significantly higher titer of cytotoxic antibodies to H‐2d and to H‐2k was obtained in the allogeneic and syngeneic sera respectively, after immunization with the in vivo C‐1 cells as compared to sera raised against the in vitro tumor line. Transplantation studies showed that both in vitro and in vivo C‐1 lines possess the same tumor‐associated transplantation antigen whose expression was non‐significantly reduced on the cultured cells.
Establishment of marek's disease lymphoblastoid cell lines from transplantable versus primary lymphomas
Authors: Calnek B. W. , Murthy K. K. , Schat K. A. 
Published: February 2007

AbstractSix new Marek's disease (MD) lymphoblastoid cell lines were established in vitro by cultivation in medium containing 2‐mercaptoethanol (2‐ME). Attempts using primary lymphoma cells were generally unsuccessful; only one of 28 lymphomas yielded a cell line and that one came from an experimentally immunosuppressed chicken. In contrast, two of seven low‐passage, and two of two established MD transplantable lymphomas grew readily in vitro. A sixth line was obtained using buffy coat cells from leukemic chicken. It was concluded that the use of transplantable tumor cells and a medium containing 2‐ME provided a combination highly sulted to the establishment of cell lines from MD.
Characteristics of hamster cells transformed by the combined action of chemical and virus
Authors: Hatch George G. , Balwierz Patrick J. , Casto Bruce C. , Dipaolo Joseph A. 
Published: February 2007

AbstractPretreatment of hamster cells with chemical carcinogen enhances transformation by a simian adenovirus, SA7. Such transformants were compared to cells transformed by SA7 alone for the presence of virus‐specified antigens, and for the ability to clone in soft agar and to form progressively growing sarcomas in hamsters. The SA7 “T” antigen content and the relative cloning efficiencies in agar of cell lines of both groups were similar. Some cell lines obtained by pretreatment with chemical carcinogen, however, produced a higher incidence of tumors, suggesting that the chemical carcinogen was involved in the transformation of cells by virus. A further indication that these cells differed from cells transformed by virus alone was obtained with MCA‐transformed fibroblast cell lines that were subsequently also transformed in vitro by SA7 to cuboidal (SA7 type) morphology. These MCA‐SA7‐transformed cells produced a higher incidence of sarcomas than cells transformed by virus alone, but a lower tumor incidence than the parental MCA line.
Induction of ebna precedes the first cellular S‐phase after ebv‐infection of human lymphocytes
Authors: Einhorn Lena , Ernberg Ingemar 
Published: February 2007

AbstractUsing a combination of immunofluorescence and autoradiography, we studied the appearance of EBNA and DNA synthesis in cord‐blood lymphocytes after infection with EBV derived from the B95‐8 cell line. EBNA appeared between 12 and 25 h after addition of the virus. DNA synthesis was detected in EBNA‐positive cells approximately 20 h after the appearance of EBNA. This shows that EBNA induction precedes the first cellular S‐phase and suggests that the cells have not yet entered the cell‐division cycle when EBNA appears. Little, if any, of the total DNA synthesis induced at this stage can be attributed to EBV‐mediated immunologic stimulation.