bluuebunny/crossref_metadata_2025_split huggingface dataset:
In vitro interference between low and high leukaemogenic variants of rauscher virus
Authors: Boyd Rosemary E. , Youn Jung Koo , Barski Georges 
Published: February 2007

AbstractCultures of the virus‐free P4bis line, originating from a C57B1 mouse, were infected in vitro with a “low leukaemogenic” variant (RC) of the Rauscher leukaemia virus (RV), prepared from long‐term cultures of this virus in syngeneic cells. Later, after different delays, these infected cultures (P4bis + RC) were superinfected with a highly pathogenic variant (RR) of the RV, obtained from short‐term cultures of RV extracted from spleens of leukaemic mice. Eighteen days after these superinfections with RR, supernatants of the doubly‐infected cell cultures (P4bis+RC+RR) and their corresponding controls were assayed for leukaemogenic potential by intraperitoneal inoculation into young adult BALB/c mice. The proportion of mice which had developed leukaemia by the 120th day after inoculation served for the evaluation of in vitro interference between the RC and RR virus variants. Even when the in vitro infection of cells with RC virus was followed only 1 h later by the RR superinfection, there was a significant difference between the proportion of leukaemic animals in the group inoculated with P4bis+RC+RR supernatant (56%) and that in the P4bis+RR positive control group (88%). With intervals of 12 days or 21 days between the two in vitro viral infections, the drop in leukaemogenicity of the doubly‐infected cultures became more accentuated; the longer the time interval, the greater was the interference effect. Indirect immunofluorescence tests made at intervals after infection of P4bis with RC showed a steady increase in the percentage of RV antigen positive cells up to the 3rd week after infection. The mechanism of the observed interference is discussed, and it is suggested that a straight relationship exists between the spread, horizontal and/or vertical, of the RC virus infection in the cultures and the blocking of their superinfection by the highly pathogenic RR virus.
Antibodies to Epstein‐Barr virus and cellular immunity in Hodgkin's disease and chronic lymphatic leukemia
Authors: Hesse J. , Andersen E. , Levine P. H. , Ebbesen P. , Halberg P. , Reisher J. I. 
Published: February 2007

AbstractAntibodies to Epstein‐Barr virus capsid antigen (VCA), early antigen (EA) and cellular immunity as measured by skin reactivity to keyhole limpet hemocyanin (KLH) and Brucella antigen (BA) were measured in 15 cases of Hodgkin's disease (HD) and 14 cases of chronic lymphatic leukemia (CLL) before treatment and one year later. Both groups of diseases were associated with elevated VCA and EA antibody levels when compared with 18 controls, and in both groups the mean titers were unchanged after therapy. A negative skin test to KLH was associated with a short survival in the HD group and was found more frequently in CLL patients with active disease. In the young HD patients, a higher EBV titer was found in pretreatment sera of non‐survivors compared with those who are still alive. There was no correlation, however, between tests for cell‐mediated immunity and humoral antibodies against EBV. The finding of similar titers in patients with depressed and normal skin reactivity indicates that the elevated titers are probably not the result of a non‐specifically depressed immune defense.
Cell‐mediated and serum blocking reactivity to tumor antigens in patients with malignant melanoma
Authors: Heppner G. H. , Stolbach L. , Byrne M. , Cummings F. J. , McDonough E. , Calabresi P. 
Published: February 2007

AbstractThe reactivity of human lymphocytes, separated from peripheral blood by procedures involving sedimentation through plasmagel and settling on a glass surface, on survival or growth of melanoma tumor cells is reported. Assay of reactivity was by either a colony inhibition in dilute agar (GEL) technique or a microcytotoxicity assay (MC). In 54 experiments with lymphocytes from normal donors, inhibition of melanoma cell viability, as compared to growth in medium alone, was seen 25 (46.3%) times, stimulation was observed seven (12.9%) times and no effect 22 (40.7%) times. These results were not influenced by matching of the lymphocyte and tumor‐cell donor for ABO blood group. Inhibition was seen less often, however, in tests with the GEL method than in those with the MC assay. Eighty‐two experiments assessed the effect of lymphocytes from melanoma patients on melanoma cell viability. Inhibition to an extent greater than that of normal lymphocytes tested at the same time was seen 65 (79.3%) times. There was no difference in the frequency of detection of inhibition with lymphocytes from patients with local, regional, or widespread disease, although the percentage inhibition was less in the latter group. No differences were seen between patients with clinically active versus inactive disease. Only one of five patients who were within a week of death was reactive. Reactivity was detected as frequently with allogeneic as with autochthonous melanoma target cells. Serum blocking factor (SBF), capable of inhibiting in vitro cell‐mediated reactivity to melanoma tumor cells, was assayed in serum from melanoma patients at various stages of disease. SBF was detected at some time in 30% of patients with local, 88.9% with regional, and 80.0% with widespread disease. It was found in 42.9% of those with clinically inactive and 70.6% with active melanoma. However, detection of SBF was found to fluctuate from sample to sample taken at different times during the course of disease in individual patients regardless of clinical status. The importance of sequential determinations of SBF activity for patient assessment is stressed.
Treatment of a mouse lymphoma by L‐asparaginase: Success depends on the host's immune response
Authors: Carter R. L. , Connors T. A. , Weston B. J. , Davies A. J. S. 
Published: February 2007

AbstractRegression of the L‐asparaginase‐sensitive Gardner lymphosarcoma was investigated in normal CBA mice and in CBA mice deficient in thymus‐processed lymphocytes (T cells). In normal animals, solid subcutaneous grafts of the tumour disappeared completely following one intraperitoneal injection of L‐asparaginase (50 IU) given 10 days after tumour inoculation. The local tumour was impalpable after 3 or 4 days and there was early and massive destruction of the graft though surviving tumour cells persisted in the vicinity of blood vessels for up to 24 h after treatment. These cells subsequently disappeared and there was an intense local inflammatory response dominated by macrophages. In mice deficient in T cells, the Gardner lymphosarcoma initially regressed as in the normal group but the small perivascular accumulations of surviving tumour cells did not disappear; they persisted and all the animals eventually died with local and disseminated lymphosarcoma 22–24 days later. Their recurrent tumours were invariably asparaginase‐resistant. These results indicate that, although the main effect of L‐asparaginase is the biochemical destruction of sensitive tumour cells, residual asparaginase‐resistant cells are normally destroyed by the host's immune response. In T‐cell‐deficient mice, the immune component does not operate effectively and asparaginase‐resistant tumour cells grow back and kill the animals. T cells appear to be involved in the immune response to the Gardner lymphosarcoma and some possible modes of action of T cells are discussed.
Contribution of host immunity to cyclophosphamide therapy of a chemically‐induced murine sarcoma
Authors: Moore Michael , Williams Dorothy E. 
Published: February 2007

AbstractThe contribution of host immune factors to the therapeutic effect of cyclophosphamide (CPA) on an antigenic chemically‐induced sarcoma (MCA‐2) transplanted in syngeneic mice with different immunological reactivity was investigated. In non‐sensitized mice, CPA failed to prevent survival of nascent tumour emboli comprising 105 cells. By contrast, the enhanced therapeutic efficiency of CPA against clinically detectable neoplasms or nascent tumours developing progressively from small inocula (104 cells) suggested that host sensitization may play a role in cyclophosphamide‐mediated regression of this tumour. The hypothesis was investigated by comparison of the effect of CPA treatment on palpable neoplasms growing in immunodepressed mice following wholebody irradiation (400 R) and specifically immunostimulated mice which had received irradiated (15,000 R) MCA‐2 cells, with their untreated immunocompetent counterparts. In the first group, the antitumour effect of CPA was noticeably weaker compared with that observed in normal mice, while in the second, the effect was markedly potentiated, so that palpable nodules comprising in excess of 5 × 106 cells underwent complete regression. Since the maximum level of resistance evoked by sarcoma MCA‐2 per se was of the order of 2 × 105 cells, the results indicate that pre‐immunization significantly augments the antitumour activity of CPA in this system. The specificity of the reaction was demonstrated by the failure of CPA to mediate complete regression of sarcoma MCA‐2 growing in mice previously immunized with normal muscle or an antigenically unrelated neoplasm (MCA‐7). Possible mechanisms for the synergistic activity of CPA and host immune factors in this tumour‐host system are discussed.
Oncogenic activity of N‐nitrosododecamethyleneimine in liver, glandular stomach and other tissues of NZO/B1 mice
Authors: Goodall C. M. , Lijinsky W. , Keefer L. , D'ath E. F. 
Published: February 2007

AbstractN‐nitrosododecamethyleneimine (NDMI), a new member of the alicyclic nitroso imine series, was synthetized and tested in NZO/Bl mice, as part of structure‐activity studies. Treated mice had significant incidences of liver and glandular stomach tumors, thought to represent the characteristic oncogenic activity of NDMI. There were also statistically significant increases in tumors of lung, duodenum and reticular tissues, but these tumors were common in controls. By contrast with the strong carcinogenic activity of lower members of the series towards pharynx and esophagus, NDMI produced no lesions at these sites. A synthesis for NDMI is given.
Distribution of basic azo‐dye‐binding protein in normal rat tissues and carcinogen‐induced liver tumors
Authors: Bannikov G. A. , Guelstein V. I. , Tchipysheva T. A. 
Published: February 2007

AbstractMonospecific antibodies against basic azo‐dye‐binding protein from the rat liver were obtained. An antigen identical to this protein was shown to be present in the liver, kidney, small intestine, ovary and testicle extracts of rats and also in liver and kidney extracts of mice. The concentration of this antigen was significantly reduced in the liver and kidney of rat embryos and in rats during the early postnatal period. Immuno‐fluorescence technique was employed to study distribution of the azo‐dye‐binding protein in sections of normal rat liver and liver tumors induced by 3′ ‐methyl‐4‐dimethylami‐noazobenzene. This protein was found in the hepatocytes of the central areas of the acinus but not in the hepatocytes of periportal zones. The azo‐dye‐binding protein was absent from poorly‐differentiated hepatomas, anaplastic carcinomas and from most adenocarcinomas. In all the highly‐differentiated hepatomas this protein was found to be uniformly distributed among the tumor cells. Thus the presence of azo‐dye‐binding protein in tumors seems to depend on the degree of cell differentiation.
Metabolism of the carcinogenic hydrocarbon benzo(a)pyrene in human fibroblast and epithelial cells
Authors: Huberman Eliezer , Sachs Leo 
Published: February 2007

AbstractMetabolism of the carcinogenic hydrocarbon benzo(a)pyrene (BP) to water and alkali‐soluble products was measured in cultured fibroblast and epithelial cells from human embryos. The alkali‐soluble products represented only a small fraction of BP metabolism. Fibroblasts from different organs from the same embryo metabolized similar amounts of BP, while those derived from different embryos can metabolize different amounts. The fibroblasts were divided into three groups which metabolized an average of 350, 850 and 3,400 μμmoles of water soluble products/106cells/3 days. No significant differences were found in relationship to the age of the embryos from 2.5 to 5 months. Fibroblasts from the endometrium of adult women metabolized less than embryonic fibroblasts. Cultures which contained more than 20% epithelial cells metabolized 3–25 times more BP than fibroblast cultures from the same embryo. Epithelial cells from different embryos also varied in the degree of BP metabolism and low epithelial activity was not necessarily associated with low fibroblast activity in the same embryo. It is suggested that there is a genetic heterogeneity in BP metabolism in fibroblast and epithelial cells, and that the higher activity of epithelial cells might be related to the higher incidence of carcinomas rather than sarcomas in humans.
In vivo and in vitro binding of carbon tetrachloride with nucleic acids and proteins in rat and mouse liver
Authors: Rocchi P. , Prodi G. , Grilli S. , Ferreri A. M. 
Published: February 2007

Abstract14C‐labelled carbon tetrachloride binds in vivo to DNA of mouse liver and to rRNA of rat liver if the animals have been pretreated with 3‐methylcholanthrene. A noticeable amount of radioactivity is also observed in liver proteins. In vitro carbon tetrachloride is activated by microsomes and pH 5 enzymes of 3‐methylcholanthrene‐treated animals to a metabolite which can react with DNA and polynucleotides; this effect is more evident if subcellular fractions from mouse liver are used.
Effect of 4‐N‐benzyldemethylrifampicin and of radiation therapy on rauscher viral leukemia in vivo
Authors: Okunewick James P. , Phillips Eleanore L. , Erhard Penny 
Published: February 2007

AbstractStudies were carried out to evaluate the therapeutic effects of 4‐N‐Benzyldemethylrifampicin (AF/ABP) and of radiation on the survival of mice infected with Rauscher leukemia virus (RLV). To assess this effect two parameters were employed. These were (a) the percentage of animals surviving 6 months after infection, and (b) the average survival time of the animals which died. The results indicate that administration of the drug shortly after virus resulted in a marked increase in the number of survivors, but without any lengthening of survival time among the animals which died of the leukemia. Administration of the drug 14 days after virus had no beneficial effect on either survival time or number of survivors. The effect of radiation 14 days after virus infection significantly increased the survival time, but did not materially affect the ultimate number of survivors at 6 months after the virus infection. Combined employment of radiation and the drug 14 days after viral infection did not show any significant improvement over the use of radiation alone. Reduction of viral leukemia‐related splenomegaly was also noted following both radiation treatment and drug treatment. However, no significant correlation could be drawn between this reduction in splenomegaly and the survival time or the number of survivors.
In utero tumor induction by murine sarcoma virus (moloney) in the rat. I. Biological characteristics
Authors: Vandeputte M. , Sobis H. , Billiau A. , Van De Maele B. , Leyten R. 
Published: February 2007

AbstractFemale R rats mated with an R male and inoculated in utero, after fetectomy, with murine sarcoma virus (Moloney), developed tumors. These tumors originated in the uterus and were of fetal origin. Intravenous or intraperitoneal injection of the virus induced similar tumors. Infectious virus could not be isolated from the tumor cells kept as transplantable lines or cultured in vitro. However, the presence of the MSV genome could be demonstrated by a direct rescue test. In non‐pregnant rats treated in the same way no neoplasms were recorded. The results are discussed in the light of current theories on the special immunological fetal‐maternal relationship.
Inheritance of susceptibility to friend mouse leukemia virus. X. Separate genetic control of two viruses in friend virus preparation
Authors: Odaka Takeshi 
Published: February 2007

AbstractSusceptibility of mice to viral components present in Friend leukemia virus (FLV) preparation, lymphatic leukemia virus (LLV) and spleen focus‐forming virus (SFFV), was studied by separately determining end point for infection of each component. Mice with Fv‐1n genotype were much more susceptible to LLV of N‐tropic FLV than those with Fv‐1b genotype. This difference in susceptibility to LLV was shown to be controlled by a single gene locus with the recessive allele for susceptibility. Mouse strains congenic except for Fv locus showed marked differences in susceptibility to SFFV according to their Fv genotypes; mice with Fvs genotype were much more susceptible to SFFV than those with Fvr genotype. These results indicate that the innate susceptibility to FLV in mice is under the simultaneous control of two separate gene loci, one locus (probably Fv‐1) for LLV multiplication and the other (Fv or Fv‐2) for proliferation of infected spleen cells (spleen focus formation and splenomegaly induction) as well as SFFV multiplication. All the data obtained support Lilly's interpretation for two‐gene control. Interaction of these two gene loci with respect to multiplication of the two viruses is discussed.
Antibodies against avian GS antigen in chickens infected naturally and experimentally with avian RNA tumor viruses
Authors: Ruoslahti Erkki , Vaheri Antti , Estola Timo , Sandelin Karin 
Published: February 2007

AbstractUsing a radioimmunoassay (RIA) we detected antibodies against one of the major group specific (gs) antigens of avian RNA tumor viruses in chickens with a naturally acquired leukosis virus infection or bearing Rous sarcoma virus (RSV)‐ induced tumors. The antibodies were absent in leukosis‐free animals, but appeared a few weeks after inoculation with infectious RSV. Out of 11 chickens with a natural or experimental infection, nine had demonstrable anti‐gs antibodies. Titers as high as 1:10,000 were observed in chicken sera, but these titers were lower than those in the sera of tumor‐bearing hamsters and guinea‐pigs. The RIA was about 10,000 times more sensitive in the detection of anti‐gs antibodies than the COFAL test. The chicken antibodies could be inhibited with the purified gs antigen and appeared to be of the IgG type. There would seem to be no complete tolerance in chickens at least to one of the major avian gs antigens. The significance of these results as related to the presence and nature of gs antigens in normal cells is discussed.
In situ hybridization of adenovirus RNA and DNA. II. Detection of adenovirus‐specific DNA in transformed and tumour cells
Authors: Dunn A. R. , Gallimore P. H. , Jones K. W. , McDougall J. K. 
Published: February 2007

AbstractThe method of in situ molecular hybridization has been used to detect adenovirus DNA in permissively and non‐permissively infected cells. Onset of viral DNA synthesis can be detected by this method in individual cells by 12 h after infection. Viral nucleic acid hybrids have been detected at the cytological level in adenovirus‐transformed and tumour cells.
Influence of age and 3‐methylcholanthrene on azo‐dye carcinogenesis and metabolism of p‐dimethylaminoazobenzene in rat liver
Authors: Decloitre Françoise , Chauveau Jean , Martin Michelle 
Published: February 2007

AbstractTwo groups of male Sprague‐Dawley rats of different ages received a carcinogenic diet containing 0.06% dimethylaminoazobenzene (DAB). Out of a group of 4‐ to 6‐ week‐old rats, 20% developed hepatomas 31/2 months after the beginning of the diet, and after 10 months the percentage of tumors reached 56%. Rats aged 10–11 weeks old did not present hepatomas before 6 months of DAB feeding; the yield was only 28% after 10 months of carcinogen ingestion. In control rats, in vitro DAB metabolites binding to DNA and proteins proceeding from microsomal activation of carcinogen decreased by 70% between 4 and 12 weeks; within the same time azoreductase activity remained constant. A single injection of 3‐methylcholanthrene (20 mg/kg) greatly increased binding but not azoreductase activity. Time‐effect was similar in treated and control rats. Results were discussed looking for age and methylcholanthrene effect on carcinogenesis‐DAB metabolism relationship.
Ultraviolet inactivation of murine leukemia virus and its assay in permissive and non‐permissive cells
Authors: Yoshikura H. 
Published: February 2007

AbstractThis study confirms the different titration patterns of murine leukemia viruses (MuLV) in permissive and non‐permissive cells reported by Hartley et al. (Lilly and Pincus, in press); the titration kinetics was one‐hit in the permissive host and two‐hit in the restrictive host. The following phenomena were also observed: (1) UV‐inactivation curves were nearly the same, regardless of whether the virus was titrated in permissive or restrictive cells. (2) Infection by MuLV of its restrictive host was enhanced by the UV‐inactivated homologous MuLV. (3) UV‐inactivated NB‐tropic virus propagated in N‐type cells enhanced plaque formation of N‐tropic virus in B‐type cells and not that of B‐tropic virus in N‐type cells. UV‐inactivated NB‐tropic virus propagated in B‐type cells enhanced plaque formation of B‐tropic virus in N‐type cells, but not that of N‐tropic virus in B‐type cells.
The effects of long‐term feeding of DDT to BALB/c mice
Authors: Terracini B. , Testa Maria Cristina , Cabral J. R. , Day N. 
Published: February 2007

AbstractA multigenerational study on the long‐term effects of three dose levels of DDT (2, 20 and 250 ppm in the diet) and one dose level of N‐nitrosodimethylamine (DMN) (0.0003% in the drinking water) was started in 1968. Each treatment was administered to two separate colonies of BALB/c mice. Treatment of parent mice started at 4‐5 weeks of age. The results observed in the first two generations are presented in this report. Survival in males was poor because of fighting. In females, the highest dose level of DDT produced liver‐cell tumours in 44% of the parent mice and 74% of the first generation mice, whereas no liver‐cell tumours were found in mice given the control diet, or lower dietary concentrations of DDT. Liver cell tumours did not give metastases, but grew after transplantation to syngeneic mice. The ability of DDT to induce liver‐cell tumours was identical in both colonies of mice given 250ppm DDT. Malignant lymphomas occurred in about 50% of the mice in all colonies given 0, 2 or 20 ppm DDT. In one of the two colonies given 250ppm DDT, the incidence of malignant lymphomas was 14%, whereas in the other it was 36%. The incidence of lung adenomas was not affected by DDT treatment. Tumours at sites other than liver, lymphatic system and lungs were highest in control mice and lowest in mice given 250 ppm DDT. However, no linear dose‐response was found, and the decrease was more obvious in the parental than in the first generation. A study on the combinations of tumours in mice with more than one tumour and an analysis of litter distribution of liver‐cell tumour‐bearing mice did not reveal any particular trend in the distribution of liver‐cell tumours. The quantitative aspects of tumour induction by DDT in BALB/c mice are compared with data from previous studies in mice. DMN consistently produced lung adenomas, liver blood cysts and haemangioendotheliomas.