bluuebunny/crossref_metadata_2025_split huggingface dataset:
The response of Xeroderma pigmentosum cells and controls to the activated mycotoxins, aflatoxins and sterigmatocystin
Authors: Stich H. F. , Laishes B. A. 
Published: February 2007

AbstractThe activation of the mycotoxins aflatoxin B1, G1, B2, G2, aflatoxicol and sterigmatocystin by 9S fraction, microsomal preparation (105,000 × g) and supernatant (105,000 × g) of livers of several species was examined. DNA repair synthesis, chromosome aberrations and clone forming capacity were used as endpoints. Cultured fibroblasts of normal persons and DNA repair deficient Xeroderma pigmentosum patients were employed as test subjects. The activation mixtures significantly increase the chromosome breaking function, lethality and DNA damaging effect (measured as DNA repair synthesis) of aflatoxin B1, G1, aflatoxicol and sterigmatocystin. The DNA repair‐deficient XP cells respond to the activated mycotoxins with a low level of unscheduled 3HTdR incorporation as compared to that of control cells, but show a highly elevated sensitivity to the chromosome‐damaging and lethal effect of aflatoxin B1 and sterigmatocystin.
DNA repair synthesis of cultured human cells as a rapid bioassay for chemical carcinogens
Authors: San R. H. C. , Stich H. F. 
Published: February 2007

AbstractThe feasibility of detection of carcinogenic chemicals using DNA repair synthesis of cultured human fibroblasts as measured by an unscheduled 3HTdR incorporation has been explored. Of 64 chemicals tested, 29 were proximate or ultimate carcinogens, 15 were precarcinogens that required metabolic activation, 16 were non‐oncogenic compounds and 4 were of unknown carcinogenicity. All directly acting carcinogens triggered a DNA repair synthesis, whereas no unscheduled 3HTdR incorporation was observed following the application of the 16 non‐oncogenic compounds. As a rule, the precarcinogens (without metabolic activation) do not elicit DNA repair synthesis. However, longer exposures and higher concentrations of the precarcinogens 2‐AAF, aflatoxin B1 and sterigmatocystin gave unscheduled 3HTdR uptake. The results suggest the suitability of using repair synthesis as endpoint, and cultured human cells as subjects in a prescreening programme for chemical carcinogens.
Specific anti‐tumor responses by cultured immune spleen cells. II. Culture supernatants induce specific anti‐tumor cytotoxicity by non‐immune lymphoid cells in vitro
Authors: Nelson Karen , Pollack Sylvia B. , Hellström Karl Erik 
Published: February 2007

AbstractSera from tumor‐bearing mice induce specific cytotoxicity to tumor cells by non‐immune lymphoid cells (antiserum‐dependent cytotoxicity or ADC). When spleen cells from BALB/c mice bearing autochthonous or syngeneic sarcomas were cultured in vitro, culture supernatants were obtained which specifically sensitized sarcoma cells to injury in vitro by normal lymph‐node cells (LNC). Culture supernatants of spleen cells from mice whose transplanted sarcomas had been excised also induced ADC. The ADC activity resided in the mouse immunoglobulin fraction of the culture supernatants and its synthesis did not depend on the presence of theta‐positive cells. Following a brief in vivo exposure to culture supernatant with known ADC activity, LNC from non‐immune mice specifically destroyed tumor cells in an in vitro assay.
Appearance of C‐type virus‐like particles after co‐cultivation of a human tumor‐cell line with rat (XC) cells
Authors: Gabelman Norman , Waxman Samuel , Smith William , Douglas Steven D. 
Published: February 2007

AbstractA serially propagated cell line (L104) was established by co‐cultivation of a lung adenocarcinoma (L‐1) from a patient with concurrent chronic lymphocytic leukemia and XC, a non‐producer rat line, known to carry the Rous sarcoma virus (RSV) genome. Karyotype of the L104 cultures revealed predominantly rat‐like patterns; however, about 5% of the cells reacted with HLA antibodies and demonstrated human isozyme patterns. Electron microscopy of L104 cells revealed the presence of C‐type particles budding from the cell membranes and in cytoplasmic vacuoles. Virus was not detected in any of the other normal lung, lung tumor or XC cells examined after co‐cultivation with XC cells. The particles isolated from tissue culture fluids had the biochemical and biophysical characteristics common to other known mammalian C‐type particles and were serologically related to the woolly monkey virus (WMV)/gibbon ape leukemia virus (GaLV) complex. Cross‐hybridization between viral 3H‐DNA transcripts and cellular RNAs from virus‐infected cells clearly show the presence of sequences in the L104 cellular RNA related to both the GaLV/WMV group of viruses and rat viruses. Hydroxyapatite chromatography reveals however that the primate‐related sequences in the viral RNA are indistinguishable from WMV in thermal elution profile. The host range of L104 virus appears to vary greatly from WMV in being xenotropic and, in the cell lines thus far tested appears, to infect only rat cells. The virus gave positive KC but negative XC assays. Inoculation of whole cells or cell‐free supernatants into weanling hamster did not result in either solid tumors or leukemia. Co‐cultivation of appropriate cell lines may represent an approach to the detection of latent viruses in human neoplasia.
Inhibition of in vitro lymphoproliferative responses to tumor‐associated antigens by suppressor cells from rats bearing progressively growing gross leukemia virus‐induced tumors
Authors: Glaser Moshe , Kirchner Holger , Herberman Ronald B. 
Published: February 2007

AbstractW/Fu rats were injected subcutaneously with low numbers of cells from the Gross leukemia virus‐induced lymphoma, (C58NT) D, which induced transient tumor growth and regression (regressors), or with high numbers of tumor cells resulting in progressive tumor growth (progressors). Spleen cells from regressors had a significant reactivity in the mixed leukocyte tumor cell interaction (MLTI), while spleen cells from progressors were unresponsive. Similarly, the responses to the non‐specific mitogens, phytohemagglutinin and concanavalin A, were suppressed in spleen‐cell cultures of progressors. Passage of spleen cells from progressors over rayon adherence columns or pretreatment with an iron/magnet technique resulted in almost complete restoration of MLTI and mitogen responses. Addition of spleen cells from progressors depressed the MLTI of spleen cells from regressors and the mitogen reactivity of normal spleen cells. Serum from progressors also suppressed MLTI and mitogen reactivity. These data indicate that, in spleens of rats bearing progressively growing tumors, suppressor cells can be demonstrated which inhibit specific reactivity to tumor‐associated antigens and non‐specific reactivity to mitogens. The presence of suppressor cells or of inhibitory factors in the serum may contribute to the immunosuppression frequently observed in tumor‐bearing hosts.
Genetic control of oncogenesis by murine sarcoma virus moloney pseudotype. I. Genetics of resistance in AKR mice
Authors: Colombatti A. , Collavo D. , Biasi G. , Chieco‐Bianchi L. 
Published: February 2007

AbstractInjection of Moloney mouse sarcoma virus (M‐MSV) in adult mice of several inbred strains revealed that all strains except AKR are highly susceptible to M‐MSV tumor development. F1 hybrids between AKR and CBA, DBA/2 or NIH mice are as resistant (93%) as the parental AKR strain, which indicates that resistance is transmitted as a dominant character. First backcross mice to the susceptible parent show a 3:1 ratio of resistant to susceptible mice. This is the expected ratio for two segregating loci which independently confer resistance. The incidence of resistant F2 mice is somewhat lower than expected. Further support for the two‐gene hypothesis was obtained in second backcross mice. None of the major genes affecting MuLV infection (Fv‐2 and H‐2) seems to play any role in this system and no linkage was found with Thy. 1 and albino, dilute, agouti and brown markers.
Genetic control of oncogenesis by murine sarcoma virus moloney pseudotype. II. A dominant epistatic susceptibility gene
Authors: Colombatti A. , Collavo D. , Biasi G. , Chieco‐Bianchi L. 
Published: February 2007

AbstractWe have shown in the preceding paper that AKR mice are highly resistant to M‐MSV tumor development, and that resistance is transmitted as a dominant character In the present studies the tumor‐response pattern of F1 hybrids between resistant AKR and susceptible strains (C57Bl/6, BALB/c and BIOBR) following injection with Moloney mouse sarcoma virus (M‐MSV) resembles that of the non‐AKR parent. Segregation is observed in first backcross (Bcl) and F2 mice, and the segregation ratios up to Bc3 mice fit a one‐gene model. The data of triple cross hybrids suggests that this dominant susceptibility gene inhibits the phenotypic expression of M‐MSV tumor resistance in some susceptible Fv‐1bb strains as well as in their hybrids with AKR. Neither Fv‐1 nor H‐2 exerts any significant influence on this complex system.
Studies of lymphocyte stimulation by intact tumor‐cell and solubilized tumor antigen
Authors: Dean J. H. , McCoy J. L. , Lewis D. , Appella E. , Law L. W. 
Published: February 2007

AbstractBALB/c mice were rendered immune to a syngeneic SV40‐induced sarcoma by subcutaneous injection of mKSA‐TU5 tissue‐culture adapted cells. Spleen cells from immune mice were examined for tumor‐cell neutralization in the Winn assay as well as in in vitro lymphocyte stimulation assays. A microculture (200 μl) lymphocyte stimulation (LS) assay utilizing immune spleen cells was employed with mixed lymphocyte/tumor‐cell cultures (MLTC) and with papain crude soluble (CS) extracts from mKSA‐TU5 cells. Specificity in the LS assay was determined using spleen cells from mice immune to other syngeneic tumors and by soluble antigenic preparation of normal BALB/c spleen cells. The Winn assay studies demonstrated that spleen cells from mKSA‐sensitized mice neutralized mKSA tumor cells and this was corroborated by their resistance to direct tumor challenge. Positive lymphocyte transformation responses in MLTC were observed when mKSA‐TU5‐sensitized spleen cells were mixed with mitomycin‐C‐treated intact tumor cells or when papain‐solubilized antigens of mKSA cells were employed, but not with non‐immune spleen cells or with a soluble antigen from normal cells. Papain‐solubilized antigen preparations employed in in vitro assays also immunized against challenge with mKSA tumor cells. Specificity of these lymphocyte transformation reactions was demonstrated with non‐sensitized lymphoid cells or lymphoid cells from mice sensitized with a syngeneic Kirsten virus‐induced sarcoma (KA‐31) or a mineral‐oil‐induced plasmacytoma (Adj‐PC5), which failed to respond. Thus, mKSA tumor surface antigens were recognized on intact tumor cells or with microgram quantities of papain‐solubilized extracts from these tumor cells. We believe the lymphocyte stimulation assay affords a method for demonstrating the presence of tumor‐specific antigen and for monitoring further purification procedures.
Detection of virus‐specific DNA sequences by quantitative in situ hybridization during infection with SV40
Authors: Langelier Yves , Mandeville Rosemonde , Simard René 
Published: February 2007

AbstractIn situ hybridization has been used as a quantitative method to study the replication of SV40 during lytic infection. Various parameters have been defined such as fixation and denaturation of cytological preparations, concentration of complementary (3H)‐cRNA and volume of buffer used for the hybridization reaction. When all these parameters are carefully controlled, a reproducibility of ±10% can be obtained for the quantitative study of the system SV40‐monkey kidney cells (CV‐1). In this system, it is evident that the synthesis of viral DNA is not localized in a special area of the nucleus and that it is not synchronized in confluent cells. Moreover, a proportion of 20 to 30% of cells are not labelled whatever the multiplicity of infection. In SV40‐transformed cells, it was not possible to detect significantly the integrated genome due either to the small size of the genome or to the fact that the number of genome‐equivalents integrated at the same place is too low to yield a radioactivity superior to background level for long periods of exposure.
Specific anti‐tumor responses of cultured immune spleen cells III. Further characterization of cells which synthesize factors with blocking and antiserum‐dependent cellular cytotoxic (ADC) activities
Authors: Nelson Karen , Pollack Sylvia B. , Hellström Karl Erik 
Published: February 2007

AbstractSpleen cells from BALB/c mice bearing syngeneic, methylcholanthrene‐induced sarcomas were cultured in vitro. In agreement with previous observations, two tumor‐specific activities could be demonstrated in the culture supernatants: the supernatants suppressed (blocked) specific lymph‐node cell‐mediated cytotoxicity directed against the respective neoplasm and they induced specific antibody‐dependent cellular cytotoxicity (ADC) mediated by lymph‐node cells from non‐immune mice. In the present study, the effects of specific depletion or enrichment of different cell types on the ability to synthesize the blocking and ADC activities was explored. Spleen cells passed through columns of Sephadex G‐10, which removed plasma cells and macrophages, no longer synthesized factors with ADC activity though synthesis of blocking factors continued. However, lysis of Thy‐1‐positive cells with antiserum and complement did abolish the synthesis of blocking factors. Spleen cells from tumor‐bearing mice were then enriched for Thy‐1‐positive cells by selective removal of macrophages and plasma cells on G‐10 columns and of immunoglobulin‐bearing cells on anti‐mouse immunoglobulin affinity columns. This T‐cell‐enriched population synthesized blocking factors and restored blocking factor synthesis in cultures depleted of Thy‐1‐positive cells. Similarly enriched spleen cells from normal control mice did not synthesize tumor‐specific blocking factors but partially restored synthesis of blocking factor in tumor‐bearer spleen cultures depleted of Thy‐1‐positive cells.
Production of epithelial and mesenchymal tumours with rat liver cells transformed in vitro
Authors: Montesano R. , Vincent L. Saint , Drevon C. , Tomatis L. 
Published: February 2007

AbstractEpithelial‐like cells originating from the livers of 10‐day and 8‐week‐old BD rats were established in culture. The cells were treated in vitro for 1 or 4 weeks with dimethyl‐nitrosamine (DMN) or N‐methyl‐N′‐nitro‐N‐nitrosoguanidine (MNNG). Although some structural changes were observed in treated cells, it was not possible to score for morphological transformation in vitro. Newborn syngeneic rats were injected with 1.5‐2 × 106 treated or 1.5‐5 × 106 control cells at various times up to 38 weeks from the beginning of treatment with the carcinogen. Following the injection of DMN‐treated cells, a total of 32 of the 42 injected rats developed tumours, of which 17 were epithelial, 10 carcinosarcomas and 5 fibrosarcomas. Following the injection of the MNNG‐treated cells into 61 rats, a total of 30 tumours were observed, including 8 carcinomas, 9 carcinosarcomas and 13 fibroscarcomas. Tumours, mainly of the mesenchymal type, were also observed in rats inoculated with control cells but at a lower frequency. The observation of mesenchymal tumours is attributed to the presence of a mixed population of epithelial and mesenchymal cells in the original culture.
Human endometrial carcinomas serially transplanted in nude mice and established in continuous cell lines
Authors: Merenda C. , Sordat B. , Mach J. P. , Carrel S. 
Published: February 2007

AbstractThree out of five human endometrial carcinomas were successfully grafted into nude mice (BALB/c/nu/nu). Two of these tumors could be maintained by serial transplantation. The morphological characteristics displayed by the grafted tumors were comparable to those of the original carcinomas. Permanent cell lines were established from these two tumors. Reinjection of cells grown in vitro into nude mice produced nodules of identical histology as compared to original solid transplants. The influence of medroxy‐progesterone acetate on tumor growth in vivo and cell proliferation in vitro was studied. This hormonal treatment did not produce any significant effect on tumor cells, either in vitro or in vivo, for the two endometrial carcinomas. After medroxyprogesterone administration, a slight but non‐significant growth inhibition of the tumor cells in vitro was observed and the tumor transplants in vivo did not appear to be influenced. The experiments illustrate the possible use of this model for testing potential anti‐cancer agents.
Sequential in vitro reactivity of lymphocytes from melanoma patients receiving immunotherapy compared with the reactivity of lymphocytes from healthy donors
Authors: Berkelhammer Jane , Mastrangelo Michael J. , Laucius J. Frederick , Bodurtha Audley J. , Prehn Richmond T. 
Published: February 2007

AbstractA microcytotoxicity technique was used to determine the sequential in vitro reactivity against melanoma cells of lymphocytes from melanoma patients receiving immunotherapy and from healthy donors. Lymphocytes were collected every 2 weeks for 2‐3 months and were stored in liquid nitrogen until use. Preliminary studies had indicated that freezing did not affect the reactivity of lymphocytes. Lymphocytes from 10 healthy donors tested against melanoma cells exhibited substantial reactivity which showed no consistent pattern over time. Lymphocytes from 9 melanoma patients exhibited increased reactivity after immunotherapy. Patterns of reactivity against melanoma cells and against bladder carcinoma cells were similar, indicating lack of specificity for melanoma antigens. Correlations with clinical course of the disease were not apparent.
Cell‐mediated cytotoxicity to chemically‐induced rat tumours
Authors: Zöller Margot , Price Michael R. , Baldwin Robert W. 
Published: February 2007

AbstractCell‐mediated immune reactions against carcinogen‐induced rat tumours were demonstrated by the in vitro microcytotoxicity test. Lymph‐node cells from syngeneic rats immunized against individual aminoazo‐dye‐induced hepatomas or 3‐methylchol‐anthrene‐induced sarcomas were cytotoxic for cells of the immunizing tumour compared with the effects of normal lymph‐node cells. Only a low level of cross‐reactivity was detectable against target cells derived from other tumours. Conversely, lymph‐node cells from tumour‐bearing rats were cross‐reactive against a range of tumour cells, suggesting that the tumour‐bearer was sensitized against a common antigen (s) as well as the individually specific antigen associated with these tumours. Lymph‐node cells were reactive at an early time (from day 2) after tumour implantation and their cytotoxic potential persisted until terminal stages of tumour growth. Spleen cells from tumour‐bearer and tumour‐immune donors also exhibited comparable cytotoxic reactivities of the same specificity as that shown by lymph‐node cell preparations. These findings are discussed in relation to the development of cell‐mediated immune responses in the tumour‐bearing rat and in immunized rats which are capable of rejecting transplanted tumour cells.
Early onset of serum blocking in a murine melanoma model
Authors: Bray Alan E. , Holt Patrick G. , Roberts Lynne M. , Keast David 
Published: February 2007

AbstractThe early onset of serum blocking of host cell‐mediated immunity was investigated in a transplantable murine melanoma model employing two in vitro assays. One of these was based on the Takasugi and Klein cytotoxicity test; the other was a new test based on the inhibition of adherence of leukocytes to a plastic surface in the presence of tumor antigen. Both tests yielded similar results, and the adherence inhibition test was more sensitive. Blocking could be detected as early as 1 h after the inoculation of 1×107 melanoma cells. Early onset of serum blocking was also demonstrable if homogenized or tissue‐cultured tumor cells were inoculated. Serum blocking under these circumstances was initially transient, declining at 24 to 48 h, but reappearing by the 4th day after inoculation. Furthermore, a functional immune system was not required for blocking factor development in this system, as evidenced by the onset of a similar pattern of blocking activity in heavily irradiated animals.
The relationship between tumorigenicity, growth in agar and fibrinolytic activity in a line of human osteosarcoma cells
Authors: Jones Peter A. , Rhim Johng S. , Isaacs Hart , McAllister Robert M. 
Published: February 2007

AbstractThe TE‐85 osteosarcoma cell line has several of the in vitro properties of malignant cells, including colony formation in agar, but has low extracellular fibrinolytic activity and no capacity to form tumors in ATS‐treated hamsters. Some TE‐85 cell clones (clones 2, 4 and 6) have increased fibrinolytic activity but do not form tumors in hamsters. TE‐85 cells infected with mammalian transformation‐defective viruses have low (FeLV) or increased (RD‐114 virus) levels of fibrinolytic activity and do not form tumors in hamsters. TE‐85 cells either nonproductively infected with Ki‐MSV or productively infected with M‐MSV (RD‐114), have fibrinolytic activity and can form tumors in hamsters. The MSV gene(s) but not colony formation in agar or extracellular fibrinolytic activity appears to be capable of rendering TE‐85 cells tumorigenic in ATS‐treated hamsters.
Strain‐dependent expression of endogenous mouse‐tropic leukemia viruses in chemically induced murine leukemias
Authors: Odaka Takeshi 
Published: February 2007

AbstractThe effects of two chemical carcinogens, nitrosobutylurea and 7,12‐dimethylbenz‐(a)anthracene, on the expression of endogenous N‐ and B‐tropic viruses were studied. The mice used were from two inbred strains, C57BL/6 and DDD‐FVr, and from 13 partially inbred strains derived from the cross of C57BL/6 with DDD‐FVr. These mouse strains are classified into three groups by the pattern of expression of endogenous viruses in normal, aged mice: (1) negative for both viruses; (2) positive for N‐tropic virus only; and (3) positive for both viruses. Mice were given the carcinogens, and were tested at various intervals by the UV‐XC procedure for the viruses in the spleens and other enlarged organs. Irrespective of the presence or absence of leukemias, the carcinogen‐treated mice showed the same pattern of expression of endogenous viruses as that of non‐treated normal mice. It can be concluded that the activation of the endogenous viruses is dependent on the mouse strains and that the growth of the activated viruses is not a necessary step for the chemical induction of leukemias.