bluuebunny/crossref_metadata_2025_split huggingface dataset:
Isolation from a transmissible lymphoid tumour (tlt) lymphoblastoid cell line of a herpesvirus similar to marek's disease virus
Authors: Nazerian K. , Lee Lucy F. , Witter R. L. 
Published: February 2007

AbstractA chicken lymphoblastoid cell line (TLT)‐6855 originally established from an avian oncornavirus‐induced lymphoma (Siegfried and Olson, 1972) was studied for the presence and expression of Marek's disease virus (MDV) genome. By nucleic acid hybridization a significant amount of MDV DNA was found in this cell line. This virus DNA, however, was not expressed in either virus‐specific intracellular or membrane antigens or the MD‐associated tumour‐specific surface antigen (MATSA). Moreover, MDV‐specific antigens could not be activated in this cell line by treatment with 5‐IdUrd. In several experiments, when chickens were inoculated with the cell line a herpesvirus was repeatedly isolated from the kidneys. This herpesvirus was antigenically similar to MDV but was low in oncogenicity for chickens.
Evidence that mulv‐induced thymic lymphoma cells possess specific cell membrane binding sites for mulv
Authors: Baird S. , Raschke W. , Weissman I. L. 
Published: February 2007

AbstractCell‐surface binding sites specific for thymotropic murine leukemia viruses were found in high concentrations on thymic lymphoma cell lines induced by this class of virus, but were detectable in much lower concentrations (if at all) in several non‐T leukemias, plasmacytomas, and normal thymocytes or spleen cells. By specific comparison, Moloney leukemia virus (M‐MuLV) binds to a lymphoma induced by M‐MuLV, but not to a thymic lymphoma induced by Gross leukemia virus (G‐MuLV); and G‐MuLV binds to an AKR lymphoma but not to the M‐MuLV‐induced lymphoma. The material which binds to these T‐lymphoma membrane sites is input virus, rather than a contaminant which copurifies with virus. Autoradiographic analysis demonstrates that a high proportion of T‐lymphoma cells possess binding sites, whereas only a rare cell in the thymus binds murine leukemia virus to the same degree. We raise and discuss the hypothesis that each T lymphoma induced by thymotropic leukemia viruses may represent the clonal descendants of the few rare cells in the normal thymocyte population which also bind these viruses.
Column separation of viral capsid antigen (vca)‐positive cells from vca‐negative cells in an epstein‐barr virus (ebv)‐producing lymphoid line
Authors: Dalianis Tina , Klein George , Andersson Birger 
Published: February 2007

AbstractVirus producing, VCA (viral capsid antigen)‐positive cells could be selectively removed from Epstein‐Barr virus (EBV)‐carrying, virus‐producer P3HR‐1 cultures by two different methods of column passage. In the first, the virus‐producing cells were covered with human EBV antibody and subsequently passaged through anti‐human‐Ig columns. In the second method, untreated P3HR‐1 cells were allowed to pass through columns of EBV receptor‐positive cell lines or, as controls, EBV receptor‐negative cells. The majority of the VCA‐positive cells were selectively removed by both techniques. The second method involves the attachment of EBV‐producer cells, known to accumulate viral envelope material in their plasma membrane, to EBV receptors. In view of recent evidence indicating an association between EBV and complement receptors, human and mouse complement were tested for their ability to block this attachment. Fresh mouse and human complement regularly exerted blocking activity, whereas heat‐inactivated human serum did not block. Heat‐inactivated mouse serum did block occasionally, but the effect was more irregular than with fresh mouse serum. Trypsin treatment of the EBV‐receptor column abolished its ability to retain VCA‐positive cells.
Genetics of murine sarcoma virus (msv)—induced tumors in akr mice: Evidence that late progressing and early regressing tumors are controlled by different genes
Authors: Colombatti A. , Chieco‐Bianchi L. , De Rossi A. , D'andrea E. , Collavo D. 
Published: February 2007

AbstractThe genetics of late appearing MSV tumors showing a progressive growth pattern in AKR mice was investigated. The late MSV tumor response in F1 hybrids depended on the genetic background of the non‐AKR parent. Within the 4‐month observation period following virus injection, (CBA × AKR)F1 (DBA/2 × AKR)F1, and (NIH × AKR)F1 developed progressing MSV tumors, which exhibited latency and growth behavior comparable to that seen in AKR mice. (BALB × AKR)F1, (B6 × AKR)F1, and (B10BR × AKR)F1 mice did not show any late MSV tumors. In contrast to early regressing M‐MSV tumors, whose development is independent of Fv‐1 genotype, late MSV tumor progression is largely a function of this gene, since all late tumors which appeared in (B10BR × AKR) × AKR were observed in Fv‐1n homozygous mice. H‐2k haplotype is a further factor in the occurrence of late MSV tumors, at least in (B6 × AKR) × AKR mice. In crosses of AKR with Fv‐1 compatible mice, tumor appearance was strongly associated with inheritance of AKR‐MuLV, and MSV recovered from late tumors of first back‐cross animals appeared to be a new pseudotype with the endogenous AKR‐MuLV. It is suggested that the host genetic control in both early and late MSV tumors is exerted mainly on the helper component of the leukemia‐sarcoma complex.
Morphological transformation of early passage Golden Syrian Hamster embryo cells derived from cryopreserved primary cultures as a reliable in vitro bioassay for identifying diverse carcinogens
Authors: Pienta R. J. , Poiley J. A. , Lebherz W. B. 
Published: February 2007

AbstractCryopreserved primary cultures of golden Syrian hamster embryo cells were used as the source of target and feeder cells for establishing an in vitro carcinogenesis bioassay. The primary culture giving the best overall response in a pretest before freezing gave positive results in 20 consecutive experiments when retested with 3‐methylcholanthrene after cryopreservation, indicating that pretested cryo‐preserved cultures can serve as a source of susceptible target cells in an in vitro carcinogenesis bioassay. Similarly prepared and cryopreserved cultures served satisfactorily as feeder cells. Susceptible positive cultures were used to test a large number of carcinogenic and non‐carcinogenic chemicals in this system. The results showed a very high positive correlation (90.8%) between morphological transformation and the reported carcinogenic activity of the chemicals. Transformation was not observed when cells were treated with a few carcinogens that may not be metabolized to their active forms by early passage hamster embryo cells. N‐2‐acetylaminofluorene transformed cells only when tested in the presence of hamster liver micro‐somes. No false positive results were obtained when non‐carcinogens were bioassayed, nor was spontaneous transformation observed in control cultures treated with medium alone, 0.2% dimethylsulfoxide or other solvents. Cultures derived from morphologically transformed colonies arising after treatment of cells with several known carcinogens were tumorigenic in vivo, confirming the correlation of morphological transformation with tumorigenicity and the validity of altered morphology as an in vitro criterion for carcinogenicity in vivo.
Cellular and humoral anti‐tumor immune responsiveness in chickens bearing tumors induced by avian sarcoma virus
Authors: Wainberg M. A. , Yu M. , Schwartz‐Luft E. , Israël E. 
Published: February 2007

AbstractA systematic comparison was undertaken of the respective abilities of normal chicken embryo fibroblast (CEF) cells, Rous sarcoma virus (RSV)‐ transformed CEF cells, avian Rous sarcoma (RS) tumor cells and murine RS cells to serve as targets and antigen donors in various assays for the detection of cellular and humoral anti‐tumor immunity in chickens bearing tumors induced by Rous sarcoma virus. As measured by a cytotoxicity procedure, avian and murine RS cells were more susceptible to the killing effects of sensitized lymphocytes than were transformed CEF which in turn were more reactive than normal CEF. In contrast, sera from tumor‐bearing animals were able to stain by indirect immuno‐fluorescence only the avian RS and transformed CEF cell types. Extracts of both transformed CEF cells and avian RS cells but not normal CEF were equally effective as inhibitors of migration of peritoneal exudate cells derived from tumor‐bearing animals. Transformed CEF were found to produce far higher quantities of transforming virus progeny than avian RS cells, although the latter were apparently able to synthesize defective viral particles. These data indicate the significant variations which may occur under experimental conditions, depending on the types of assays and target cells employed.
Immunogenicity of solubilized tumor antigen extracted from P1798 murine lymphoma cells or isolated from tumor‐bearer ascites fluid and reactivity with anti‐thy‐1.2 antiserum
Authors: Gordon William C. , Baechtel F. Samuel , Goetz Gregory , Prager Morton D. 
Published: February 2007

AbstractSolubilized antigen was prepared from P1798 lymphoma cells by sonication, 3 M KCI extraction, or isolated from the ascites fluid of syngeneic tumor‐bearing BALB/c mice. Antigen was detected and quantitated by its ability to block activity of anti‐P1798 serum raised in syngeneic mice, as assayed by cytotoxic and indirect immunofluorescence tests. It was established that the reaction was immunologically specific as the P1798 antigen did not inhibit the binding to L1210 lymphoma cells of antisera raised against L1210 in syngeneic DBA/2 or allogeneic BALB/c mice. Vaccination of BALB/c mice with different subcellular fractions of sonicated antigen or with ascites fluid resulted in protection against a live P1798 challenge with results comparable to those obtained using iodoacetamide‐modified tumor cells. Solubilized antigen prepared by each of the three methods eluted from a Bio‐Gel A5m agarose column exclusively in an early peak that had a molecular weight estimated to be greater than 2×106. This column‐fractionated antigen was shown to cross‐react with antiserum raised against Thy‐1.2 antigen, which is present on P1798 cells. The purified P1798 antigen sedimented at 200,000 g and was shown to protect syngeneic mice in immunoprophylactic tests.
Immunologic responses to a murine mammary adenocarcinoma. I. Passive transfer of immunity by sera from tumor‐bearing mice
Authors: Yamamura Yasuhiro , Virella G. , Haskill J. S. 
Published: February 2007

AbstractDBA/2 mice bearing a syngeneic mammary adenocarcioma T1699 produced high levels of tumor‐specific antibody, detected by indirect immunofluorescence and subsequently identified as the IgG2a subclass. Tumor‐bearer sera passively administered to normal recipients protected the animals from subsequent challenge with T1699 tumor cells but not from challenge with a non‐cross‐reacting syngeneic tumor, SaD2 fibrosarcoma. Administration of sera prior to tumor challenge was found to be more effective than treatment after the challenge. The protective effect of sera appeared to parallel both antibody titers and appearance of concomitant immunity; however, sera absorbed with T1699 cells, with the indirect fluorescent antibody titers reduced more than 100‐fold, conferred an almost identical level of protection. Immune suppression of serum recipients before serum transfer abolished the effect, suggesting that protection depended on a cellular immune response by the host in addition to the possible protective effect(s) of humoral antibody.
Alpha‐1 antitrypsin (AAT) and alphafoetoprotein (AFP) in sera of patients with germ‐cell neoplasms: Value as tumour markers in patients with endodermal sinus tumour (yolk sac tumour)
Authors: Talerman A. , Haije W. G. , Baggerman L. 
Published: February 2007

AbstractSerum alphafoetoprotein (AFP) and serum alpha‐1 antitrypsin (AAT) were determined in 24 patients with germ‐cell neoplasms of the gonads and extragonadal sites and in two patients with hepatocellular carcinoma. In the majority of the patients serial determinations were performed. All seven patients with testicular seminoma and four patients without evidence of active disease had normal levels of serum AAT and AFP. The remaining 13 patients with germ‐cell neoplasms had tumours containing endodermal sinus tumour (yolk‐sac tumour) elements. All these 13 patients had elevated levels of serum AFP and the levels were high or very high in most cases. Nine of these 13 patients had raised serum AAT, although the elevation above normal levels was only slight in a number of cases. When serial determinations were performed serum AAT levels frequently followed the pattern of serum AFP levels, but the AAT levels were frequently within normal limits and therefore the interpretation of the results was difficult, and much less reliable as compared with those for serum AFP. The elevation of serum AAT levels following the recurrence of the tumour was found to occur much later and was much less marked than elevation of serum AFP, which occurred early, showed a large rise and was a reliable marker of tumour recurrence in patients with germ‐cell neoplasms containing endodermal sinus tumour elements. It is therefore considered that, although there is good evidence that serum AAT is produced by endodermal sinus tumour elements, serum AAT is not a useful monitor of disease activity in these patients, especially when compared with serum AFP, the value of which is well recognized. Serum AAT may be a useful tumour marker in patients with hepatocellular carcinoma, and this aspect should be investigated further.
K cell mediated lysis of cultured colon carcinoma and urinary bladder carcinoma cells induced by monospecific antisera against carcinoembryonic antigen (CEA) and two CEA‐related normal glycoproteins
Authors: Hammarström S. , Troye M. , Wahlund G. , Svenberg T. , Perlmann P. 
Published: February 2007

AbstractAntibody dependent lymphocyte (K cell) mediated lysis of tumor cells in vitro was used to assay for cell surface associated carcinoembryonic antigen (CEA) and two CEA‐related normal tissue components, “normal glycoprotein” (NGP) and biliary glyco‐protein I (BGP I). Three tumor cell lines were used as target cells. These were HT‐29, colon carcinoma, T‐24, urinary bladder transitional cell carcinoma and Mel‐1, malignant melanoma. To induce lysis we used the IgG‐fraction of specific rabbit and monkey anti‐CEA sera and of specific rabbit anti‐NGP and anti‐BGP I sera, respectively. Purified human lymphocytes were used as effector cells. HT‐29 was efficiently killed by low concentrations of rabbit anti‐CEA and less efficiently by monkey anti‐CEA. T‐24 and Mel‐1 were not lysed by anti‐CEA. HT‐29 and T‐24 were lysed by low concentrations of anti‐BGP I. In contrast only HT‐29 was lysed by anti‐NGP. Only a fraction of the tumor cells was killed by the different antisera although kinetic studies showed that the lytic reaction was complete well before the end of the eighteen hour incubation period used in the assay. Anti‐CEA and anti‐BGP I gave 30–40% corrected lysis of HT‐29. With anti‐NGP the corresponding figure was 10–20%.
Comparative studies on adult donor lymphocytes infected by EB virus in vivo or in vitro: Origin of transformed cells arising in co‐cultures with foetal lymphocytes
Authors: Rickinson A. B. , Finerty S. , Epstein M. A. 
Published: February 2007

AbstractCo‐cultures were set up between equal numbers of mononuclear cells from the blood of EB virus‐infected individuals, either acute IM patients or healthy seropositive adult donors, and foetal cord blood mononuclear cells of the opposite sex. The cell lines arising in the co‐cultures were of mixed origin, with foetal cells predominating in many cases. In contrast, when mononuclear cells from seronegative adult donors were first infected with EB virus in vitro and then 5 to 12 days later co‐cultured with a large excess of foetal cells of the opposite sex, the cell lines which arose were almost exclusively derived from the adult donor despite the fact that a small minority of the virus‐infected adult cells released infectious virus capable of transforming the co‐cultivated foetal cells. The experiments suggest that EB virus‐infected cells present in the blood of IM patients and seropositive donors do not possess the capacity for unlimited in vitro growth shown by seronegative adult donor lymphocytes experimentally infected with the virus.
Familial leukemia and inherited chromosomal aberration
Authors: Cervenka Jaroslav , Anderson Renner S. , Nesbit Mark E. , Krivit William 
Published: February 2007

AbstractThis communication contributes a family with 12 cases of cancer and two cases of leukemia. Chromosomal analysis was performed on three occasions, 9 months apart, In unaffected first‐degree relatives, we have demonstrated high frequency of tetraradial figures: in parents, 1:243 mitoses, and in all first‐degree relatives, 1:328 mitoses. The rate of chromosomal breakage was moderately elevated in comparison with carefully matched controls, mainly in father (6.17), mother (4.01) and one sister (4.07). G‐banded and C‐banded karyotypes revealed no structural chromosomal abnormality in relatives of leukemic children. This family is one of five leukemic families investigated. Analogous methods of chromosomal analysis have been employed in all, but chromatid exchange figures and elevated chromosomal breakage were detected only in the presently reported pedigree. It has been postulated that in this family there exists a possible relation between increased incidence of chromatid exchange figures and increased tendency to leukemia.
Competition for cytotoxic immune capacity against A ‘syngeneic’ mouse tumour distributed at two sites
Authors: Chassoux D. , Maclennan I. C. M. , Munro T. R. 
Published: February 2007

AbstractNormal C3H mice will develop fatal ascites after the intraperitoneal injection of as few as 100 BP8 cells. However, mice can be immunized so that they can specifically reject an intraperitoneal challenge of 107 of these C3H‐derived tumour cells. This paper investigates a phenomenon in which the capacity of immunized mice to reject an intraperitoneal challenge of tumour cells is lost between two to seven days after tumour cells have been given subcutaneously. Investigation of this temporary loss of capacity to reject the intraperitoneal challenge of tumour suggests that this might be due to the attraction of cytotoxic immunity to the site of subcutaneous injection. The possibility that this phenomenon is due to blocking factors, tumour overload, suppressor cells or enhancing antibody has been investigated but experimental results are given which do not favour these explanations.
Tumor regression after intralesional injection of emulsified trehalose‐6,6′‐dimycolate (cord factor): Efficacy increases with oil concentration
Authors: Yarkoni Eliyahu , Meltzer Monte S. , Rapp Herbert J. 
Published: February 2007

AbstractInjection of emulsified trehalose‐6,6′‐dimycolate (TDM), a mycobacterial glycolipid, into transplants of an established, syngeneic murine fibrosarcoma induced complete regression of tumor in a number of animals. The number of animals in which tumor regressed completely depended on the amount of oil in the emulsion. The anti‐tumor activity of the TDM emulsion containing the highest concentration of oil was equivalent to that of living BCG.
Expression of viral protein P27 in avian sarcoma virus‐transformed mammalian cells and helper‐dependent rescue of rous sarcoma virus
Authors: Popovič M. , Svoboda J. , Suni J. , Vaheri A. , Pontén J. 
Published: February 2007

AbstractAvian sarcoma virus (ASV)‐transformed mammalian cells, known to be either virus‐producing, virogenic or non‐virogenic, were tested for viral gene products: for p27 by radioimmunoassay and for group‐specific (gs) antigens by the complement fixation test. Clones of B77 virus‐producing RBI rat tumour cells had p27 concentrations ranging from 10 to 80 ng/mg cellular protein; the poor virus‐producing clone had the lowest levels of p27 and gs antigen. Treatment of the clones with halogenated pyrimidines, BrdUrd and IdUrd, had little effect. Virogenic mammalian cell lines XC, LWC3 cells and human 118MG/EH cells transformed by the Prague, Schmitt‐Ruppin and Engelbreth‐Holm strains of ASV, respectively, were analyzed for p27, for gs antigens, tumour induction in chickens and focus formation after fusion of the X‐ray‐irradiated cells with chicken fibroblasts. Concentrations of p27 and of gs antigens and tumour induction by intact cells were approximately the same in both rat XC cells and human 118MG/EH cells. Treatment with BrUrd or IdUrd increased the level of p27 in the latter cell line. On the other hand, rat LWV3 cells had no detectable p27 or gs antigens but their tumourinducing activity in chickens was fifty‐fold higher. Non‐virogenic rat TWERC cells, transformed by the Prague strain of RSV, had low detectable levels of p27 and of gs antigens. These cells did not produce tumours in chickens or foci when fused with chicken fibroblasts. The only, and very effective, way of rescuing RSV from TWERC cells was the fusion of TWERC cells with RAV‐1‐preinfected cells. After inoculation of a mixture of 2×104 cells treated with inactivated Sendai virus, tumours were induced in 50% of the chickens. Both the host‐range and virus neutralization studies indicated that the rescued TWERC virus had avian subgroup C specificity and not the specificity of the helper virus. The rescued virus had a one‐hit titration pattern in duck embryo fibroblasts, indicating that the virus was non‐defective for infection and transformation of these cells.
Incomplete viral genome in a non‐virogenic mouse tumour cell line (RVP3) transformed by prague strain of avian sarcoma virus
Authors: Svoboda J. , Popovič M. , Sainerová H. , Mach O. , Shoyab M. , Baluda M. A. 
Published: February 2007

AbstractTwo cell lines, RVP3 and RVA4, derived originally from mouse tumours induced by the Prague and Schmidt‐Ruppin strain of RSV, respectively, were studied. All attempts failed to induce infectious virus production in RVP3 cells by fusion with chicken fibroblasts even if the cells were infected with avian leukosis viruses. Also, attempts to rescue the viral genome by transfection were unsuccessful. RVP3 cells harboured 31–45% of the viral genome sequences, as was shown by molecular hybridization, and therefore they were designated cryptovirogenic. The tumour cell line RVA4 did not contain any detectable viral sequences. The significance of the detection of the incomplete Rous virus genome sequences in mammalian cells is discussed.
RNA‐reverse transcriptase complex from cultured human myeloma‐leukemia cells
Authors: Sawada Hiroyoshi , Tashima Masaro , Nakamura Toru , Uchiyama Takashi , Sagawa Kimitaka , Takatsuki Kiyoshi , Uchino Haruto , Ito Yohei 
Published: February 2007

AbstractA high molecular weight RNA‐reverse transcriptase complex in the culture media of peripheral leukocytes obtained from two Japanese patients with myeloma‐leukemia was detected by demonstration of a 3H‐uridine peak and a peak of DNA polymerizing activity banding at a density of 1.15–1.19 g/ml. The enzyme in the complex was able to utilize poly(rA) · d(pT)10 or poly (rC) · d(pG)12–18, but not poly (dA) · d(pT)10 or (dT)12–18, as template‐primers. The sucrose density sedimentation analysis revealed that RNA in the complex sedimented at a location of approximately 50s and 20–30s.