bluuebunny/crossref_metadata_2025_split huggingface dataset:
Effect of solvents on methylcholanthrene‐induced carcinogenesis in mice
Authors: Reddy A. Lakshma , Fialkow Philip J. 
Published: February 2007

AbstractWe have shown previously, with X‐chromosome linked phosphoglycerate kinase (PGK) cell markers, that the fibrosarcomas induced in mice by subcutaneous injection of 0.2–2.0 mg of methylcholanthrene (MCA) dissolved in olive oil had a multicellular origin. In this study we used a constant dose of MCA injected subcutaneously and compared the effects on tumorigenesis of using benzene or olive oil as the solvents. The benzene and olive oil groups differed in tumor incidence (100% versus 50%), location (muscle versus skin), and type (rhabdomyosarcomas versus fibrosarcomas). Each of the nine olive‐oil MCA‐induced tumors showed both PGK enzyme types, whereas 13 of 16 tumors induced by MCA in benzene displayed only a single PGK type. This difference in PGK phenotypes suggests that the MCA‐benzene neoplasms arose from one or a few cells. We conclude from these results that the nature of the solvent plays an important role in the type and number of cells from which tumors induced by subcutaneous injection of MCA arise.
Carcinogenicity of analgesics: Long‐term treatment of sprague‐dawley rats with phenacetin, phenazone, caffeine and paracetamol (acetamidophen)
Authors: Johansson Sonny L. 
Published: February 2007

AbstractSix groups of male Sprague‐Dawley rats were treated with phenacetin, phenazone or caffeine in the diet or with combinations of these chemicals. Another group received paracetamol in the diet and a further group received only the control diet. The rats were treated for up to 117 weeks. Renal pelvic tumors were only seen in rats treated with phenacetin or phenazone alone or in combination with caffeine, phenazone having slightly greater activity toward the urinary tract than phenacetin. Phenacetin, however, had a greater overall carcinogenic effect, inducing 31 malignant tumors. The urinary tract and the kidneys had the highest incidence of tumor followed by squamous‐cell carcinomas of the head and neck. Half of the rats treated with phenacetin, phenazone and caffeine in combination developed hepatomas. The explanation may be that the addition of phenazone and caffeine altered the metabolism of phenacetin, increasing the production of N‐hydroxy‐phenacetin, a known liver carcinogen. The justification of using phenacetin as a human analgesic must be seriously questioned, and further studies with phenazone are required.
Susceptibility to killing by bcg‐activated macrophages associated with ‘spontaneous’ neoplastic transformation in culture
Authors: Tucker Robert W. , Meltzer Monte S. , Sanford Katherine K. 
Published: February 2007

AbstractNon‐tumorigenic and ‘spontaneously’ transformed tumorigenic paired cell lines derived from mouse, rat, or hamster embryonic tissues were examined for their susceptibility to killing by mouse peritoneal macrophages activated in vivo by infection with Mycobacterium bovis, strain Bacillus Calmette‐Guérin (BCG). Susceptibility to killing was measured by the extent of clearing in a confluent layer of target cells overlying an area of adherent macrophages or by the release of 3H counts from target cells prelabelled with [3H]‐thymidine. Only tumorigenic lines showed complete clearing by activated macrophages; the reaction occurred regardless of species differences between macrophages and target cells. The degree of clearing increased with increasing ratio of macrophages to target cells. Normal macrophages from uninfected mice did not produce a clearing reaction. The macrophage reaction discriminated between non‐tumorigenic and tumorigenic cells with short tumor latent periods (<100 days) even when neoplastic and non‐neoplastic cells were derived in culture from the same cell. The more tumorigenic lines (i.e., shortest latent period) tended to be more susceptible to killing. Thus, cells spontaneously transformed in culture are more susceptible to killing by activated macrophages than are their non‐neoplastic counterparts. In two cloned lines the enhanced susceptibility to macrophage killing appeared to be a late manifestation of the neoplastic change.
Reactivation of epstein‐barr virus‐specific cytotoxic t cells by in vitro stimulation with the autologous lymphoblastoid cell line
Authors: Rickinson A. B. , Moss D. J. , Allen D. J. , Wallace L. E. , Rowe M. , Epstein M. A. 
Published: February 2007

AbstractUnfractionated mononuclear (UM) cells and T cells freshly prepared from the blood of adult donors were co‐cultivated in microtest plate wells with progressively lower numbers of cells from the autologous EB‐virus‐transformed B‐cell line. The fresh cells present in co‐cultures from EB virus antibody‐negative (seronegative) donors regularly facilitated autologous cell line outgrowth, monitored after 4 weeks, whereas outgrowth was markedly inhibited in the corresponding co‐cultures from seropositive donors. Larger‐scale co‐cultures, set up at a ratio of 80–100 fresh UM cells to one autologous virus‐transformed B cell, were harvested after 8 to 12 days and the T‐cell subpopulation was examined for cytotoxicity both by growth inhibition and by chromium release assays. Cytotoxic T cells were generated exclusively in seropositive donor co‐cultures and were strongly active against the autologous virus‐transformed cell line without affecting either autologous uninfected B cells or any of a range of EB virus genome‐negative target cell lines chosen as sensitive indicators of non‐specific cytotoxicity. Recognition of allogeneic EB‐virus‐transformed cells was restricted to those whose HLA‐A and/or B and/or C antigen expression matched that of the effector cells themselves; moreover target cell lysis was specifically inhibited in the presence of monoclonal antibodies binding to these HLA antigens. The results indicate that EB‐virus‐specific HLA‐restricted memory T cells, present in the blood of previously‐infected individuals, can be reactivated in vitro using the established autologous virus‐transformed cell line as a stimulus. The reactivated cytotoxic cells appear to recognize a virus‐induced lymphocyte‐detected membrane antigen, LYD‐MA, analogous to that first invoked to explain the cytotoxic response to primary EB virus infection observed during infectious mononucleosis.
in vitro motility of cells from human epidermoid carcinomas. a study by phase‐contrast and reflection‐contrast cinematography
Authors: Haemmerli Gisela , Str Peter 
Published: February 2007

AbstractThe motile behavior of six cell lines derived from human squamous carcinomas (two from the larynx, four from the tongue) was studied by cinematography under phase‐ and reflection‐contrast illumination. The recorded cell activities consist in spreading, stationary and translocative motility, and aggregate formation. Within this common pattern, quantitative modifications (≪sub‐patterns ≪) are stable properties of the individual cell lines. Such modifications are particularly evident with regard to the dynamic texture of the aggregates which ranges from loose, netlike structures to compact islands with smooth borders. Accordingly, the intensity of cell traffic within and around the aggregates varies considerably. It is discussed to what extent the in vitro motility of the carcinoma cell populations reflects their behavior in the organism and thus the significance of cell movements for invasion.
Characterization of human keratinocyte
Authors: Peehl Donna M. , Stanbridge Eric J. 
Published: February 2007

AbstractIntraspecific human cell hybrids were created by fusing normal epidermal keratinocytes with carcinoma (HeLa) cells. All of the hybrids were epithelial in morphology and exhibited a bright cytoskeletal pattern after indirect immunofluorescent labelling by antibody against keratin. Like the normal parental cells, the hybrid populations had organized arrays of microfilaments, and expressed low levels of surface fibronectin, predominantly in short ≪stitches ≫ at cell boundaries. None of the cells expressed collagen type I, as expected of epithelial cells. Subcutaneous injection into nude mice revealed that the tumorigenic phenotype was initially suppressed in certain of the hybrids. However, cells of these lineages tested at later population doublings, and other hybrid clones tested at early population doublings, formed very small, non‐progressive nodules. Histologically, these nodules resembled moderately to well‐differentiated squamous‐cell carcinomas. The properties in vitro and in vivo of these epithelial hybrids are compared to those of human fibroblast × HeLa hybrids.
Alkaline phosphatase expression in human cell lines derived from various malignancies
Authors: Benham Frances J. , Fogh Jørgen , Harris Harry 
Published: February 2007

AbstractA search for expression of heat‐stable placental‐type alkaline phosphatase (ALP) has been carried out in 19 unselected human tumor cell lines, known not to be HeLa. All cell lines showed measurable ALP activity and in 15 of the lines at least low levels of a heat‐stable, presumptively placental‐type ALP were detected. In five of these lines where the level of this heat‐stable activity was sufficient, further investigation (immunologic, inhibition and electrophoretic studies) demonstrated that this ALP was placental‐type in its characteristics and clearly different from liver/bone/kidney or intestinal ALPs. In 10 lines the heat‐stable activity was too low to allow further characterization. In four lines no heat‐stable activity could be detected. The thermolabile ALP activity in these various lines was liver/bone/kidney in type. This study suggests that the placental ALP locus may be expressed at least at low levels in a much higher proportion of tumors and tumor cell lines than previously reported. The findings, taken together with recent reports that low levels of placental‐type ALP are present in some normal adult tissues (cervix, Goldstein et al., 1980; testis, Chang et al., 1980), indicate that so‐called ‚ectopic’︁ synthesis of placental ALP in tumor cells may not necessarily be due to derepression of a structural locus which is completely unexpressed in normal adult tissues. It may represent an enhancement of expression in malignancy or there may be clonal expansion of a particular cell type which normally expresses the alkaline phosphatase at a high level.
Murine embryonal carcinoma cells: Universal targets for mammalian nk cells?
Authors: Stern Peter , Gidlund Magnus , Kimura Arthur , Gr Kjell‐Olov , Wigzell Hans 
Published: February 2007

AbstractNatural killer (NK) cells from mice lyse murine teratocarcinoma stem cells in accordance with their appropriate cellular, genetic and interferon inducible features. In addition, rat and human putative NK cells were found to exhibit cytotoxicity of these embryonal carcinoma stem cells. By contrast, endodermal cells derived from such stem cells, either as cell lines or by recent induction with retinoic acid, were relatively resistant to effectors from all three mammalian species tested. Attempts to elicit a murine T‐cell response to embryonal carcinoma by secondary in vitro stimulation failed. As previously shown, T killers directed to H‐2 determinants were unable to lyse the MHC lacking embryonal carcinoma cells. The use of lectin ‘glues’, a procedure supposedly capable of revealing the total cytotoxic T‐cell potential regardless of specificity, also failed to elicit lysis of these target cells. We have therefore failed to find evidence for T‐cell recognition or lysis of embryonal carcinoma while NK cells from different species seemingly regard these latter cells as ‘universal’ targets.
Comparative antineoplastic activity against p388 leukemia of 9‐β‐d‐arabinofuranosyladenine (area) and 9‐β‐(2′‐azido‐2′‐deoxy‐d‐arabinofuranosyl)adenine (arazide)
Authors: Lee Sang H. , Thomas Linda K. , Unger Frank M. , Christian Rudolf , Sartorelli Alan C. 
Published: February 2007

AbstractThe anticancer effects of 9‐β‐(2′‐azido‐2′‐deoxy‐D‐arabinofuranosyl)adenine (arazide) were compared to those of 9‐β‐D‐arabinofuranosyladenine (araA) in P388 leukemia cells. Arazide was less susceptible than araA to deamination by a partially purified preparation of adenosine deaminase from P388 cells. This corresponded to significantly more cytotoxicity by arazide than by araA to P388 cells in culture; however, neither agent prolonged the survival time of mice bearing this experimental tumor. Coadministration of these agents with an inhibitor of adenosine deaminase, 2′‐deoxycoformycin (2′dCF), led to marked antineoplastic activity with arazide. Thus, daily administration of arazide (12.5–25 mg/kg per day) with 2′dCF (0.25 mg/kg per day) for 6 consecutive days to mice bearing the P388 leukemia resulted in 50% of the animals surviving for at least 50 days. In combination with 2′dCF, arazide levels higher than 25 mg/kg per day × 6 showed host toxicity as expressed by major loss in body weight and by decreased survival times of leukemia‐bearing mice. AraA plus 2′dCF in the same regimen produced only slight increases in survival time. [3H]‐Thymidine incorporation into DNA of P388 cells was inhibited by more than 90% following administration of a therapeutic dose of arazide and 2′dCF to leukemia‐bearing mice, and inhibition of the formation of DNA persisted for at least 24 h. Under the same experimental conditions, araA and 2′dCF caused less inhibition of DNA biosynthesis and more rapid recovery occurred. Neither arazide nor araA caused inhibition of incorporation of radioactive uridine or leucine into acid‐insoluble material. The results indicate that arazide, which is considerably more water‐soluble than araA, is also superior to araA as an antineoplastic agent when employed in combination with 2′dCF on a once‐a‐day schedule × 6, and suggest that this action is the result of potent and long‐lasting inhibition of DNA synthesis.
Androgen, estrogen and progestin binding sites in human leukemic cells
Authors: Danel Laurence , Martin Pierre , Escrich Edouard , Tubiana Nicole , Fiè Denis , Saez Simone 
Published: February 2007

AbstractSex steroid binding capacity was investigated in malignant cells from 32 patients with acute non‐lymphoblastic leukemia (25 patients with acute myeloid leukemia, 4 with subacute leukemia, 3 with chronic myeloid leukemia in blast crisis) and 30 patients with acute lymphoblastic leukemia. Specific binding of labelled steroids was characterized either by competition assay in cytosol fraction or by whole‐cell incorporation. In some cases further characterization of the receptor complex was attempted by sucrose gradient centrifugation and gel filtration column. The results show the presence of specific binding sites for dexamethasone (22/32 in non ALL and 30/30 in ALL), for estrogens (11/15 in non‐ALL and 5/12 in ALL), for progestins (8/25 in non‐ALL and 5/13 in ALL) and for androgens when RI881 was used as ligand (8/21 in non‐ALL and 5/10 in ALL patients) but only in 1/13 non‐ALL patients and no ALL patients when labelled 5α DHT was used. These results indicate that the blast cells from patients with acute leukemia contain specific proteins binding steroids with a high affinity. Our results for dexamethasone receptors are similar to those described in the literature in ALL and non‐ALL.
Extracellular matrix proteins characterize human tumor cell lines
Authors: Alitalo Kari , Keski‐oja Jorma , Vaheri Antti 
Published: February 2007

AbstractExtracellular matrix proteins synthesized and secreted by adherent human tumor cell lines were analyzed using metabolic labelling with glycine and proline in the presence of ascorbate, polypeptide analysis by polyacrylmide gel electrophoresis, affinity chromatography, collagenase digestion, and immunofluorescence staining. The results showed a characteristic pattern of matrix proteins for each tumor cell type. Tumor cell lines of mesenchymal origin produced mostly interstitial types (I and III) of collagen and fibronectin. Carcinoma cell lines secreted only basement membrane proteins, type IV collagen, laminin and fibronectin, but not interstitial collagens. A melanoma and a rhabdomyosarcoma cell line produced type V of procollagen that has not previously been described in cell culture. Neuroblastoma cells were shown to be phenotypically heterogeneous also with respect to matrix protein production. We propose that the analysis of extracellular matrix proteins may serve as an adjunct in the classification of human tumors.
Fibronectin from human germ‐cell tumors resembles amniotic fluid fibronectin
Authors: Ruoslahti Erkki , Jalanko Hannu , Comings David E. , Neville A. Munro , Raghavan Derek 
Published: February 2007

AbstractThree human germ‐cell tumors established as xeno‐grafts in immunosuppressed mice were shown to produce fibronectin. Immunoperoxidase tissue staining with a specific antiserum revealed human fibronectin in some tumor cells. The cyst fluid which accumulated in the tumors contained human fibronectin as shown by a species‐specific radioimmunoassay. Human fibronectin was isolated from two of the tumor fluids and compared to previously characterized fibronectins. Sodium dodecyl sulfate/polyacrylamide gel electrophoresis and gel electrofocusing showed that the germ‐cell fibronectins resembled amniotic fluid fibronectin with regard to subunit molecular weight and isoelectric point. The distinct features of the amniotic fluid and germ‐cell tumor fibronectin suggest that such fibronectins may provide new oncodevelopmental markers.
Monoclonal anticolon carcinoma antibodies in complement‐dependent cytotoxicity
Authors: Herlyn D. M. , Koprowski H. 
Published: February 2007

AbstractHybridoma‐derived monoclonal anticolon carcinoma (ACC) antibodies mediated specific complement‐dependent cytotoxicity (CDC) against human colon carcinoma cells either grown in culture or obtained directly from patients. These ACC antibodies did not lyse normal colonic mucosa or other normal and malignant human cells. Absorption of these antibodies to cells of established colon carcinoma cell lines totally eliminated their specific lytic capacity. ACC antibodies were able to bind in vivo to colon carcinoma cells grown in nude mice but did not bind to lung or kidney cells from tumor‐bearing animals. These monoclonal antibodies did not, however, inhibit the growth of colon carcinoma tumor cells in nude mice.
Mouse fibroblasts transformed by rous sarcoma virus express a virus‐specific non‐virion transplantation antigen
Authors: Prat Maria , Tarone Guido , Comoglio Paolo M. 
Published: February 2007

AbstractRous sarcoma virus (RSV)‐transformed fibroblasts from different animal species a serologically detectable virus‐induced non‐virion cell surface antigen (VCSA), whose expression is controlled by the transforming viral srcgene and by a cellular gene. Now, by in vivo immunization, we have found that RSV‐transformed fibroblasts from different mouse strains share a virus‐specific transplantation antigen. In fact, only animals immunized with irradiated syngeneic or allogeneic fibroblasts transformed by RSV, but not animals immunized with cells transformed by different oncogenic agents, rejected a lethal dose of syngeneic RSV‐induced tumor cells. Immunoprecipitation tests with monospecific antisera showed that the expression of this antigen did not correlate with the presence of intracellular viral proteins other than the src gene product pp60src. However, hyperimmunization of mice with hamster or quail fibroblasts transformed by RSV, that express a high level of pp60src, did not induce transplantation resistance. It is concluded that the expression of both the serologically‐defined VCSA and the transplantation antigen is the result of the interaction of pp60src with host cell gene product(s) rather than the simple exposure of pp60src at the outer cell surface.
A genetic approach to the role of energy metabolism in the growth of tumor cells: Tumorigenicity of fibroblast mutants deficient either in glycolysis or in respiration
Authors: Franchi A. , Silvestre P. , Pouysségur J. 
Published: February 2007

AbstractTo analyze the role of the cell energy metabolism in the expression of the malignant phenotype, we isolated fibroblast mutants with specific defects either in aerobic glycolysis or in respiration. From the anchorage‐independent and tumorigenic subclone (023) of Chinese hamster lung fibroblasts, we selected two mutants. The first, DS7, is deficient in aerobic glycolysis and glucose transport as a consequence of a block in phosphoglucose isomerase activity. DS7 is strictly dependent upon respiration for cell viability. The second mutant, GSK3, is unable to oxidize glucose as a result of a defect in oxidative metabolism, therefore its energy for growth relies exclusively on aerobic glycolysis. When injected into nude mice, these two mutant cells have kept the capacity to form tumors. For both mutants we observed an increase in the latency of tumor formation and a decreased tumorigenicity only for the respiration defective cells. The tumoral cells analyzed after passaging in vivo have retained the respective phenotypes, glycolysis‐ and respiration‐, of the injected cells. Finally, from the anchorage‐dependent and non‐tumorigenic Fisher rat fibroblast cell line, FR 3T3, we isolated mutants with a 6‐fold derepressed aerobic glycolysis and high glucose transport rate. In spite of this transformed character, these mutants (GSR 16/24) have kept the normal growth characteristics of the parent FR 3T3 (anchorage dependency and non‐tumorigenicity). These results indicate that only one of the two energy metabolisms of the mammalian cell ‐ respiration or aerobic glycolysis ‐ is enough for the expression of the malignant phenotype. Therefore, the high aerobic glycolysis of tumoral cells should be regarded as a non‐essential character of tumoral growth.
Effect of bacillus calmette‐guéarin cell wall skeleton on the induction of the cytotoxic and suppressor T cells against syngeneic tumor in the mouse
Authors: Koyama Shohei , Fujimoto Shigeyoshi , Tada Tomio , Sakita Takao 
Published: February 2007

AbstractThe effect of Bacillus Calmette‐Guérin cell wall skeleton (BCG‐CWS), which is one of the well‐established immunopotentiators, on the induction of either cytotoxic or suppressor T cells against syngeneic tumor S1509a was investigated by an in vitro assay system. BCG‐CWS showed an apparent augmenting activity in the induction of cytotoxic T cells against a syngeneic tumor when it was administered subcutaneously into mice with mitomycin C (MMC)‐treated tumor cells in a form of oil‐in‐water emulsion. In addition, cytotoxic T cell activity was dominantly generated in regional lymph nodes. Furthermore, the immunized animals developed stronger resistance against the second inoculum of the same viable tumor cells. However, BCG‐CWS had no effect on the induction of suppressor T cells in tumor‐bearing host (TBH), and could not induce cytotoxic T cells against the homologous tumor in TBH in which suppressor T cells had been readily activated. The growth of tumor was neither suppressed nor enhanced, even if an oil‐attached BCG‐CWS was administered in TBH.