bluuebunny/crossref_metadata_2025_split huggingface dataset:
Alterations in chromosomal proteins in C3H/HeN mice with spontaneous primary hepatocellular carcinomas
Authors: Rodriguez Lewis V. , Becker Frederick F. 
Published: February 2007

AbstractThe chromosomal proteins from chromatins of normal and background liver and spontaneous primary hepatocellular carcinomas (PHC) of C3H/HeN mice were examined by high resolution acid‐urea and sodium dodecyl sulfate (SDS) polyacryl‐amide gel electrophoresis. Before gel analysis, the histone and non‐histone chromosomal proteins (NHCP) from the various tissues studied were separated by affinity chromatography. No qualitative or quantitative differences in histone content were detected in any of the chromatins studied. Tumor and background chromatins did, however, exhibit higher NHCP content than normal tissues. When NHCP were fractionated on SDS polyacrylamide gels, the appearance of 10 new unique NHCP, many of which were of high molecular weight, was found to accompany the manifestation of malignancy in these C3H/HeN mice. Conversely, the abundance of a number of individual NHCP decreased precipitiously in PHC chromatin; and, additionally, two high‐molecular‐weight NHCP present in normal chromatins were not detectable in background and PHC chromatin. A number of NHCP were found to be unique to each of the chromatins studied. The progressive increase in total number of NHCP in background and PHC chromatin when compared to normal chromatin suggested that such changes in NHCP might indicate progression towards malignancy. The acquisition of new high‐molecular‐weight NHCP, the loss of some high‐molecular‐weight NHCP, and the decrease in individual NHCP found for mouse PHC correlate well with findings of previous studies in other systems in which malignant transformation was induced with some agent. It appears then that changes in NHCP accompany both spontaneous and induced malignant transformation, and that such changes may reflect alterations in gene expression known to accompany malignancy.
Mouse mammary tumor virus (MMTV) antigen(s) are present on B lymphocytes of BALB/c mice
Authors: Charyulu Vijaya , Sigel M. Michael , Durden Donald L. , Lopez Diana M. 
Published: February 2007

AbstractImmunofluorescence studies using a polyvalent anti‐MMTV serum revealed the presence of MMTV antigen(s) on the surface of spleen cells from the low mammary tumor incidence mouse strain BALB/cCrgl. Upon separation of the splenocytes on nylon‐wool columns the populations of cells exhibiting positive fluorescence were nylon‐adherent. These cells were considered to be B lymphocytes by the following criteria: presence of surface immuno‐globulin (Slg), absence of Thy‐1 antigens, enhanced responses to B‐cell mitogens and decreased reactivity to T‐cell mitogens. In order to ascertain the specificity of the cell surface immunofluorescence reaction, blocking studies were performed. Immunofluorescence was blocked by preincubation of the antiserum or with purified MMTV, but not by R‐MuLV. Non‐specific binding of the anti‐MMTV to Fc receptors present on B lymphocytes was ruled out by the use of Fab′2 fragments of IgG from the various sera. Double label immunofluorescent studies with rhodamine‐conjugated anti‐mouse Slg Fab′2 fragments and rabbit anti‐MMTV Fab′2 with fluorescein‐conjugated goat anti‐rabbit Fab′2 showed the simultaneous appearance of both labels in the nylon‐adherent splenocytes. These results suggest the expression of viral polypeptide(s) encoded by an endogenous MMTV on the surface of B‐type splenocytes in mice devoid of intact viral particles.
Lymphocyte‐mediated lysis of tumor cells in vitro (ADCC), induced by serum antibodies from patients with urinary bladder carcinoma or from controls
Authors: Troye M. , Hansson Y. , Paulie S. , Perlmann P. , Blomgren H. , Johansson B. 
Published: February 2007

AbstractIgG fractions from serum of patients with transitional‐cell carcinoma of the urinary bladder (TCC), patients with carcinoma of the prostate (CC) and healthy donors (HD) were tested for their capacity to induce antibody‐dependent lymphocyte‐mediated cytotoxicity (ADCC) to tumor cells in vitro. Lymphocytes from healthy donors were selected for low natural cytotoxicity to the target cells from established cell lines of TCC or other origins. IgG was prepared by adsorption of serum to Sepharose‐bound protein A from Staphylococcus aureus and subsequent acid elution. When tested against a panel of six different target cells, most individual IgG preparations from all three donor groups contained antibodies inducing ADCC to some of the target cells. When IgG preparations from 11 untreated TCC patients were studied for ADCC induction to the TCC target T24 and the colon carcinoma HT29, cytotoxicity to T24 was, on an average, significantly higher than that to HT29. For IgG preparations from 18 TCC patients, treated with radiotherapy, a similar difference was seen but was not statistically significant. IgG preparations from 11 patients with carcinoma of the prostate and from 12 healthy donors did not show this difference. Moreover, while individual IgG preparations from untreated TCC patients were, on the average, significantly more cytotoxic to T24 than those from either of the two control groups, no such differences were seen when HT29 was the target. On the contrary, IgG preparations from patients with prostatic carcinoma were significantly more cytotoxic to HT29 than those from healthy donors. The results suggest that TCC patients develop a disease‐related humoral immune response, superimposed on a “natural” immunity to a variety of antigens on the target cells used. The nature of the antigens involved in these reactions remains to be established. However, the results are compatible with previous findings, in these patients, of a bladder‐tumor‐related cellular cytotoxicity, to a large extent caused by the patients' own antibodies.
Surface glycoproteins of normal and neoplastic glia cells in culture
Authors: Lubitz Werner , Westermark Bengt , Peterson Per A. 
Published: February 2007

AbstractTwo normal and seven malignant human glia lines grown in vitro were labelled by lactoperoxidase catalysed iodination. The labelled cell surface glycoproteins were isolated by lectin affinity chromatography and compared by SDS gel electrophoresis. The glia and the glioma lines possess a common characteristic glycopro‐tein pattern. Seven glycoproteins in the molecular weight range between 70,000 and 220,000 daltons and several minor components of low molecular weight could be distinguished. The expression of the glycoproteins was independent of the passage number or the growth conditions although the expression of the different glycoproteins showed quantitative differences for the individual cell lines. The differences found in the tumor lines were either due to an amplification or decrease in the expression of the different glycoproteins and/or their accessibility to the lactoperoxidase‐catal‐ysed labelling.
Long‐term T‐cell‐mediated immunity to epstein‐barr virus in man. IV. Development of T‐cell memory in convalescent infectious mononucleosis patients
Authors: Rlckinson A. B. , Moss D. J. , Pope J. H. , Ahlberg N. 
Published: February 2007

AbstractUnder appropriate culture conditions, EB virus infection of lymphocytes from seropositive donors leads to regression of transformation, and this was shown previously to be due to activation in a secondary immune response of T lymphocytes inhibitory for the autologous lymphoblastoid cell line. Regression can be quantified by determining the number of cells required for its expression. To investigate the development of memory T cells with EB‐virus specificity in the primary infection, a comparison was made of the capacity for regression of lymphocytes from 16 cases of infectious mononucleosis (IM) and 13 normal donors. With 9 normal seropositive donors a mean lymphocyte concentration of 4.6 × 105/ml was required to achieve 50% regression. In contrast, with 8 cases of IM tested within I week of onset, a much higher mean lymphocyte concentration (3.7 × 106/ml) was necessary. Six of these IM cases, and another not tested in the first week, were tested on several occasions between 5 and 23 weeks after onset, and showed a slight reduction in the mean cell concentration required for regression (1.5 × 1O6/ml). Six additional IM cases were tested 23–83 weeks after onset by which time the cell concentration required for 50% regression (mean = 4.5 × 1O5/ml) had reached the level shown by normal seropositive donors. Regression did not occur with lymphocytes from seronegative donors, even at the highest cell concentration. Recombination cultures of T‐cell‐de‐pleted and T‐cell‐enriched lymphocyte populations from 3 IM cases in ratios of 1:7 to 7:1 showed that the failure of regression in acute IM was not due simply to lack of sufficient numbers of T cells. The results indicate that EB‐virus‐specific memory T‐cell activity as detected by the regression test is absent in the acute phase of IM, becomes evident at low levels 5–23 weeks after onset, and reaches a maximum after about 6 months.
H‐2 associated resistance to leukaemia transplantation: Natural killing in vivo
Authors: Carlson George A. , Melnychuk David , Meeker Mary Jane 
Published: February 2007

AbstractNatural resistance in vivo was studied by injecting non‐immunized mice with leukaemia cells prelabelled with the thymidine analogue 131I‐iododeoxyuridine. There was a decrease in the survival of the leukaemia cell inoculum as determined by whole‐body gamma counting, and a failure of the leukaemia cells to survive in the spleens of mice which were not H‐2 identical with the transplant. H‐2‐associated resistance could be measured within 24 h of leukaemia inoculation and was strongest in the spleen and absent from the liver. Although all strains of mice tested were able to resist H‐2 non‐identical cells, resistance in irradiated (800‐900 R) mice was restricted to certain strains and their F1 hybrids, notably those of the C57BL family. Resistance in both non‐irradiated and irradiated mice was not due to classical immunological rejection. Mice with either genetic or induced T‐cell deficiency showed full resistance, and circulating preformed antibody could not account for the rejection observed. Treatment with silica or with 89Sr abrogated natural resistance in non‐irradiated as well as irradiated animals; these treatments had previously been shown to abolish both bone‐marrow graft rejection in irradiated mice and in vitro natural killing. Resistance against leukaemia transplantation in irradiated C57BL mice appeared to depend on Hh‐I (H‐2D) incompatibility between the host and the graft, again suggesting that bone‐marrow graft rejection, and perhaps natural killer activity, is a subset of a more general paraimmune or non‐adaptive rejection mechanism.
Carcinogenicity of dapsone in mice and rats
Authors: Griciute Laima , Tomatis L. 
Published: February 2007

AbstractDapsone (4,4′‐diamino‐diphenyl sulfone) has been tested for possible carcinogenicity in long‐term animal experiments. BDIV rats and C7BL mice received a 3.5% aqueous suspension of dapsone by intragastric intubation. Treatment was started in pregnant females during the last part of pregnancy, continued during lactation, then given to the offspring after weaning, five times a week for 104 weeks. The dose administered was 100 mg/kg to both rats and mice; total doses ranged from 10–16 g per rat and 1.2–1.4 g per mouse. Separate groups of animals received a combined treatment of dapsone with urethane or benzo (α) pyrene, to investigate the possible additive or synergistic action of dapsone with known carcinogens, as well as the possible inhibiting effect of dapsone on carcinogenesis. Unusual tumours, viz. spleen sarcomas (related to severe fibrosis of the spleen) were detected in male rats, and higher morbidity from C‐cell thyroid carcinomas was observed in treated rats of both sexes than in control rats. There was no evidence that dapsone can modify the action of other chemical carcinogens. It was noted that: (1) although the increase in the incidence of turnours in dapsone‐treated animals over that observed in untreated controls is statistically significant, the increase is relatively low; (2) the tumours appeared after lifetime treatment with maximum tolerated doses; (3) in rats, spleen sarcomas were observed mostly in males; this may indicate a possible hormone‐dependence of the observed carcinogenic effect. The present results therefore provide only limited evidence of carcinogenicity of dapsone in rats.
Protein‐A antibody‐binding (PAAB) technique for detection of tumor‐associated membrane antigen (TAMA) of lewis lung carcinoma
Authors: Veltri Robert W. , McKolanis John R. , Rockoff S. David , McIntire K. Robert 
Published: February 2007

AbstractXenoantisera were prepared in rabbits against intact paraformaldehyde‐fixed Lewis lung carcinoma (LLCa) cells and membrane solubilized proteins extracted with Triton X‐100 and 3M KCI. The antisera were analyzed for antibodies to tumor‐associated membrane antigens (TAMA) by means of a solid‐phase radioimmunoassay (RIA). The immunoassay employed 125I‐labelled Staphylococcus aureus protein A (SPA) to detect specific antibody binding to glutaraldehyde‐fixed Lewis lung tumor target cells. The protein‐A antibody‐binding (PAAB) method is rapid, sensitive and reproducible. The PAAB revealed a possible LLCa‐TAMA as evidenced by the reactivity of xenoantisera raised to LL paraformaldehyde tumor cell vaccine (TCV) and LL tumor Triton X‐I00 (TTri) and 3M KCI (TKCI) extracts of membrane preparations. The reactivity of our antisera followed linear dose‐response kinetics but the degree of reactivity decreased from anti‐TCV to anti‐TTri to anti‐TKCI respectively. The LL‐TAMA demonstrated specificity since our antisera did not significantly cross‐react with normal C57BL/6 cellular antigens or other known murine tumor‐associated surface antigens of virally and chemically‐induced tumor systems.
HLA antigens in stomach cancer
Authors: Nomura Abraham , Glober Gary A. , Terasaki Paul I. , Stemmermann Grant N. 
Published: February 2007

AbstractHLA antigens were identified for 99 Japanese patients with stomach cancer and for 222 controls in Hawaii. There were 68 patients with the intestinal / other histological type of stomach cancer and 31 patients with the diffuse type who may be genetically predisposed towards developing the disease. No significant differences in antigen frequency were noted between cases of the diffuse or intestinal/other histological type and the controls, or between the diffuse and intestinal/other type stomach cancer cases.
Space‐time clustering of Burkitt's lymphoma in East Africa: Analysis of recent data and a new look at old data
Authors: Siemiatycki J. , Brubaker G. , Geser A. 
Published: February 2007

AbstractForty cases of Burkitts' lymphoma (BL) in North Mara, Tanzania, with onset between 1971 and 1977, were analysed for evidence of space‐time clustering. Previous analyses in East Africa had produced conflicting results. The Knox method used in those analyses dichotomizes the space and time scales and does not take into account the degree of closeness. The Mantel method, a generalization of Knox's, does permit closeness between pairs of cases to enter into computations. To see whether this method could clarify matters, previously reported data sets from West Nile, Uganda and North Mara were reanalysed. Unexplained differences were found between West Nile and North Mara with respect to age, sex and temporal distributions of BL, and between the eastern and western parts of North Mara with respect to incidence. In West Nile between 1961 and 1965, there was clustering. All of the Mantel analyses and a few of the Knox analyses were highly significant (p< 0.0025). Since 1966, evidence of clustering is weak. In North Mara, there was no statistical evidence of space‐time clustering between 1971 and 1977, as there was none between 1964 and 1970. The conflicting results in East Africa are compatible with a model involving several factors which «move about», or with a single factor which is sporadic in some areas but constant in others. Alternatively, artifactual biases or coincidence may have created or wiped out the appearance of clustering. Results of space‐time clustering analyses permit little discrimination between infectious and non‐infectious etiologic hypotheses. Either one type or both may be operating.
Evidence for type‐C retrovirus production by Burkitt's lymphoma‐derived cell line
Authors: Yaniv Abraham , Gotlieb‐Stematsky Tamar , Vonsover Ami , Perk Kalman 
Published: February 2007

AbstractBurkitt's lymphoma cell line, P3HR‐1, was found to secrete virions with properties of known type‐C RNA tumor viruses. The viral particles had a buoyant density of 1.16 g/ml in sucrose gradients and contained a highmolecular‐weight RNA and an RNA‐instructed DMA polymerase. The viral polymerase was active in an endogenous reaction requiring the presence of the four deoxyriboside triphosphates and manganese ions, and was sensitive to RNase. The DNA product of the endogenous reaction specifically hybridized to P3HR‐I viral 60 to 70S RNA. Electron microscopic examination of ultrathin sections of P3HR‐I cells revealed immature, mature and budding virions typical of type‐C retroviridae. Nucleic acid hybridization assays showed no sequence homology between the genome of P3HR‐I virus and avian myeloblastosis virus, murine oncornaviruses, simian sarcoma virus or RD114 virus.
Stable bone‐marrow‐derived cell line producing transforming avian acute leukemia virus OK 10
Authors: Pfeifer Susan , Kallio Annikki , Vaheri Antti , Pettersson Ralf , Oker‐Blom Nils 
Published: February 2007

AbstractA stable bone‐marrow‐derived cell line, OK‐BM, producing transforming avian acute leukemia virus OK 10, was established. The cell line has been maintained in culture for over 4 years and 405 passages. The cells grow rapidly in suspension, have a low serum requirement, display a uniform morphology and perpetually release transforming OK 10 virus. No transforming helper virus was detected by interference assay. The cells have a chromosome complement of the chicken. Characterization of the cells indicates that they are of myeloid origin and have properties characteristic of proliferating transformed macrophages.
Retinoids inhibit the mitogenic activity of tumourpromoting phorbol esters on human lymphocytes
Authors: Abb Jochen , Deinhardt Friedrich 
Published: February 2007

AbstractThe tumour‐promoting agents 12‐0‐tetradecanoyl‐phorbol‐13‐acetate (TPA) and phorbol‐12,13‐dibutyrate (PDB)1 are potent mitogens for human peripheral blood lymphocytes. In contrast, the non‐cocarcinogenic substance phorbol lacks lymphocyte‐activating properties. Non‐toxic levels of retinoic acid (RA) or retinyl acetate (RAt) inhibit the phorbol‐ester‐induced lymphocyte proliferation. Selective inhibition of phorbol‐ester‐stimulated lymphocyte blastogenesis required the near‐concurrent addition of retinoids. Differences in the sensitivity of phorbol‐ester‐stimulated lymphocyte subpopulations to the antagonistic action of RA or RAt, respectively, suggest that the inhibitory effect of retinoids may not be due to a common mode of action. Lymphocyte cultures may provide a useful model system for studies of the mechanisms of action of both phorbol esters and retinoids.
Correlation between perchloric‐acid‐soluble serum proteins, cellular immunity and tumor‐cell burden
Authors: Hakim Anwar A. 
Published: February 2007

AbstractSeveral in vitro‐cultured neoplastic cells, particularly human mammary carcinoma and malignant melanoma cells, shed or secrete glycoproteins which are tumorspecific. These compounds contain N‐acetylneuraminic acid (NANA), and they differ from the bulk of serum proteins and glycoproteins in being soluble in perchloric acid. The present studies examined the relation between perchloric acid soluble serum proteins (PA‐proteins), and N‐acetylneuraminic acid (PA‐NANA) and the number of R3230 AdCa implanted into syngeneic Fischer rats. A graded number of R3230 AdCa cells from a mammary rat adenocarcinoma was implanted into separate groups (20 rats/group) of imbred 12‐ to 16‐week‐old female Fischer rats. At 0, 24,48, 72, 196 h, and at 6, 9, 12, 15 and 21 days after tumor cell implantation, blood was examined for protein and NANA levels, and spleen cells for migration inhibition. Vibrio cholerae neuraminidase (VCN)‐treated formalinized tumor cells were used as the antigen. Animals which received 100 R3230 AdCa cells/animal showed a progressive increase in PA‐proteins and PA‐NANA 48 h after implanting the tumor cells. The serum PA‐protein and PA‐NANA levels were time‐dependent and increased with the number of implanted tumor cells. Maximum levels were found in sera from blood drawn 196 h or later from animals which received 1,000 tumor cells/rat or more. At 72 h or more after tumor cell implantation, spleen cells from animals which received 100 or more R3230 AdCa cells per animal were inhibited on contact with VCN‐treated formalinized R3230 AdCa cells. The magnitude of inhibition increased with time and with number of implanted tumor cells. A maximum of 85% inhibition was attained with spleens from animals 196 h after implantation of 100 R3230 AdCa cell/animal, or from animals 72 h after implantation of 103 or 104 R3230 AdCa cells/animal.
Does whole‐body hyperthermia therapy involve participation of the immune system?
Authors: Roszkowski W. , Wrembel J. K. , Roszkowski K. , Janiak M. , Szmigielski S. 
Published: February 2007

AbstractThe effect of micro‐wave whole‐body hyperthermia on tumor growth and lung metastasis counts was examined in adult BALB/c mice. The effective therapy with hyperthermia prolonging mean survival time of the animals and causing tumor regression resulted in concomitant depression of anti‐tumor immunity measured in vivo. The beneficial effect of preimmunization of animals with killed tumor cells on subsequent challenge with live tumor cells was completely abrogated by hyperthermia treatment. It is postulated that this form of therapy is directly related only to heat sensitivity of tumor cells and that there is no profitable participation of the immune system in the anti‐tumor effect of wholebody hyperthermia.
Cells from chemically induced mouse sarcomas retain tumor‐specific transplantation antigenicity during prolonged passage in vitro
Authors: Walker Rondi , Hellstroöm Ingegerd , Hellström Karl Erik 
Published: February 2007

AbstractTumor‐specific transplantation antigens (TSTA) expressed by cells from transplantable lines of 3‐methyl‐cholanthrene‐induced BALB/c sarcomas were maintained over a 26‐week culture period, which represented 2–32 passages in vitro. Cells from in vitro‐passaged sarcomas were immunogenic in that they induced specific resistance in syngeneic mice to challenge with cells from the same sarcoma. They were also immunosensitive in that their outgrowth in syngeneic mice was prevented when they were mixed with lymph‐node cells from mice immunized with in vivo‐passaged cells from the respective sarcoma.