bluuebunny/crossref_metadata_2025_split huggingface dataset:
Cellular immunity to human urinary bladder carcinoma. I. Correlation to clinical stage and radiotherapy
Authors: O'Toole C. , Perlmann P. , Unsgaard B. , Moberger G. , Edsmyr F. 
Published: February 2007

AbstractAs tested in vitro in a microcytotoxicity assay, purified peripheral blood lymphocytes from patients with carcinoma of the urinary bladder have a specific destructive effect on primary cultures of autologous and allogeneic tumour target cells, as well as on bladder carcinoma cell lines. No specific effect is observed on cells derived from normal tissues or tumour cells of other histogenic origin. Serial tests made on individual patients have shown that the incidence of lymphocyte cytotoxicity varies with the clinical staging of the disease. While 88% of patients with localized tumours, stage T1‐T2, have a response before treatment, the corresponding figure for those with T3‐T4 stage tumours is 41%. Local radiotherapy in tumour doses of 3,500–8,400 R either destroyed or diminished existing cytotoxicity. The response remained depressed as long as irradiation was continuous. After therapy all patients with T2 stage tumour redeveloped a response, usually within 7 days. While 80% of T3 patients had cytotoxicity at this time, the incidence in T4 cases was 50%. In some T3 and T4 patients no response redeveloped after radiotherapy or conversely a response was induced by the treatment. Patients lacking cytotoxicity after therapy invariably had distant metastases and/or large residual tumours detected within 3 months. Weak post‐therapy cytotoxicity was usually accompanied by development of recurrent tumour or distant metastases during a 9‐month observation period; this was not seen in patients whose post‐irradiation cytotoxicity was strong during this time. In the absence of viable tumour the post‐irradiation response seems to wane with time. Evidence for this comes from patients tested 1‐10 years after radiotherapy. Here the presence of cytotoxic lymphocytes was usually associated with viable tumour. The majority of patients clinically tumour free had no response. Maintenance of lymphocyte cytotoxicity, as measured in this system, therefore appears to require the presence of either viable tumour or tumour‐derived material. This cytotoxicity is inhibited however by large viable tumours and also metastases.
Cellular immunity to human urinary bladder carcinoma. II. Effect of surgery and preoperative irradiation
Authors: O'Toole C. , Perlmann P. , Unsgaard B. , Almgård L. E. , Johansson B. , Moberger G. , Edsmyr F. 
Published: February 2007

AbstractA group of patients with carcinoma of the urinary bladder treated by local resection or total cystectomy were studied in regard to tumour specific cytotoxicity of their lymphocytes. Only one in a group of five, treated by transurethral resection, had cytotoxic lymphocytes when tested within 1 yr after surgery. This patient alone in the group had a residual growing tumour at the time of testing. Total cystectomy in five patients led to complete disappearance of cytotoxicity in two and almost complete disappearance in a third. One patient was negative both before and after surgery. These four patients were free of macroscopic tumour when tested 4–8 weeks after surgery. The patient whose lymphocytes were strongly cytotoxic after surgery had suspected residual tumour foci in the urethra at 5 weeks after operation. Preoperative irradiation of the tumour produced a systemic response which was maintained after total cystectomy in three of four patients for at least 3–7 months. The patient who was negative when tested after cystectomy was in poor general health. All four patients were clinically tumour‐free at the time of post‐operative lymphocyte sampling. These results favour the interpretation that the maintenance of a cellular response to this tumour is dependent on the presence of tumour material in the body. Stimulation of the immune response measured may be produced or maintained by localized primary tumours or by material released systemically as a result of tumour necrosis.
Effect of host strain and H‐2 type on spontaneous regression of murine leukemia
Authors: Dietz Michael , Rich Marvin A. 
Published: February 2007

AbstractThe susceptibility of 14 mouse strains to a regressing and a conventional strain of Friend leukemia virus was studied. A comparison of leukemia incidence and latent period to leukemia development demonstrated that, for all mouse strains, the susceptibility to both viruses was the same.Leukemia regression occurred in 10 of the 12 mouse strains susceptible to regressing Friend virus (RFV). Regression of leukemia in mice inoculated with conventional Friend Virus (CFV) occurred primarily in those mouse strains homozygous for the H‐2k allele. RFV‐induced leukemia regression was observed in mice homozygous for H‐2a, H‐2q, H‐2s, H‐2d, and H‐2k. The H‐2 locus does not appear to be a determinant in leukemia regression.
DNA repair following exposure of human lymphocytes to 4‐nitroquinoline‐1‐oxide
Authors: Jacobs Allan J. , O'Brien Richard L. , Parker John W. , Paolilli Patricia 
Published: February 2007

AbstractThe carcinogen 4‐nitroquinoline‐1‐oxide (4NQO) is known to induce unscheduled DNA synthesis when administered to a number of mammalian cells. This effect was demonstrated in human lymphocytes. The degree of unscheduled DNA synthesis was found to be correlated with time and with 4NQO concentration. 4NQO was demonstrated to inhibit DNA replication in actively dividing lymphocytes.In addition, human lymphocytes treated with the mitogen phytohemagglutinin‐M (PHA‐M) were allowed to incorporate bromodeoxyuridine (BUdR) into one chain of DNA in replicative synthesis. Following this, the BUdR was removed and the cells were incubated with 4NQO and tritiated thymidine. DNA isolated from these cells was fractionated by cesium chloride gradient centrifugation into a BUdR‐containing fraction of replicated DNA and a light fraction of DNA which had not yet replicated when incubated with BUdR. 3H‐thymidine was found in the heavy fraction of DNA from 4NQO‐treated cells which contained no newly replicated DNA. It was concluded that this represented repair synthesis.
Cellular reactions against Burkitt lymphoma cells. I. Colony inhibition with effector cells from patients with Burkitt's lymphoma
Authors: Hewetson John F. , Golub Sidney H. , Klein George , Singh Surjit 
Published: February 2007

AbstractA micro‐assay colony inhibition (CI) test has been developed for studying cell‐mediated reactions against lymphoblastoid target cells. The assay makes use of the ability of the target cells, but not the effector cells, to grow in discrete colonies in semi‐solid medium. Peripheral blood leukocytes from patients with Burkitt's lymphoma and nasopharyngeal carcinoma, and from controls, were used as effector cells in this assay against the Burkitt lymphoma derived lymphoblastoid cell line P3HR‐I. Only five of the 62 samples from patients with these diseases inhibited colony formation by more than 30%. When phytohemagglutinin‐stimulated cells were used in the CI test, colony formation was greatly reduced. CI activity of PHA‐stimulated cells appeared to be correlated to the degree of stimulation, as determined by incorporation of tritiated thymidine. Preliminary data indicate that lymph‐node cells, but not peripheral leukocytes, tested against autochthonous and allogeneic cell lines, are capable of significant colony inhibition.
Cellular reactions against Burkitt lymphoma cells. II. Effector cells obtained by allogeneic stimulation in mixed leukocyte cultures
Authors: Golub Sidney H. , Hewetson John F. , Svedmyr Erik A. J. , Singh Surjit 
Published: February 2007

AbstractA new colony inhibition test has been employed to detect effector cell activity of normal human leukocytes after stimulation with allogeneic cells. The responding cells in one‐way mixed leukocyte culture show strong activity in this assay, and effector cell activity is at least in part antigenically specific. Specificity of the CI activity was found to be dependent on the dose of effector cells added and the nature of the stimulator cell used. Stimulation with allogeneic leukocytes yielded a response which was strongly restricted in its CI activity to the appropriate target cell, while stimulation with Burkitt lymphoma‐derived cell lines resulted in CI activity which was cross‐reactive with other BL‐derived cell lines. These data indicate the presence of cross‐reactive antigens on two LCL lines derived from Burkitt lymphomas which can sensitize normal leukocytes to yield a cytotoxic response.
Spontaneous appearance of cytopathology and rat C‐type virus (WF‐1) in a rat embryo cell line
Authors: Bergs Victor V. , Pearson Gary , Chopra Harish C. , Turner Willie 
Published: February 2007

AbstractAn established line (WF‐1) of Wistar/Furth rat embryo cells spontaneously developed cytopathology after about 2 years in vitro. The cellular changes appeared within 5–7 days after subculturing of the cultures and consisted of altered rounded and fusiform cells with dark, prominent nuclei. These changes increased after removal of bovine amniotic fluid from the culture nutrient but were not apparent if the cultures were subcultured at 3–4 day intervals. Most of the altered cells were viable, but they failed to multioly under the conditions employed. Electron microscopical examination of the WF‐1 cells revealed numerous extracellular and budding C‐type virus particles. The cells, when inoculated into rats, produced progressively growing fibrosarcomas which also contained C‐type particles. Initially the WF‐1 virus failed to produce visible effects in the REL line of Sprague‐Dawley rat embryo cells. Several months later, upon concentration and banding at 1.16 g/cm3 in a sucrose gradient, low‐titered infectious virus of about I TCID50 per 10,000 virus particles was recovered. This produced foci of predominantly viable rounded cells in REL cultures similar to those induced by the C‐type virus (RMTDV or BV‐1) previously isolated from chemically induced rat mammary tumors. Immune BV‐1 serum prevented the WF‐1 virus from producing these cellular effects. Tests for properties characteristic of murine leukemia viruses (gs‐1 antigen, gs‐3 interspecies antigen, and the XC reaction) were negative indicating that the WF‐1 virus was not a mouse virus. These observations suggested that upon prolonged cultivation in vitro the WF‐1 rat embryo cells spontaneously liberated a rat C‐type virus related to the BV‐1. Whether the cell‐altering and partially lethal effects produced by the WF‐1 virus were due to some cytopathic C‐type particles in a generally non‐cytopathic population or reflected the concentration of only one biological type of particles needs further study.
Bias in an African cancer registry
Authors: Templeton A. C. , Bianchi Alexis 
Published: February 2007

AbstractThe returns of the Kampala Cancer Registry, Uganda, which registers cases diagnosed in the whole of the country, have been analysed to discover if changes in patterns of registration have occurred over a 20‐year period. The age distribution has remained surprisingly constant. Comparison with the best data available in the country, from a relatively small area adjacent to the main teaching hospital, suggests that in the first years of study deeply placed tumours were only half as likely to be diagnosed as more superficially placed lesions. Registration of cancer in females was about half as efficient as in males. Registration bias has diminished as social patterns have evolved and as hospitals have become more accessible but it still considerable. Similar changes occurred in all regions in Uganda which vary markedly in social, ethnic and climatic backgrounds and it is highly likely, therefore, that a similar bias is operating in cancer studies elsewhere in Africa.
Réctions d'hypersensibilité retardée avec des lignées de cellules tumorales humaines cultivées in vitro chez des malades porteurs de tumeurs cérébrales malignes
Authors: Febvre H. , Maunoury R. , Constans J. P. , Trouillas P. 
Published: February 2007

AbstractLes cellules cultivées in vitro à partir de tumeurs cérébrales humaines se comportent comme des antigènes forts qui permettent de caractériser l'état d'immunité cellulaire des patients atteints d'affection néoplasique. Cette antigénicité croisée, fortement évocatrice de la présence d'un antigène tumoral commun, différent de l'antigène de transplantation associé aux tumeurs, paraǐt pouvoir ětre utilisée dans une certaine mesure dans le diagnostic précoce du processus néoplasique, au měme titre, par exemple, que la cuti‐réaction tuberculinique, mais ne peut préjuger en aucune manière de l'évolution de la maladie. Ces résultats demandent à ětre confirmés sur une plus large échelle. Quoi qu'il en soit, l'isolement de l'antigène et l'expérimentation in vitro nécessaires à l'interprétation des faits observés en clinique se poursuivent.
Embryonic antigen expression in chemically induced rat hepatomas and sarcomas
Authors: Baldwin R. W. , Glaves Dorothy , Vose B. M. 
Published: February 2007

AbstractEmbryonic antigens were detected at the surface of carcinogen‐induced rat hepatoma and sarcoma cells by their reactivity in membrane immunofluorescence tests with sera from multiparous rats. These sera also showed complement‐dependent cytotoxicity for plated target tumour cells, and lymph‐node cells from multiparous rats were similarly cytotoxic when compared with the effects of cells from normal virgin age‐matched controls. These embryonic antigens could be demonstrated on embryonic cells but not on cultured normal adult rat liver cells or lung fibroblasts. The tumour‐associated embryonic antigens were shown to be common to both tumour types and so differ from the individually distinct antigens associated with these carcinogen‐induced tumours which play a major role in immune rejection responses.
Tumorigenicity and agglutination by concanavalin a of Chinese hamster cells and their hybrids
Authors: de Micco Ph. , Berebbi Monique 
Published: February 2007

AbstractIn a previous work we studied the relationship between tumorigenicity and the karyological data of a somatic hybrid derived from two lines of Chinese hamster cells, of which one was tumorigenic and the other had lost its tumorigenicity. In this work, we show the relationship between the two factors previously studied and the agglutinating ability of these cells by Concanavalin A. In order to do this, we first derived a coefficient α to express quantitatively the agglutinating ability with Concanavalin A. This coefficient was a function of the latency period, the time necessary to reach the platform level of agglutinating ability and the degree of agglutination of the cells in presence of a fixed quantity of cells and Concanavalin A. The highly tumorigenic DC‐3F cell line gave a high a value, the non‐tumorigenic DC‐3F/ADX/Aza had a much lower value and the overall hybrid population (HyC) had an intermediary value for α. The clones and the tumors studied show a correlation between the value and the tumorigenicity of the cells involved. The karyological analysis showed, inter alia, a possible correlation between the presence of a marker M2 and a particularly low a coefficient.
Incidence of group‐specific (gs) antigens of type C tumor viruses in spontaneous neoplasms of BALB/cCr mice
Authors: Peters Robert L. , Spahn Gerard J. , Rabstein Louise S. , Turner Horace C. , Huebner Robert J. 
Published: February 2007

AbstractThe incidence of species‐specific gs antigen of the C‐type RNA tumor viruses in the spleen and tumor tissues of BALB/cCr mice (mostly female) with spontaneous neoplasms was determined by the complement fixation (CF) test. Spleen extracts from mice with neoplasms of the reticuloendothelial system (all involving the spleen) were much more frequently positive for gs antigen than spleens of age‐ and sex‐matched normal mice. Among mice with non‐leukemic, solid tumor malignancies the incidence of gs antigen in spleen tissue was elevated, but not significantly, above that found for mice of comparable age, which had no histologic evidence of malignancy. Extracts of tumor tissue from these same tumor‐bearing mice revealed variable incidences of positive reactions exceeding those found for normal connective tissues from the same tumor‐bearing mice. Cell lines derived from solid tumors had uniformly higher rates of gs antigen incidence when compared to the donor tumor or spleen tissues.
The transformation of BHK 21 hamster cells by simian virus 40
Authors: Wiblin C. N. , Macpherson I. A. 
Published: February 2007

AbstractAlthough BHK 21 cells remain refractory to direct transformation by SV40 virus even at multiplicities of infection as high as 104 PFU per cell, transformed derivatives may be produced by cocultivation of the untransformed cells with monkey cells infected with SV40 virus.The characteristics of a cloned SV40‐transformed line (C13/SV) have been studied. The cells showed several of the properties of BHK 21 cells transformed by other oncogenic viruses. High‐passage variants of the line (C13/SV‐M) metastasized from the primary tumour that they induced in hamsters. Metastatic foci were the result of dissemination of the cells, and not due to the release of infectious SV40 virus from implanted cells.Comparisons between the in vitro and in vivo growth properties of C13/SV and C13/SV‐M cells did not reveal a correlation with metastasizing ability. The C13/SV‐M cells also retained those properties of transformed cells that are probably associated with surface alterations, although the SV40‐specific transplantation antigen may be partially absent or masked in these cells.
The SV40 S antigen; A carcinoembryonic‐type antigen of the hamster?
Authors: Berman Leonard D. 
Published: February 2007

AbstractIn addition to hamster tumor cells induced or transformed by SV40, hamster anti‐SV40 S (Surface) antiserum also reacted with non‐SV40‐exposed cell lines spontaneously induced (BHK 21) or transformed by heterologous oncogenic DNA and RNA viruses in the indirect membrane fluorescent antibody test. The antiserum titered equally with both BHK and SV40‐transformed cells and the reaction could be absorbed with either of these cell lines, or with hamster embryo. The antiserum also reacted with early hamster embryo cells, although various organ cells from late fetuses, newborns and adults were negative. Mouse cell lines spontaneously induced (BALB/c‐3T3) or transformed by SV40 and adenovirus 12 were also non‐reactive. The results suggest that the antigen in question is a hamster somatic antigen present during embryonic life and derepressed in lines of actively growing cells.
Inhibitory effects of BCG on adenovirus tumorigenesis: Dependence on administration schedule
Authors: Ankerst Jaro , Jonsson Nils 
Published: February 2007

AbstractThe cumulative incidence of tumours was registered in CBA mice inoculated with adenovirus type 12 when newborn and treated with BCG in different ways during the latency period. A single subcutaneous dose of BCG at 3–4 weeks of age had a preventive effect, while no prevention could be recorded after a single BCG dose at 9 weeks of age or eight BCG injections at intervals of 1 week. Sera obtained during the latency period were tested for capacity to block lymph‐node cell‐mediated tumour immunity. Blocking activity was detectable in pooled serum of the mice which had been infected with BCG at 9 weeks of age, already at 10 weeks, i.e. 1 to 2 weeks before the appearance of palpable tumours. Blocking activity could not be demonstrated in a serum pool from control mice until 14 weeks after virus inoculation, at which time sera from mice inoculated with BCG at the age of 3 weeks were still negative. The results indicate that the effect of BCG upon tumour development is dependent upon the point of time of BCG treatment and further suggest that BCG treatment initiated at a stage when serum blocking activity is already present can further stimulate the production of blocking factors and tentatively promote tumour development.
Ultrastructural localization of concanavalin a receptors in normal and SV40‐transformed hamster and rat cells
Authors: Bretton R. , Wicker R. , Bernhard W. 
Published: February 2007

AbstractThe distribution of receptor sites for concanavalin A at the surface of normal and SV40‐transformed hamster cell cultures has been studied with the electron microscope after application of the Con A‐peroxidase method. Both normal and transformed cells show a strongly positive reaction. Although it has not been possible in single cases to distinguish with certainty between normal and transformed cells, the cell‐coat reaction of the majority of malignant hamster cultures shows a striking tendency to be more unevenly distributed than in normal controls. This remains true for cultures after relatively few or after many passages, and for lines derived from in vivo induced tumors or from in vitro transformed cultures. This observation confirms results obtained in this laboratory from hamster cells transformed by Polyoma virus or Adenovirus 12. However, in a few rat fibroblast cultures transformed by SV40 virus, we have so far not seen any difference in the cell‐coat reaction between normal and transformed cells. The possible reasons for the more irregular distribution of the cell‐coat reaction product of transformed hamster cells compared to normal controls are discussed.
Mechanism of resistance of Yoshida sarcoma to nitrogen mustard. II. Further evidence for suppressed transport of nitrogen mustard
Authors: Inaba Makoto , Moriwaki Ayako , Sakurai Yoshio 
Published: February 2007

AbstractSensitivity of Yoshida sarcoma lines resistant to nitrogen mustard (HN2) was not enhanced by pretreatment in vitro with SH‐blocking agents such as 2,2′‐dithiodi‐pyridine. This fact seems to indicate that content of cellular sulfhydryl groups did not play a great role in acquisition of resistance to HN2. No difference was observed between the sensitive and resistant lines in retention rate of HN2 bound to DNA of the cells during incubation of the cells in an HN‐free medium. These results suggested no considerable difference in the ability to repair DNA in both lines.Further evidence was added for suppressed transport through the cell membranes of the resistant lines. Damage to cell membranes was proved by vital staining when a concentration of SH‐blocking agents in the pretreatment reached a certain level, and the binding rate of HN2 to DNA of the resistant lines was recovered almost to the same level of the sensitive line by this pretreatment.However, the binding rate of the sensitive line was not changed by pretreatment with the blocking agents at any concentrations.