bluuebunny/crossref_metadata_2025_split huggingface dataset:
Effect of bnu treatment on leukaemogenesis in lethally irradiated akr mice restored with bone‐marrow and spleen cells
Authors: Shisa H. , Legrand E. , Daculsi R. 
Published: February 2007

AbstractThe leukaemogenic effect of N‐butyl‐N‐nitrosourea (BNU) was studied in normal and thymectomized AKR mice which were lethally irradiated and restored with either bone‐marrow (BM) or spleen cells from (AKR × AKR/T1ALD)F1 donors. In some instances T1ALD thymic cells were added to the restorative inoculum. It was possible to determine the origin of the leukemic cells by the metacentric marker chromosomes of T1ALD. The T‐ or B‐cell characteristics were further ascertained by the cytotoxicity test for θ antigen and the EAC rosette test. All leukaemias whether thymic (TLS) or extra‐thymic (ETL), developed from donor bone‐marrow or spleen cells and never from the injected thymic cells. In non‐thymectomized animals BNU increased the percentage of TLS and shortened their latency. Most of TLS which occurred after BNU treatment of BM‐restored mice were θ‐negative whereas the majority of TLS which occurred in controls and in spleen‐restored animals were θ‐positive. This suggests that during their maturation process BM‐derived T precursors transit through a θ‐negative compartment. This compartment does not reach a similar size during the maturation process of the spleen‐derived precursors. Adding thymic cells to the restorative inoculum enhanced leukaemogenesis and suppressed θ‐negative TLS in BM‐restored mice. Thymectomized mice, restored either by BM or spleen, had a low incidence of ETL which was not significantly increased by BNU treatment except in the case of mice restored with spleen cells. The leukaemic cells of one ETL were θ‐positive whereas all the other leukaemias had no detectable T or B marker. The percentage of ETL was higher in thymectomized mice treated with BNU alone than in those previously subjected to irradiation and restoration. These results strongly suggest that a θ‐negative T precursor could be involved in extra‐thymic leukaemogenesis but the possible involvement of a B precursor cannot be ruled out unless experiments are carried out with specific markers of T‐ and B‐cell sub‐classes.
The presence of herpesvirus saimiri genomes in virus‐transformed cells
Authors: Fleckenstein Bernhard , Müller Ingrid , Werner Jürgen 
Published: February 2007

AbstractHerpesvirus saimiri (H. saimiri) ‐transformed cells contain both types of viral DNA, unique L‐DNA and highly repetitive H‐DNA. DNA from spleen and lymph‐node autopsies of two tumor‐bearing marmoset monkeys contained 0.14–0.75 / viral L‐DNA and 0.115–1.08 / H‐DNA. This amount of H‐DNA would be equivalent to the presence of 14–130 M‐genomes per diploid tumor tissue cell. Six virus‐transformed lymphoid cell lines, two of them virus‐producing, contained 0.69–2.27 / H‐DNA and more than 0.72–1.95 / L‐DNA. These concentrations of H‐DNA sequences correspond to 83–274 M‐genome copies per lymphoid tissue culture cell. The majority of viral genomes in transformed non‐producer lymphoid cell lines appeared to be defective, since part of the L‐sequences present in virions were found to be deleted in the genome copies of transformed cells. There was a relative excess of repetitive H‐sequences in all transformed cells in regard to the ratio of H‐DNA/L‐DNA in M‐genomes of H. saimiri virions.
Augmentation of natural cytotoxic reactivity of mouse lymphoid cells against syngeneic and allogeneic target cells
Authors: Herberman Ronald B. , Nunn Myrtel E. , Holden Howard T. , Staal Steven , Djeu Julie Y. 
Published: February 2007

AbstractThe levels of natural cell‐mediated cytotoxicity against tumor cells in young BALB/c and BALB/c nude mice could be augmented by inoculation of a variety of mouse tumor cells or of mouse thymocytes. In older mice with low levels of spontaneous cytotoxic reactivity, inoculation of tumor cells led to rapid appearance of cytotoxicity. This augmented cytotoxicity reached a peak 3 days after inoculation, and then declined rapidly. The specificity of the augmented cytotoxicity appeared to be the same as that seen with natural cell‐mediated cytotoxicity. The detected antigens were restricted to mouse tumor cells and thymocytes, and were absent on cells from other species. The effector cells after boosting also had the same cell surface characteristics as the natural cytotoxic effector cells, being non‐adherent, non‐phagocytic, and only weakly sensitive to treatment with anti‐theta serum plus complement. In addition to this boosting by mouse tumor cells, marked increases in the levels of cytotoxicity were caused by a variety of murine viruses, including murine sarcoma virus and lymphocytic choriomeningitis virus. These effector cells also had the same properties as those seen with natural cytotoxic effector cells. The results indicate that the levels of natural cell‐mediated cytotoxicity in conventional and athymic BALB/c mice can be consistently and rapidly boosted by inoculation with tumor cells or viruses. This should provide a valuable tool for better understanding of the mechanisms responsible for the expression of natural cytotoxicity and its relevance to in vivo resistance to tumor growth.
Tumor cell locomotion—a factor in metastasis formation? influence of cytochalasin b on a tumor dissemination pattern
Authors: Hagmar B. , Ryd W. 
Published: February 2007

AbstractThe influence of Cytochalasin B (CB) on TA3 ascites tumor cells was studied in vivo in order to assess whether CB‐induced cell paralysis would affect the transplantation behavior of the cells and in particular tumor distribution after IV cell infusion (“experimental metastases”). Tumor cell pre‐treatment with CB (1 μg/ml) did not alter the SC or IV transplantability of TA3 cells. Pre‐treatment with 10 μg/ml CB, in contrast, consistently increased the incidence and number of extra‐pulmonary tumor takes from IV transfused cells. The amount of pulmonary tumors was not significantly altered. SC transplantability was not affected by 10 μg/ml CB. The importance of cell mobility and cell surface topography for tumor cell nidation in vessels is discussed.
Felv epidemiology in los angeles cats: Appraisal of detection methods
Authors: Gardner Murray B. , Brown John C. , Rongey Robert W. , Dworsky Ruth , Charman Howard P. , Gilden Raymond V. , Stephenson John R. , Huebner Robert J. , Hauser Duane E. , Diegmann Frank , Howard Edwin 
Published: February 2007

AbstractWe investigated the reliability of the fixed cell indirect fluorescent antibody (IFA) peripheral blood smear test as an index of systemic infection with FeLV. Positive results with this test were found to correlate well with detectable FeLV p30 antigen in bone‐marrow smears by IFA, in serum and tissue by competition immunoassays, and with type‐C particles in bone marrow or spleen by electron microscopy. Most cats with lymphoma, anemia or infectious peritonitis were positive for FeLV and showed a poor or absent antibody response to FeLV p30, gp70, and FOCMA antigens. Most older cats with lymphoma, carcinoma, or sarcoma were negative for FeLV expression and also lacked these FeLV‐related antibodies. Detectable immunologic response to FeLV p30 and gp70 proteins and a high‐titered FOCMA antibody response were generally restricted to certain healthy cats exposed to FeLV. Antibody to endogenous RD‐114 viral p30 and gp70 was not detected in any of a large number of feline sera tested. The prevalence of FeLV‐related diseases and immunologic responses to FeLV in healthy cats was directly correlated with the degree of FeLV exposure. By using the IFA blood smear and FOCMA antibody tests one can monitor the horizontal spread of FeLV in multi‐cat households and accurately predict the FeLV disease susceptibility or resistance of individual cats in such environments.
Epidemiology of Hodgkin's disease in the young
Authors: Gutensohn Nancy , Cole Philip 
Published: February 2007

AbstractMany features of Hodgkin's disease (HD) among adolescents and young adults suggest that it has an infectious etiology. However, the proposal that HD is a contagious disease which can be transmitted by patients or their close contacts has not been substantiated. An alternative infectious disease model is suggested by analogy with paralytic poliomyelitis (PP). For both diseases, the peak age of incidence is delayed as living conditions improve. For both, increased risk is associated with higher social class and small family size. Like PP, HD may be a rare manifestation of a common infection with the probability of disease development increasing as age at infection is delayed. This analogy is supported by the report that the risk of HD is higher for persons who had a low frequency of childhood infectious diseases. If this model is valid, HD patients represent no hazard to their contacts. However, the incidence of HD among young adults may increase in the coming decade because of the current high standard of living and small family size.
A comparative study of the localization of CEA and NCA2 in cancerous and normal gastrointestinal tissues
Authors: Burtin P. , Sabine M. C. , Chavanel G. 
Published: February 2007

AbstractThe histological localization of CEA in gastrointestinal tissues was re‐evaluated after absorption of anti‐CEA antiserum with NCA2, another normal antigen cross‐reacting with CEA. This absorbed antiserum showed clearly the presence of CEA in colonic tumors and some non‐cancerous colonic mucosae, obtained even from non‐cancerous patients. In contrast, some of the gastric adeno‐carcinomas we studied were stained very weakly by absorbed anti‐CEA antiserum, althouth non‐absorbed antiserum (or serum absorbed with NCA alone) labelled them strongly. The same difference in reactivity between both antisera was observed in intestinal metaplasia. The localization of NCA2 was studied with a specific antiserum, previously absorbed with CEA and NCA. NCA2 was found to be a noromal cytoplasmic and mucus‐associated antigen of gastrointestinal tissues. It was present also in fetal stomach and colon. Sections of gastric and colonic tumors as well as intestinal metaplasia of gastric mucosae always reacted brilliantly with absorbed anti‐NCA2 antiserum.
Cell kinetics and immunogenicity of lymphoma cells treated with 5‐(3,3‐dimethyl‐1‐triazeno) imidazole‐4‐carboxamide (DIC) in vivo
Authors: Silvestrini R. , Testorelli C. , Goldin A. , Nicolin A. 
Published: February 2007

AbstractA cycle of treatment with antineoplastic compounds may alter the immunologic properties of experimental tumors leading to an increased survival of syngeneic hosts as compared to that observed with the original parental tumors. However, a loss of growth potential in drug‐treated tumors might account for this preferential rejection by syngeneic or by allogeneic animals. In the present study the cell cycle kinetics of parental (L1210 and L5178Y) and DIC‐altered leukemic cells (L1210/DIC; L5178Y/DIC) has been evaluated by the establishment of labelled mitosis curves. The in vitro DNA synthesis and cell loss were also investigated. The experimental results indicate that no significant differences in the above properties were present for parental and corresponding drug‐treated leukemic sublines. Immunodepressed allogeneic mice were more resistant to lymphoma challenge when inoculated with the DIC‐sublines than with the parental lines. On adoptive transfer of immune lymphocytes there was increased survival of allogeneic animals challenged with DIC cells, attributable to an additional immune response to DIC‐induced antigens. Thus, parental or DIC‐tumors showed similar tumorigenic characteristics, and the increased allogeneic host survival to DIC‐cell challenge may be attributed to an additional immune response of the animal against DIC‐induced antigens.
Immune response of athymic nude mice to papovavirus SV40 tumor‐associated antigens
Authors: Tevethia Satvir S. , Waneck Gerald , Tevethia Mary J. 
Published: February 2007

AbstractThe requirement of T cell functions in the induction of immune response to SV40‐specific transplantation rejection antigen and intranuclear tumor antigen was studied using athymic nude mice. The results obtained indicated that virus‐immunized athymic nude mice were unable to reject SV40 tumor cell challenge, and sensitized lymphocytes capable of inhibiting tumor growth in vivo could not be demonstrated in the spleens of virus‐immunized mice. Athymic nude mice bearing tumors induced by virus‐free SV40‐transformed BALB/c cells failed to develop antibodies to intranuclear T antigen. Athymic nude mice also failed to respond to viral antigens. Thus it can be concluded that T cell functions are required in the induction of cellular immune response to SV40‐specific transplantation rejection antigen and in humoral immune response to SV40‐specific T antigen and virion antigen.
Immunologic responses to a murine mammary adenocarcinoma. II. Monocyte effector activation by humoral factors
Authors: Yamamura Yasuhiro 
Published: February 2007

AbstractSera from DBA/2 mice bearing a syngeneic T1699 mammary adenocarcinoma not only induced specific antibody‐dependent cellular cytotoxicity (ADCC) mediated by monocytes (and/or macrophages) but also armed (activated) such effector cells into specific killer cells in vitro. Removal of specific anti‐tumor antibody (IgG2a subclass) by absorption with T1699 cells abolished the ADCC activity at the level of target cell coating but did not alter the level of effector‐arming activity. Fractionation on Sephadex G‐20 indicated more than one factor capable of inducing specific monocyte‐mediated lysis of target cells in vitro, including immune complexes, free IgG2a 7S antibody (ADCC), and another factor(s) with a molecular weight very close to that of 7S immunoglobulins.
Loss of specific natural cell‐mediated cytotoxicity with absorption of natural antibodies from serum
Authors: Akira D. , Takasugi M. 
Published: February 2007

AbstractWhen effector cells from most individuals are tested directly against a number of target cells for cell‐mediated cytotoxicity, most of the reactivity is non‐selective. This apparent non‐selectiveness is a result of specific activity against multiple antigens on target cells by each effector suspension. The specific reactions can be demonstrated through competitive inhibition of natural cell‐mediated cytotoxicity. The specific inhibition of cytotoxicity by competitor cells directed our attention toward the determination of specificity to the effector cell surface. Natural cell‐mediated cytotoxicity was decreased when effector cells were treated with proteolytic enzymes or low pH and regained when these cells were incubated in serum, suggesting an antibody on cell surfaces of the effector cell. Reconstitution of trypsinized effector cells with absorbed serum resulted in selective loss of cytotoxicity against the absorbing cell. To determine the role of the effector cell and the role of antibodies in natural cell‐mediated cytotoxicity, effector cells from two different persons were reconstituted in the same absorbed sera. The selective pattern achieved was similar. When effector cells from the same individual were reconstituted with two different sera absorbed in the same way, the selective pattern achieved showed greater differences. We concluded that natural antibodies loosely attached to effector cells provided the specificity of natural cell‐mediated cytotoxicity.
Differential induction of Epstein‐Barr virus‐related antigens in heterokaryon cultures
Authors: Yamamoto K. , Osato T. 
Published: February 2007

AbstractDifferent patterns of induction of Epstein‐Barr virus (EBV)‐related antigens were observed in heterokaryons produced by Sendai virus‐mediated fusion of producer and non‐producer human lymphoblastoid cells with various other cell types. EBV‐related early antigens (EA) and viral capsid antigen (VCA) could obviously be induced in heterokaryons between producer cells (P3HR‐1 and QIMR‐WIL), normally expressing these antigens at very low frequency, and human FL or HeLa cells. Positive cells were detected as early as 3 h after fusion and there often followed a rapid increase in positive cells. In contrast, in heterokaryons between non‐producer cells (Raji and NC‐37) and FL or HeLa cells, only EA but not VCA was induced. EA induction was also evident in fusion of human lymphoblastoid cells with monkey cells (Vero) but with mouse cells (L‐M (TK−) C11D and MCB‐2) no EBV induction occurred. The EBV induction in heterokaryons was significantly enhanced by 5‐iododeoxyuridine treatment.
ESTROGEN AND PROGESTOGEN CYTOSOL RECEPTORS IN HUMAN BREAST CARCINOMA
Authors: May‐Levin F. , Guerinot F. , Contesso G. , Delarue J. C. , Bohuon C. 
Published: February 2007

AbstractThe authors have studied Estrogen (RE) and Progestin (RP) cytosol receptors in 379 human breast carcinomas: 281 tumors suitable for surgery, 26 pseudo‐inflammatory tumors, 52 metastases and 20 recurrences. They have used an exchange technique with estradiol for RE and a synthetic compound, R 5020, for RP. The results point out that high rates of RE correlate with post‐menopausal women and high rates of RP with pre‐menopausal women. Tumours are considered receptor‐positive when the binding sites concentration exceeds 100 fmoles/g tissue. Using this as a base 32% of the tumors are RE and RP negative. Considering only the positive tumors, 54% contain both receptors, 31% only RE and 15% only RP. The percentages are also given in terms of the hormonal state of the patients. The results are discussed in terms of Mc Guire's hypothesis that both receptors are necessary to obtain a positive response to hormonal therapy. Correlation between histology and receptors is also discussed.
Intra‐tumour host cells of transplanted rat neoplasms of different immunogenicity
Authors: Moore Keith , Moore Michael 
Published: February 2007

AbstractThe nature of host‐derived cells present in serial transplants of five tumours of variable immunogenicity in syngeneic NW rats was investigated. Single‐cell suspensions obtained by tumour disaggregation in papain‐collagenase‐DNase (PCD) mixture were quantitatively analysed for cells with Fc receptors by formation of erythrocyte‐antibody (EA) rosettes; for cells with receptors for the third component of complement (C3) by formation of erythrocyte‐antibody‐complement (EAC) rosettes; for macrophages by the uptake of polystyrene particles and/or phagocytosis of membrane‐bound EA rosettes and for T cells by means of rabbit anti‐rat thymocyte serum (ATS). In addition, the total host cell content of two neoplasms (MC40A and SP22) was determined by immunofluorescence analysis of tumours grown in (NWxPVG/c) F1 hybrids, using NW anti‐PVG/c antiserum. There was close correspondence between the host cell content of these tumours as determined by immunofluorescence and summation of total EA‐RFC and T lymphocytes, indicating the probability that EA‐RFC were of host, rather than tumour, origin. This latter population consisted of macrophages and non‐phagocytic Fc+ cells and these, together with T cells, constituted the major infiltrative components. Host cells were most evident in the two neoplasms (MC40A, MC57) which were immunogenic, where macrophages, non‐phagocytic Fc+ cells and T lymphocytes were present in approximately equivalent proportions. (Total host cells: 42% and 45% respectively.) For the nonimmunogenic tumours (AAF 57, SP1 and SP22) host cells accounted for ± 15% of the enzyme‐dispersed suspension. However, analysis of cellular infiltration as a function of time after injection of cultured tumour cells revealed that the macrophage content of MC40A, AAF 57 and SP22 was greatest when the tumours first became clinically manifest and thereafter rapidly declined to the levels observed in serial transplants. EA‐RFC were represented almost wholly by macrophages in AAF 57 and SP22, whereas in MC40A the declining macrophage population was replaced by non‐phagocytic Fc+ cells, the precise identity of which was not established. The results indicate that cellular infiltration of established neoplasms correlates with their immunogenicity; that this host cell component comprises non‐phagocytic Fc+ cells and T cells as well as macrophages; but that the macrophage content is significantly greater when tumours are first palpable than at later stages of development, even in neoplasms which evoke no transplantation immunity.
Bovine leukemia virus specific antibodies among French cattle. I. Comparison of complement fixation and hematological tests
Authors: Levy D. , Deshayes L. , Guillemain B. , Parodi A.‐L. 
Published: February 2007

AbstractComplement fixation (CF) and hematological studies were performed on 517 cows living in normal conditions in different geographical areas of France. The animals belonged to three different categories: (1) multiple or single case herds, in which lymphosarcomas had been detected in the past five years. (2) Leukemia free herds of high risk regions. (3) Leukemia free and apparently unexposed herds. Positive animals were found with both methods in the first two categories but not in the third. Persistent lymphocytosis and CF antibodies were more frequent in leukemia than in exposed but leukemia free herds. Approximately 2 times more animals were found positive by serologic than by hematologic tests. The mean geometrical titer of CF antibodies was higher in lymphocytotic than in normal animals and highest in lymphosarcomatous cows. Persistent lymphocytosis was first detected in 3‐years‐old animals whereas 22% of younger cows were positive in the CF test.
The metabolic activation of 7‐methylbenz(a)anthracene: The induction of malignant transformation and mutation in mammalian cells by non‐K‐region dihydrodiols
Authors: Marquardt H. , Baker S. , Tierney B. , Grover P. L. , Sims P. 
Published: February 2007

AbstractFour different dihydrodiols derived from 7‐methylbenz(a)anthracene have been tested, together with the parent hydrocarbon, for their ability to induce the in vitro malignant transformation of mouse M2 fibroblasts and mutations in V79 Chinese hamster cells. In the transformation tests with the non‐K‐region dihydrodiols, the 3,4‐diol was the most active dihydrodiol tested and the 8,9‐diol was also more active than 7‐methylbenz(a)anthracene itself; the 1,2‐diol showed only slight activity. The K‐region dihydrodiol, the 5,6‐diol, which cannot be directly metabolized to a vicinal diol‐epoxide, was inactive. These differences in biological activity were similar to those apparent in the results from the mutagenicity tests. The data support the general hypothesis that non‐K‐region dihydrodiols, which can be metabolized to vicinal diol‐epoxides, are important in the metabolic activation of the carcinogenic polycyclic hydrocarbons and, when taken together with other results, indicate that 3,4‐dihydro‐3,4‐dihydroxy‐7‐methylbenz(a)anthracene is most probably involved in the metabolic activation of 7‐methylbenz(a)anthracene presumably following conversion into the related diol‐epoxide, 3,4‐dihydro‐3,4‐dihydroxy‐7‐methylbenz(a)anthracene 1,2‐oxide.