bluuebunny/crossref_metadata_2025_split huggingface dataset:
Cell‐mediated reactivity to antigens shared by moloney‐virus‐induced lymphomas (LSTRA) and certain 3‐methylcholanthrene‐induced mouse sarcomas
Authors: Hellstrom I. , Hellstrom K. E. , Zeidman L. , Bernstein I. D. , Brown J. P. 
Published: February 2007

AbstractSpleen cells (SC) both from BALB/c mice whose primary Moloney sarcoma virus (MSV)‐induced sarcomas had spontaneously regressed and from normal, untreated BALB/c mice, were co‐cultivated for 5 days with mitomycin‐C‐treated LSTRA cells; LSTRA is a BALB/c Moloney lymphoma which shares cell surface antigens with MSV‐induced sarcomas. These SC, referred to as CMR and CU cells, respectively, were shown to be cytotoxic to LSTRA cells in 3 h 51Cr‐release assays; CMR cells showed, in most cases, the greatest lytic activity against LSTRA targets. The same SC were also reactive, in 20‐h microcytotoxicity and 51Cr‐assays, against target cells from a variety of transplanted sarcomas induced by 3‐methylcholanthrene (MCA) in BALB/c mice. The highest reactivity was seen when CMR or CU cells were tested against target cells from sarcoma lines that expressed an NB‐ecotropic MuLV cross‐reacting serologically with Moloney virus. Reactivity against isotope‐labelled tumor cells expressing MuLV‐associated cell surface antigens could be competitively inhibited by adding unlabelled tumor cells expressing such antigens. Finally, Winn assays were performed in which CMR cells strongly inhibited the outgrowth of cells from three sarcoma lines that express the NB‐ecotropic MuLV. There was less but significant inhibition of cells from some other MCA sarcomas, either negative for the expression of MuLV‐associated antigens or expressing the N‐ecotropic endogenous BALB/c MuLV. CU cells enhanced tumor outgrowth in Winn assays at least as often as they inhibited it.
Low natural killer‐cell activity and immunoglobulin levels associated with smoking in human subjects
Authors: Ferson M. , Edwards Anne , Lind Anne , Milton G. W. , Hersey P. 
Published: February 2007

AbstractPrevious studies have shown that smoking is associated with a high incidence of certain malignancies and a high incidence of metastatic spread of melanoma. The purpose of the present study was to examine whether this high incidence of malignancy could be associated with certain aspects of immune function believed to be important in restricting tumour growth. Age‐and sex‐matched smoking and non‐smoking normal subjects and male, smoking and non‐smoking melanoma patients, were studied for the natural killing (NK) activity of their blood leukocytes against cultured melanoma and Chang cells. The levels of the various immunoglobulin classes in their sera and the E rosette levels of the normal subjects were also assessed. The results indicate that the NK activity of blood leukocytes from both normal subjects and melanoma patients who smoked was significantly lower against cultured melanoma cells than that of non‐smokers. Smokers were also shown to have lower IgG and IgA Immunoglobulin levels in their sera compared to non‐smokers but no differences in the percentage of E‐rosetting (T) cells was detected. Recent studies provide some basis for the belief that the low NK activity and immunoglobulin levels in smokers may be related. These results further suggest that a closer examination of the effects of this environmental hazard on the immune system and its relation to malignancy is needed.
Isolation and characterization of lymphocytes and macrophages from solid, malignant human tumours
Authors: Svennevig Jan‐L. , Lövik Martinus , Svaar Helge 
Published: February 2007

AbstractIn mechanically prepared cell suspensions from 17 solid, malignant human tumours, 0.5–5.0% (mean 2.0%) lymphocytes and 1.0–28.0% (mean 7.4%) macrophages were found. Mononuclear cells (MC) were isolated using the Böyum technique. From each biopsy weighing 1–4 g, on average, 1.3×106 lymphocytes and 0.8×106 macrophages were reco vered. The tumour‐infiltrating lymphocytes (TIL) were characterized with regard to T and B markers. The proportion of TIL‐forming rosettes with SRBC (T cells) was 43%, which was significantly less than for peripheral blood lymphocytes (PBL) from cancer patients (58%), or normal controls (80%), On average, 15% of the TIL were B cells, whereas 42% had no T‐or B‐cell markers. Macrophages (TIM) were identified by non‐specific esterase staining and phagocytosis. In four cases the tumour cells were also stained with a‐naphthyl butyrate. Corresponding findings were made on esterase‐stained cryostat sections from four tumours. Macrophages were found within and around the tumour tissues, occasionally localized to necrotic areas, but in most cases with no sign of necrosis of the surrounding cells. In some tumour cell suspensions typical clusters of lymphocytes and macrophages were seen. Total lymphocyte and T‐cell counts were markedly reduced in the peripheral blood of cancer patients, whereas total monocyte counts were within the normal range.
A 14q+ chromosome in a B‐cell acute lymphocytic leukemia and in a leukemic non‐endemic Burkitt lymphoma
Authors: Slater R. M. , Philip P. , Badsberg E. , Behrendt H. , Hansen N. E. , Van Heerde P. 
Published: February 2007

AbstractChromosome analysis using banding staining techniques was carried out on cells from a B‐cell acute lymphocytic leukemia (ALL) of the Burkitt type and a case of non‐endemic Burkitt lymphoma presenting as ALL. In both patients a marker chomo‐some 14q+ was found which was morphologically identical to those reported for endemic and non‐endemic Burkitt lymphoma and a few other B‐cell malignancies. However, the origin of the translocated segment could not be identified in either case. In addition, both patients had a 13q+ chromosome with a breakpoint in the 13q3 region but involving different material of unknown origin. Other marker chromosomes in the B‐cell ALL included rearrangements of chromosome arms 1q and 6q. Serial studies showed that cells with a partial duplication of the long arm of chromosome No. 1, in addition to the 14q+ chromosome, were important in the karyotype evolution of the malignant cell population. In this patient the 14q + chromosome had a brightly fluorescing satellite region indicating the probable monoclonal development of the leukemic cell population. From this and other reports it appears that the B‐cell type of ALL is characterized by a 14q+ chromosome. Because of the pathological and cytogenetic similarities between certain types of B‐cell ALL and Burkitt lymphoma it is suggested that they may be different manifestations of the same disorder.
The role of the macrophage in Marek's disease: In vitro and in vivo studies
Authors: Haffer Keith , Sevoian Martin , Wilder Martin 
Published: February 2007

AbstractMacrophages from Sand K‐strain Leghorn chickens, susceptible and resistant to Marek's disease (MD) respectively, were studied to determine the macrophage contribution to the dynamics of MD infection, tumorigenesis and genetic resistance to this disease. In vitro studies demonstrated that macrophages from both strains were similar in their responses toward JM strain of Marek's disease virus (MDV) and JM‐1 tumor cells. Macrophages were observed to phagocytize JM virus, but the interiorized virus was not seen to replicate within the macrophage or induce antigenic changes of the cell membrane. Clearance of JM‐1 tumor cells was by both cytolytic and phagocytic mechanisms. In vivo selective suppression of macrophage functions by antimacrophage serum or trypan blue inoculations resulted in significantly elevated viral titers and increased tumorigenesis, as compared to infected, non‐suppressed or non‐infected control groups. Results from this study indicate that genetic susceptibility or resistance to MD, as exhibited by Sand K‐strain chickens, respectively, is not controlled at the macrophage level. The role of the macrophage in MD infection appears to be specifically surveillance.
Enhancement of host cell reactivation of ultraviolet‐irradiated herpes simplex virus by caffeine, hydroxyurea and 5‐bromodeoxyuridine
Authors: Fogel Marian , Yamanishi Koichi , Rapp Fred 
Published: February 2007

AbstractEnhancement of host cell reactivation (HCR) of ultraviolet (UV)‐irradiated herpes simplex virus (HSV) was demonstrated in cell cultures pretreated with caffeine, hydroxyurea, or 5‐bromodeoxyuridine (Brd Urd). The effect of caffeine on HCR was shown to depend on the time of drug treatment with respect to infection. In cultures treated with caffeine during the course of virus replication, the infectivity of irradiated HSV was reduced about nine‐fold, while cultures pretreated with the drug before infection showed an increase in infectivity. The extent of HCR enhancement depended on the time interval between treatment with caffeine and infection, drug concentration, and the UV irradiation dose to which HSV was exposed. Magnitude of enhancement of HCR by caffeine differed in various cell species. The results suggest that enhanced HCR of UV‐irradiated HSV by DNA antimetabolites is associated with DNA repair activated in consequence of cell DNA damage.
Immune suppression in BALB/c mice bearing the plasmacytoma TEPC‐183: Evidence for normal lymphocyte but defective macrophage function
Authors: Joshua D. E. , Brown G. , MacLennan I. C. M. 
Published: February 2007

AbstractThis paper analyses impairment of the primary immune response of mice bearing the plasmacytoma TEPC‐183. Healthy animals and mice bearing the reported non‐immunosuppressive tumour MOPC‐104E were used as controls. The defect was shown to affect both primary IgG and IgM responses to chicken cells (CRBC) and to be related to tumour size. However, the primary immune depression could be overcome either by increasing the antigen dose or by using Freund's complete adjuvant together with antigen. Secondary responses were also depressed. This depression was more pronounced if the animals was primed after, rather than before, tumour implantation. Further studies involved the measurement of primary immune responses of immunologically deprived syngeneic mice, after they had been reconstituted with cells from normal or tumour‐bearing mice. Lymphocyte reconstitution experiments were carried out in mice which had been irradiated with 950R. Various lymphoid preparations from TEPC‐183‐bearing mice were as effective as those from healthy controls in reconstituting primary immune responses. When mice were deprived of macrophage function by the method of Gorczynsky et al. (1971) using large doses of horse red cells macrophage preparations from normal mice were able to partially restore primary immune responsiveness. However, macrophages from TEPC‐183‐bearing mice were unable to bring about such restoration. It is concluded that the impairment of the primary immune response of mice bearing the plasmacytoma TEPC‐183 is due to a macrophage, rather than a lymphocyte, abnormality. However, none of these transfer studies suggested that positive suppression of primary immune responses was being mediated by cells from TEPC‐183‐bearing mice.
Methylation of DNA in target and non‐target organs of the rat with methylbenzylnitrosamine and dimethylnitrosamine
Authors: Fong Louise Y. Y. , Lin Hsiang Ju , Lee Clara Lai Hing 
Published: February 2007

AbstractThe sites of labelling of DNA with [14C]methyl groups from methylbenzylnitrosamine and dimethylnitrosamine were studied in rat oeso‐phageal epithelium and liver. All four combinations of tissue and carcinogen were studied. Tissues were labelled in vitro and the DNA contained therein purified and hydrolysed (pH 1, 37° C) to free purines and apurinic acid. Quantitative analysis was performed with the aid of thin‐layer chromatography. The apurinic acid and 7‐methylguanine fractions were found to be extensively labelled. Smaller amounts of radioactivity were found in O6‐methyl‐guanine and some of the methylated adenines. The same carcinogen produced different patterns of labelling in oesophageal and liver DNA. The proportion of O6‐methylguanine to 7‐methylguanine was higher when the methylating agent was a carcinogen specific for the organ.
Serological detection of a polyoma‐tumor‐associated membrane antigen
Authors: Klein George , Ehlin Barbro , Witz Isaac 
Published: February 2007

AbstractSyngeneic antisera raised against three polyoma tumors, SEYF‐a, SESO and SEWE, of strain ABY, A and ASW origin, respectively, contain antibodies directed against multiple specificities. One specificity is cross‐reactive for the three polyoma tumors, but appears to be absent from a large variety of other tumors tested. Other, more “public” antigens are shared with a variety of other tumors of viral or non‐viral origin. Five different public specificities of this type have been demonstrated and to some extent defined. Since the SEWE ascites tumor, with the shortest passage history, is much less liable to induce antibodies against the public specificities than the long‐passaged SEYF‐a and SESO, it is likely that the corresponding antigenic determinants arise as a result of passenger virus pick‐up during continued passage, or are due to secondary cytogenetic changes.
Cell‐mediated mutagenesis in cultured chinese hamster cells by polycyclic hydrocarbons: Mutagenicity and DNA reaction related to carcinogenicity in a series of compounds
Authors: Wigley Caroline B. , Newbold Robert F. , Amos Jacqueline , Brookes Peter 
Published: February 2007

AbstractThree potycyclic hydrocarbons, benz(a)anthracene, 3‐methylcholanthrene and 7,12‐dimethyl‐benz(a)anthracene, have been studied in a cell‐mediated mutagenesis system using BHK 21 cells to metabolize the hydrocarbons and V‐79 cells as targets for detecting induced cytotoxicity and mutation. In large‐scale experiments, the DNA of V‐79 cells was analyzed by column chromatography to determine the nature and true extent of reaction of hydrocarbons with deoxyribonucleosides. Products with DNA formed by the two carcinogenic compounds were qualitatively very similar to those reported to occur in vivo and in primary cell cultures. Binding indices were calculated from the tritium content of DNA‐hydrocarbon products, related to overall metabolism, for these two compounds together with benzo(a)pyrene and 7‐methylbenz(a)‐anthracene using data from a previous study. These values reflected differences in carcinogenic potency between the compounds. Induced mutation frequencies were related to the extent of DNA reaction with each compound. At equivalent extents of DNA reaction with hydrocarbon products, levels of induced mutation were not significantly different.
Carcinogenic action of low‐dose cyclophosphamide given orally to sprague‐dawley rats in a lifetime experiment
Authors: Schmähl D. , Habs M. 
Published: February 2007

AbstractIn a lifelong experiment Sprague‐Dawley rats received cyclophosphamide (CP) in drinking water. Daily doses of 2.5 (I), 1.25 (II), 0.63 (III), and 0.31 (IV) mg/kg body weight were given to groups of 40 male and 40 female rats five times a week. The median survival time (MST) of treated rats proved to be dose‐dependent. In rats treated with dose I the MST was 638 days for males and 642 for females, in those given dose IV it was 906 days for males and 934 days for females. The percentage of control animals with malignant tumors was 11% for males and 15% for females. The corresponding figures for CP‐treated animals ranged from 32 to 43% for male rats and from 30 to 35% for females. At doses I, II, and III CP proved to be carcinogenic (p vs control <0.05). No carcinomas of the urinary bladder were found in controls but one female showed a benign papilloma of the bladder. However, 17 CP‐treated rats died with carcinomas of the urinary bladder and, remarkably, only one of these was a female. In addition, 18 male and 10 female animals showed benign tumors of the same organotropy. No leukemia was diagnosed in controls, but in CP‐treated rats leukemia was found in 8 male and 11 female animals. These findings support the evidence emerging from case reports in humans showing an increased risk of cancer of the urinary bladder as well as of leukemia in patients treated with CP.
Idiopathic mammary tumors in BALB/c mice
Authors: Moore Dan H. , Sarkar Nurul H. , Holben Jane A. , Sheffiel Joel B. 
Published: February 2007

AbstractA colony of BALB/c mice consisting of two sublines with a high incidence of mammary tumors was examined for the presence of a mammary tumor virus (MuMTV). The mammary tumor incidences in the two sublines were 18% and 35% at average tumor age 19–20 months. Over a period of 8 years, their milk at third to tenth lactations were monitored for the presence of MuMTV antigen, and the milk and tumors were examined for the presence of B particles. Neither antigen nor B particles were found. Milk and tumor extracts from the higher mammary tumor line were also assayed for MuMTV bioactivity by intraperitoneal inoculation of weanling C57BL, BALB/c, and Rlllf females. No response was obtained, except possibly in Rlllf. Both the MuMTV antigen incidence and the tumor incidence in inoculated Rlllf mice were somewhat elevated over controls. The question remains unanswered as to whether there is an active MuMTV in our colony of tumor‐bearing BALB/c mice and, if there is, whether it is associated with B particles.
Assessment of the use of the Salmonella mutagenesis assay to determine the influence of antioxidants on carcinogen‐induced mutagenesis
Authors: Rosin Miriam P. , Stich H. F. 
Published: February 2007

AbstractThe Salmonella mutagenesis assay was used to study the influence of antioxidants on the mutagenic activities of carcinogens. The assay allowed us to determine which antioxidant would affect a carcinogen's in vitro mutagenic activity as well as to estimate the relative effectiveness of each antioxidant as a carcinogen inhibitor. Antioxidants studied included cysteamine, disulfiram, butylated hydroxyanisole, propyl gal late, sodium selenite, sodium bisulfite, α‐tocopherol succinate and sodium ascorbate. The mutagenic activity of N‐methyl‐N'‐nitro‐N‐nitrosoguanidine was most effectively inhibited by cysteamine and sodium bisulfite with selenite, propyl gallate and sodium ascorbate being only slightly less effective. Propyl gal late, selenite and cysteamine had a similar ability to inhibit N‐acetoxy‐2‐acetylaminofluorene‐induced mutagenesis, whereas the addition of sodium bisulfite, sodium ascorbate and disulfiram had no detectable inhibitory effect on this carcinogen. Butylated hydroxyanisole and α‐tocopherol succinate did not affect the mutagenic activity of either carcinogen. It was also observed that dimethyl sulfoxide, when used as a solvent, could significantly affect the measurement of an antioxidant's efficiency as an inhibitor of carcinogen‐induced mutagenesis. The results obtained indicate the necessity of studying an antioxidant's effect on numerous carcinogens prior to drawing any conclusions as to the potential use of the antioxidant as a carcinogen inhibitor.
Increased monocyte‐mediated cytostasis of lymphoid cell lines in breast and lung cancer patients
Authors: Jerrells Thomas R. , Dean Jack H. , Richardson Gary , Cannon Grace B. , Herberman Ronald B. 
Published: February 2007

AbstractPeripheral blood mononuclear cells of most normal adults and patients with breast or lung cancer were found to inhibit [3H]thymidine uptake by lymphoid cell lines in a growth inhibition assay. At effector target cell ratios between 5:1 and 20:1, lung cancer patients and breast cancer patients, when compared to normal individuals, demonstrated significantly greater inhibition of [3H] thymidine uptake by a human lymphoid cell line (F‐265). The effector cells were adherent and were probably monocytes. Sephadex G‐10 column passage or adherence to plastic removed most growth‐inhibitory activity. Adherent cells recovered from plastic flasks (88–94% monocytes) were strongly growth‐inhibitory. Lung cancer patients receiving BCG immunotherapy were found to have an apparently increased activity compared to patients not treated with BCG. The possible mediation of the growth inhibition by release of prostaglandins was suggested by the reduced cytostatic effects in the presence of indomethacin. Growth‐inhibitory activity was not species‐restricted, since human effector cells and also effector cells from tumor‐bearing mice were reactive against the human target cell and against a murine lymphoma line (RBL‐5). Natural killer (NK) cells did not appear to contribute appreciably to the observed cytostasis, since the levels of their activities did not correlate, and human NK cells are non‐adherent and have little reactivity against F‐265 or RBL‐5. The inhibition of [3H]thymidine uptake by target cells was demonstrated to be a good reflection of actual inhibition of proliferation, since incubation of adherent cells from cancer patients with F‐265 resulted in similar degrees of reduction in the number of target cells and in [3H]thymidine uptake.
Demonstration of placental alkaline phosphatase in human breast cancer
Authors: Wada H. Garrett , Shindelman Jeffrey E. , Ortmeyer Ann E. , Sussman Howard H. 
Published: February 2007

AbstractThe screening of a series of 11 metastatic breast tumors for the presence of the placental isoenzyme of alkaline phosphatase (EC 3.1.3.1) by RIA revealed one strong producer. The alkaline phosphatase of this tumor was characterized with respect to its immunochemical cross‐reactivity, inhibition by L‐phenylalanine and levamisole, subunit molecular weight (Mr) and isoelectric point (pl) in two‐dimensional electrophoresis, and one‐dimensional peptide map. In all parameters of the characterization, the tumor alkaline phosphatase was similar to placental alkaline phosphatase, except for subunit molecular weight which was slightly lower (60,000 versus 64,000 for the placental isoenzyme). No strong placental alkaline phosphatase producers were found among 16 primary tumors examined by RIA. The screening of patients' sera for the placental alkaline phosphatase using RIA indicated elevated levels over post‐menopausal controls in 20% of the metastatic patients. Only 3% of the primary patients had elevated serum levels. These results suggest that the placental isoenzyme of alkaline phosphatase may be a useful tumor marker for recurrent breast cancer.
Differential inducibility of Epstein‐Barr virus in cloned, non‐producer raji cells
Authors: Bister Klaus , Yamamoto Naoki , Hausen Harald Zur 
Published: February 2007

AbstractCells of the human lymphoblastoid non‐producer line Raji were cloned in soft agar. Individual colonies were isolated and analyzed for their inducibility of the Epstein‐Barr virus‐associated early antigen (EA). The induction of EA by the tumor promoter TPA varied among the different cell clones. Clones with very high and very low inducibility of the resident Epstein‐Barr virus genome were further analyzed. Constant differences in the inducibility of EA were observed after activation by tumor promoters, 5‐iododeoxyuridine or antibodies to human IgM. Induction of EA synthesis by super‐infection with Epstein‐Barr virus from the P3HR‐1 line, however, did not vary among the clones tested. No differences in expression of the Epstein‐Barr virus‐associated nuclear antigen (EBNA) were noted in cells of clones with high or low susceptibility to EA induction. DNA reassociation kinetics demonstrated that Raji cells with high susceptibility to EA induction contained a significantly higher number of Epstein‐Barr virus genome equivalents per cell than cells with low susceptibility. Treatment of Raji cells with the tumor promoter TPA did not change the ratio of Epstein‐Barr virus‐specific DNA to cellular DNA.