bluuebunny/crossref_metadata_2025_split huggingface dataset:
Antagonistic action of retinoic acid and teleocidin on the proliferation and epidermal growth factor binding of rat hepatoma cells
Authors: Kaneko Yoshiyasu 
Published: February 2007

AbstractRat hepatoma cells were cultured in a medium with suboptimal concentration of fetal calf serum. In this low serum culture, retinoic acid inhibited the cell proliferation and enhanced the number of receptors for epidermal growth factor (EGF). On the contrary, teleocidin, a possible naturally occurring tumor promoter from Streptomyces, was a weak mitogen and inhibited EGF binding. A concurrent treatment of AH66 cells with these two compounds showed that they acted antagonistically. Retinoic acid inhibited the mitogenic action of teleocidin, while teleocidin suppressed the retinoic‐acid enhancement of the number of EGF receptors. Retinoic acid could not prevent the alterations of the cell surface properties induced by a prolonged treatment with teleocidin. Furthermore, these two compounds appeared to be involved in the regulation of glycoprotein synthesis and the stimulation of cellular glycoprotein synthesis by retinoic acid was abolished by teleocidin. The present data suggest that retinoic acid selectively antagonizes the mitogenic action of teleocidin, and also indicate that the hepatoma cell cultures appear to provide a useful system for exploring the mechanisms of action of both retinoic acid and teleocidin.
Suppressor cell activity in melanoma patients. II. Concanavalin A‐induced suppressor cells in relation to tumor growth and suppressor T‐cell subsets
Authors: Werkmeister J. , Phillips Georgina , McCarthy W. , Hersey P. 
Published: February 2007

AbstractThe relative proportions of T, B and Tγ suppressor cells were determined sequentially in peripheral blood of melanoma patients before and after surgery. Concanavalin A (Con A)‐induced suppression against lymphocyte mitogenesis of melanoma patients and age‐matched controls was measured concurrently. The mean percentage of Tγ cells was significantly higher (p < 0.001) in melanoma patients before surgery (21.8 ± 5.4) compared to a group of age‐matched controls (14.9 ± 5.4). There was a tendency for the proportion of Tγ cells in patients to decrease after surgery, although the relative levels of Tγ were still significantly elevated (p < 0.05) 6–8 weeks after surgery when compared to normal controls. The mean percentage of T and B cells in melanoma patients before and after surgery was comparable to that observed in normal controls. The degree of Con‐A‐induced suppression in patients increased significantly after surgery particularly at 6–8 weeks (p < 0.02). No difference in Con‐A‐induced suppressor cell activity was observed between melanoma patients and controls before or after surgery. An inverse relationship was found between the amount of Con‐A‐induced suppression and percentage of Tγ cells in melanoma patients before surgery. Similar associations were not apparent in patients after surgery or in normal control populations. The inverse correlation of Con‐A‐induced suppression with Tγ cell numbers suggests that the former may measure potential suppressor cell activity whereas the Tγ cells may indicate active suppressor cells. The significance of these findings for the monitoring of suppressor cell activity in vivo and their role in suppression of immune responses in melanoma patients is discussed.
Influence of serum thymic factor (FTS) on radiation‐induced leukaemogenesis in thymectomized akr mice
Authors: Legrand E. , Daculsi R. , Bach J. F. , Duplan J. F. 
Published: February 2007

AbstractThe influence of serum thymic factor (FTS) on extrathymic leukaemogenesis induced in thymectomized AKR mice by fractionated sub‐lethal irradiation was studied. Thirty‐day‐old thymectomized mice were submitted to four doses at weekly intervals (1.75 Gy) and thereafter treated with FTS (I ng) for 9 days. Two groups were restored with either bone marrow or spleen cells prior to FTS treatment. In another group, mice were treated with FTS (12 ng) for I month after thymectomy and prior to irradiation. Results indicated that primarily irradiation and FTS, and, to a lesser extent, restoration and age of the mice at the time of their first radiation exposure influenced leukaemogenesis. Irradiation increased the spontaneous low incidence of extrathymic leukaemia (5 %) up to 50 %. Although nothing is yet known about the expression of endogenous retroviruses in thymectomized AKR mice, the possible expression of leukaemogenic recombinants, either identical to or different from mink‐cell‐focus‐inducing viruses (MCF), might explain this enhancing effect of radiation on leukaemogenesis. Mice developed two types of leukaemias: “null” leukaemias whose cells bore no detectable antigen or surface immunoglobulin, and B leukaemias. Among the null leukaemias, two kinds could be distinguished: “early” ones which were observed before 450 days, and in which BM and spleen were similarly involved, and “late” ones which displayed the same characteristics as B leukaemias, i.e. delayed appearance (after 450 days) and splenic origin. Although FTS did not modify the overall frequency of leukaemias, it increased significantly the incidence of the “early” null ones. It had no effect on the frequency or the latency of late null and B leukaemias. Any population of negative T cells sensitive to FTS could be an acceptable candidate for “early” null leukaemogenesis. The origin of “late” null leukaemias remains an open question.
Non‐specific cytotoxic cells generated in vitro in response to a weakly immunogenic murine adenocarcinoma. In vivo correlations
Authors: Pope Barbara L. , Justice Robert L. , Sarma Chander , Martin W. John 
Published: February 2007

AbstractTumor 85 adenocarcinoma cells, which are very weakly immunogenic for C3H/HeN (C3H) mice, provide a model tumor system for studying the parameters of induction of a cell‐mediated immune response which does not appear to be a traditional cytotoxic T‐cell or NK‐cell response. Mice pre‐immunized with irradiated tumor 85 cells are protected about 50% of the time from a challenge of viable tumor 85 cells although it is never possible to protect 100% of the immunized mice. Optimal protection is observed in mice immunized with 106 irradiated tumor 85 cells 14 days prior to challenge. Protection is also observed if mice are immunized with C3H or C3HfeB/HeN (C3Hf) tumors originally induced by the same carcinogen as that used to induce tumor 85. The injection of carrageenan I h before challenge completely reverses the protection observed in immunized mice and tumors grow faster in carrageenan‐treated immunized mice than in normal mice. Two populations of cells obtained from cultures of spleen cells stimulated by tumor 85 cells appear to prevent tumor growth in vivo. One population, which is cytotoxic for tumor 85 cells in vitro, is nylon‐wool‐adherent and expresses Thy 1.2 The second population, which is not observed to be cytotoxic in a 51Cr release assay, is phagocytic.
Effects of carcinogen and/or mutagen on normal and gonadotropin‐primed ovaries of mice
Authors: Rao A. Ramesha 
Published: February 2007

AbstractThe influence of pregnant mare serum gonadotropin (PMSG) on the induction of ovarian tumors by carcinogen (DMBA) and/or mutagens (EMS and BMS) has been studied in Swiss albino mice. Priming of the ovaries of 6‐week‐old mice with PMSG (50 lU/mouse) 24 h before intragastric intubation of DMBA (5 mg/mouse) resulted in a significant increase in ovarian tumors when harvested 6 months after the treatment. A similar experiment done on 8‐week‐old mice yielded confirmatory results. Mutagens (EMS and BMS) failed, at given dose levels (200 mg/kg and 300 mg/kg body weight), to induce tumors in normal as well as PMSG‐primed ovaries. Nor could these mutagens enhance DMBA‐induced tumor incidences in normal or PMSG‐primed ovaries. Pretreatment of animals with PMSG‐enhanced DMBA‐induced oocyte depletion and also increased the DMBA‐3H activity in the ovaries. The augmentation of DMBA‐induced tumors in PMSG‐primed ovaries could be due to increased uptake of DMBA and increased depletion of oocytes. It is also possible that PMSG‐primed ovaries provided more proliferating granulosa cells (and macromolecules) for the interaction of DMBA (or its metabolites) and thereby increased the chances of cell transformation in the ovaries.
Cytostasis of tumor cell lines by granulocytes from cancer patients and normal human donors
Authors: Korec S. , Herberman R. B. , Cannon G. B. , Reid J. , Braatz J. A. 
Published: February 2007

AbstractGranulocytes of normal human donors were previously shown to have cytostatic activity in vitro against a variety of tumor cell lines. In the present study, we have compared the levels of granulocyte‐mediated cytostatic activity in cancer patients and normal donors. In an initial study of 25 tumor‐bearing patients and 21 individuals with benign or no disease, decreased cytostatic activity was observed in 84% of the cancer patients. Nine cancer patients with no evidence of disease had reactivity in the normal range. Granulocytes separated by a one‐step method on a double Ficoll‐Percoll gradient showed decreased reactivity. This procedure eliminated the differences previously detected between tumorbearing patients and controls. Addition of either pooled normal AB human serum or autologous serum to the assay restored the reactivity. Only with autologous serum and not with allogeneic serum, were the differences between tumor‐bearing patients and controls again seen. Therefore, in a subsequent study, we examined the effect of serum on cytostasis by normal granulocytes that were isolated on double gradients. We observed lowered serum restorative activity (SRA) in 41 of the 46 (89%) tumor‐bearing patients tested. Fractionation of sera by Sephadex G‐200 chromatography indicated that SRA of both cancer patients and normal donors was in the 100,000 molecular weight region.
Tumoricidal activity of macrophages isolated from human ascitic and solid ovarian carcinomas: Augmentation by interferon, lymphokines and endotoxin
Authors: Peri Giuseppe , Polentarutti Nadia , Sessa Cristiana , Mangioni Costantino , Mantovani Alberto 
Published: February 2007

AbstractPeripheral blood monocytes and macrophages from ascitic or solid tumors were obtained from 50 patients with advanced (Stage III or IV) ovarian carcinoma. Blood monocytes and peritoneal macrophages from 76 patients undergoing surgery for benign gynecological diseases were used as controls. Macrophages were 30% (range 0.2–62) and 2% (range 0.2–4) of mononuclear cell suspensions from ascitic and solid tumors, respectively. Cytolytic activity was measured as release of [3H]‐thy‐midine from prelabelled mKSATUS (TU5) target cells at an effector to target cell ratio of 20:1. Peripheral blood monocytes and tumor‐associated macrophages had baseline cytotoxicity lower than or similar to that of control peripheral blood and peritoneal macrophages respectively. In vitro exposure to partially purified human fibroblast interferon, lymphokine supernatants or endotoxin augmented the cytotoxicity of mononuclear phagocytes, and no significant difference was observed between control and ovarian cancer effector cells from peritoneal effusions. In four patients, macrophages were isolated from the solid tumor or from the malignant effusion and tested in parallel: in two out of four subjects, macrophages from the solid neoplasm showed defective cytotoxicity compared to ascites effector cells from the same subjet. When primary ovarian carcinoma cultures were used as targets, tumor cells from two out of five patients tested were relatively resistant to activated macrophage cytotoxicity. Thus, tumor‐associates macrophages from ascitic or solid ovarian neoplasms showed no evidence of activation, in terms of spontaneous cytotoxicity or responsiveness to stimuli: it appears unlikely that small numbers of non‐activated macrophages present within primary ovarian carcinomas act as a significant mechanism of restraint of neoplastic growth, at least at this anatomical site.
Biphasic depression of macrophage function after tumor transplantation
Authors: Normann Sigurd J. , Schardt Martin , Sorkin Ernst 
Published: February 2007

AbstractTumor bearing produces a biphasic depression of macrophage inflammatory responses. Macrophage accumulation was measured on nitrocellulose filters in DA rats transplanted with a syngeneic DMBA‐induced fibrosarcoma and in SJL/J mice transplanted with a firstgeneration histiocytic lymphoma. The early phase defect was observed 2–5 days and 4–12 days after tumor transplantation in rats and mice respectively. Although transient, its duration could be prolonged by increasing the number of tumor cells injected. An interval of normal responses separated this early defect from a second or late‐phase defect which began midway in the clinical course and persisted until death. Transplantation of syngeneic liver cells increased macrophage responses in DA rats but had no effect in SJL/J mice. The demonstration of a bisphasic anti‐inflammatory effect following tumor transplantation suggests that low doses of tumor cells are effective in inhibiting macrophages and that tumor bearing may alter macrophage responses by more than one mechanism.
Studies on lung tumours. V. Susceptibility of mice to dimethylnitrosamine‐induced tumour formation in relation toH‐2 haplotype
Authors: den Engelse L. , Oomen L. C. J. M. , Valk M. A. Vander , Hart A. A. M. , Dux A. , Emmelot P. 
Published: February 2007

AbstractMale mice of the strain A/Sn, of its congeneic partner strain A.SW, C57BL/105cSnA (abbreviated: B10), and of two congeneic strains on a B10 background (B10.A and B10.AKM) were investigated for their susceptibility to lung tumour induction by dimethylnitrosamine (DMN) administered either by intraperitoneal injection or in the drinking water. Strain B10 (haplotypeH‐23) proved to be very resistant, whereas strains A/Sn (H‐2b) and A.SW (H‐2s) were highly susceptible. The introduction of the haplotypesH‐2aandH‐2min the resistant strain B10 resulted in a significant increase in sensitivity towards DMN‐induced lung tumour formation. Lung tumour incidences in male (B10.A × B10)F1, hybrids, receiving DMN in drinking water, were found to be intermediate between, and significantly different from, the incidences of identically‐treated parent strains B10.A and B10. Males of back‐cross (B10.A × B10) × B10 BC1proved to be of low susceptibility to lung tumour formation by DMN, tumour incidence being very low and not significantly different from that observed in identically‐treated B10 males. It is concluded that, at least in the model system of B10‐derived congeneic strains,H‐2haplotype is one of the factors important in determining susceptibility towards DMN‐induced lung tumours. Comparison of C3Hf (H‐2k), C3H/Sn (H‐2k) and the latter's congeneic strains C3H.B10 (H‐2b) and C3H.NB (H‐2p) of male mice showed that these strains were moderately susceptible to both lung tumour and hepatoma formation by DMN. Accordingly, the presence of anH‐2haplotype from a lung‐tumour‐resistant strain (H‐2b, B10) on the background of a strain of intermediate susceptibility (C3H) does not decrease susceptibility to lung tumour formation. The results were considered in the light of theH‐2haplotype dependence of spontaneous lung tumours, and consequently attention has been paid to the histological types of the induced and spontaneous lung tumours.
RNA oncovirus expression in N‐methyl‐N‐nitrosourea‐induced lymphomas in mice
Authors: Pintér A. , Börzsönyi M. 
Published: February 2007

AbstractRNA oncovirus expression was investigated in thymic lymphomas induced by N‐methyl‐N‐nitrosourea (MNU) in (C57BL/6 × DBA/2)F1(BDF1) mice. Out of 15 newborn mice injected with 20 mg/kg MNU, five developed thymic tumours of T‐cell origin. Virus production of thymic cells from tumorous and normal animals was studied by an infectious center assay. All five tumours released ecotropic (mouse tropic) virus. No xenotropic or dualtropic mink cell focus‐inducing virus was found. No virus was obtained from thymus cells taken from six normal mice killed between 83 and 124 days; however, an ecotropic virus was cultured from the thymus of a 134‐dayold normal mouse. According to these results, the MNU‐induced thymic lymphoma development in BDF1, mice is accompanied by activation of endogenous ecotropic virus, whereas spontaneous activation also occurs in older mice.
Immunohistologic evidence for the role of antibody and macrophages in regression of the murine T1699 mammary adenocarcinoma
Authors: Key Marc , Haskill J. Stephen 
Published: February 2007

AbstractThe regression or progression of the T1699 murine mammary adenocarcinoma was analyzed with histologic and immunohistologic techniques to determine the tissue distribution of both macrophages and antitumor antibody. Changes in integrity of tumor blood vessels were apparent during tumor growth and regression. Tumors at early stages of growth were invaded in the capsule by multiple vascular branches which later permeated the tumor. Following the appearance of anti‐tumor antibody in the serum, these vessels often showed immune complex deposition which preceded vessel leakage, destruction and hemorrhage. After these changes, tumor cells appeared coated with antibody. Macrophages appeared predominantly in the tumor capsule during early stages of tumor growth, while at later stages they were observed within tumors most prominently near the edge of growing hemorrhagic and necrotic areas. As tumors regressed, connective tissue septation lined by macrophages became apparent. Phagocytosis of seemingly intact tumor cells was common and appeared to account for much of the loss in tumor cell numbers. In immunosuppressed animals (ATXBM, 450R) in which tumor progression always occurred, the above features were markedly diminished or absent. This model emphasizes the interplay of many factors in tumor regression. These include immune complex deposition, blood vessel destruction, macrophage infiltration and connective tissue development, all of which are associated with tumor regression and seem to be infrequent and/or inconsequential during progressive tumor growth.
Glycosphingolipids of K562 cells: A chemical and immunological analysis
Authors: Suzuki Akemi , Karol Robin A. , Kundu Samar K. , Marcus Donald M. 
Published: February 2007

AbstractThe K562 cell line, which was established from a patient with chronic myeloid leukemia in blast crisis, was thought to be myeloid, but recent data indicate that it is an undifferentiated erythroid cell line. We have found that the glycosphingolipid content of these cells differs considerably from that of mature erythrocytes. Globotetraosylceramide, the most abundant glycolipid of mature red cells, was not detected in K562 cells, and neither was globotriaosylceramide. The predominant neutral glycolipids of K562 cells are monohexaosyl‐ceramides, which are a mixture of glucosyl‐ and galactosylceramides, and lactotriaosyl‐ and lactoneote‐traosylceramides were also detected. Secondly, gangliosides which contain N‐acetylgalactosamine were much more abundant than those containing N‐acetylglucosamine in K562 cells, in contrast to erythrocytes. The most abundant ganglioside of K562 cells, GM2, is present in trace quantities in erythrocytes. A third major difference between these two cells lies in their relative proportions of neutral glycolipids and gangliosides. The molar ratio of neutral glycolipids/gangliosides is approximately 15:1 in erythrocytes and 1:1 in K562 cells. These striking differences between K562 cells and mature erythrocytes indicate that glycolipids may be useful cell surface markers of normal erythrocyte differentiation, and of erythroleukemias.
Regulation of gene expression by tumor promoters. II. Control of cell shape and developmental programs for macrophages and granulocytes in human myeloid leukemic cells
Authors: Liebermann Dan , Hoffman‐Liebermann Barbara , Sachs Leo 
Published: February 2007

AbstractRegulation of the developmental programs for macrophages and granulocytes has been analysed, using two‐dimensional gel electrophorels of the cytoplasmic protein changes, in a human myeloid leukemic cell line (HL60) that can be induced to differentiate to macrophages by the macrophage and granulocyte‐inducing (MGI) protein and the tumor promoter 12‐O‐tetradecanoyl‐phorbol‐13‐acetate (TPA), and to granulocytes by dimethylsulfoxide (DMSO). Studies on the protein changes induced by the different inducers showed a similar developmental program for macrophage differentiation induced by MGI or TPA, which differed from the beginning from the granulocyte program induced by DMSO. Comparison with normal cells from human peripheral blood has shown that the developmental programs induced in the HL60 cells are relevant to the normal programs of differentiation for these two cell types. Unlike MGI and DMSO, TPA induces rapid attachment of the HL60 cells to the surface of the Petri dish. Combined treatment with TPA and DMSO showed cell attachment, extensive spreading of the cells, the regulation of specific proteins and expression of the macrophage program. The addition of TPA to cells induced for the granulocyte program by DMSO resulted in cell attachment and spreading and a switchover from the granulocyte to the macrophage program. The results indicate that cells in suspension can express either the macrophage or granulocyte program depending on the inducer, and that changes in cell shape associated with cell attachment induced by TPA can regulate specific proteins and restrict the developmental program to macrophages. It is suggested that the in vivo environment of cells in relation to the possibilities for cell adhesion, which can be regulated by tumor promotors, may play a major role in determining the developmental program of myeloid and other cell types.
Morbidity from cancer in La Paz, Bolivia
Authors: Ríos‐Dalenz Jaime , Correa Pelayo , Haenszel William 
Published: February 2007

AbstractData from a population‐based Cancer Registry in La Paz, Bolivia, are presented. The city is located at approximately 4,000 meters above sea level and has a strong cultural influence consisting of Aymará Indians immigrating from the altiplano. Incidence rates in females are high for cancer of the cervix, the gallbladder and the thyroid gland. Males display unusually high rates of testicular cancer. Stomach cancer rates are lower than among other Andean populations. Smoking‐related cancer and cancers related to sex‐hormones are lower than average in incidence. Cancer of the nasal mucosa and paranasal sinuses is unusually high in frequency.