bluuebunny/crossref_metadata_2025_split huggingface dataset:
A fine fibrous silica contaminant of flour in the high oesophageal cancer area of North‐East Iran
Authors: O'Neill C. H. , Hodges G. M. , Riddle P. N. , Jordan P. W. , Newman R. H. , Flood R. J. , Toulson E. C. 
Published: February 2007

AbstractWe report here the discovery and characterization of a fibrous mineral contaminant of the diet in that area of north‐east Iran where oesophageal cancer has a very high incidence. This contaminant has a smoothly tapering shape and is between 50 and 150 μm long. The greatest diameter is between I and 10 μ and this decreases to a sharply pointed tip with a radius of curvature of between 0.25 and 0.60 μm. Electron microscope X‐ray analysis shows that this fibre consists almost entirely of silica. It is free from alkali metals, aluminium and iron, and therefore differs from other known natural or manmade mineral fibres. Examination of the seeds of more than sixty different species of weed known to contaminate the wheat in this area of the Middle East shows that the fibre originates from the seeds of the common Mediterranean grass Phalaris minor. This seed bears fibres of the same dimensions, composition and birefringence, borne upon the inflorescence bracts which envelop the pericarp of the seeds of this and other members of the Phalaris genus. They are broken off from the seed when the wheat is milled but persist in the flour, where up to 3,000 are found in each gram. Similar fibres can be isolated in quantity from the seeds of related species which are grown commercially, and they have a similar size and composition. When cells of the 3T3 mouse fibroblast line are exposed to these fibres in semi‐solid suspension culture, their proliferation is stimulated more than 100‐fold. We present an hypothesis for the involvement of these plant mineral fibres in the aetiology of oesophageal cancer in Iran and in other areas of high incidence.
The humoral antibody response of rats immunized with chemically modified syngeneic brain cells and glioma cells
Authors: Stavrou D. , Hultén Mariette , Anzil A. P. , Bilzer Th. 
Published: February 2007

AbstractSix‐month‐old Fischer rats (F344) were given the carcinogen methylnitrosourea in their drinking water. Of the induced brain tumors, four were established in culture and propagated as 78FR‐G‐219 (pleomorphic glioma), 78FR‐G‐299 (astrocytoma), 78FR‐G‐284 and 78FR‐G‐344 (mixed glioma) permanent lines. All cell lines produced S‐100 protein and grew as tumors when inoculated s.c. or i.c. in syngeneic hosts. A comparative study of the antigenicity of these lines at different passage levels was carried out using native and chemically modified cells. Syngeneic rats were immunized with cells conjugated with dimethylsulfate and trinitrobenzene sulfonic acid. The immune response was characterized and quantified by an indirect immunofluorescence method and by a complement‐dependent microcy‐totoxicity test. Chemical modification of the tumor cells enhanced antigenicity of the treated cells. The best results were attained with trinitrobenzene sulfonic‐acidtreated cells and constituted a two‐fold increase in the cytotoxicity index. Cytotoxicity values varied in the different cell lines. Antisera raised with trinitrobenzene sulfonic‐acid‐modified cells of all lines cross‐reacted with cells of all lines. Cytotoxicity values were insignificantly reduced by absorbing the antisera with a variety of syngeneic tissues. Antisera raised against native syngeneic brain cells showed virtually no cytotoxicity for glioma cells. Antisera raised against syngeneic brain cells treated with trinitrobenzene sulfonic acid, however, were slightly cytotoxic for normal brain cells and glioma cells as well. The results of the present studies show that antigenicity of glioma cells can be definitely raised with trinitrobenzene sulfonic acid treatment. Furthermore, it would seem that haptenization of glioma‐associated antigens may be a promising approach to the study of glioma—host interactions.
Characterization of a serum factor stimulating the differentiation of myelomonocytic leukemic cells
Authors: Burgess Antony W. , Metcalf Donald 
Published: February 2007

AbstractCulture of WEHL‐3B myelomonocytic leukemic cells in semi‐solid agar medium containing serum from mice injected with endotoxin serum (ES) led to the development of maturing granulocytes and macrophages in most leukemic colonies. ES contains high levels of granulocyte‐macrophage colony‐stimulating factor (GM‐CSF), a regulator known to stimulate differentiation of these leukemic cells, but an antiserum which neutralized >85% of the GM‐CSF in ES did not suppress the differentiation‐inducing activity of ES on WEHI‐3B cells. The active factor in endotoxin serum stimulating differentiation in WEHI‐3B leukemic cells (GM‐DF) was separated from most of the GM‐CSF by gel filtration using Ultrogel AcA44. The residual CSF associated with the GM‐DF appeared to stimulate selectively granulocytic colonies. Disproportionation of GM‐DF and GM‐CSF was observed in ES fractions obtained using concanavalin‐A/Sepharose chromatography: none of the GM‐DF bound to this matrix, whereas 40% of the GM‐CSF bound and was eluted with competing α methylglucopy‐ranoside. Although no separation of GM‐CSF and GM‐DF was obtained using DEAE‐Sepharose, non‐isoelectric focusing in amphoteric buffers indicated charge differences between the differentiation factor and several sub‐species of GM‐CSF. Sequential purification of GM‐DF from ES using 40 ‐ 70 % ammonium sulfate precipitation gel filtration and phenyl‐Sepharose chromatography resulted in a 25‐fold purification. In all fractionation procedures used, a sub‐species of GM‐CSF, stimulating granulocyte colony formation, was consistently associated with partially purified GM‐DF, but some subspecies of GM‐CSF clearly lacked any capacity to induce differentiation in the leukemic cells. The observations suggest that the factor in post‐endotoxin serum most efficient in enforcing differentiation in myelomonocytic leukemic cells may be a subset of GM‐CSF molecules with a selective capacity to stimulate granulocyte colony formation by normal cells.
The effect of bursectomy on the adoptive transfer of resistance to Marek's disease
Authors: Powell P. C. , Rennie M. , Ross L. J. N. , Mustill Brenda M. 
Published: February 2007

AbstractImmunization with inactivated viral antigens protected chickens against Marek's disease. Non‐immunized chickens could be protected by injections of spleen cells but not of serum from immunized, histocompatible donors. Chickens rendered agammaglobulinaemic by bursectomy and irradiation could also be immunized against Marek's disease by inoculation with viral antigens, but spleen cells from these immunized, bursectomized and irradiated donors did not confer protection on the recipients into which they were injected. It was concluded that, although in the bursectomized, immunized donors cell‐mediated immunity alone was able to provide a fair degree of protection against Marek's disease, the protection afforded against the disease by spleen‐cell transfer was at least partly attributable to the transfer of antibody‐producing cells, and that humoral immunity, while not being an absolute requirement for resistance, is normally an important component of the resistance mechanism.
Adhesion of metastatic and non‐metastatic carcinoma cells to glass surfaces
Authors: Cottler‐Fox M. , Ryd W. , Hagmar B. , Fox C. H. 
Published: February 2007

AbstractAdhesion in vitro is described in cells from a tumor pair originating from a single methylcholanthrene‐induced mouse carcinoma. One member of this tumor pair shows a high incidence of metastases while the other does not metastasize. Cells from the non‐metastasizing carcinoma were found to form close and focal contacts with a glass substrate consecutively, as do normal mouse kidney epithelial cells. Cells from the metastasizing carcinoma, however, had only limited areas of close contact and generally failed to form focal contacts. It is suggested that this alteration in cell‐substrate adhesion contributes to the release and mobility of metastatic cells.
Demographic patterns for nasopharyngeal carcinoma in the united states
Authors: Levine Paul H. , Connelly Roger R. , Easton John M. 
Published: February 2007

AbstractDemographic and pathologic information on over 1,000 newly diagnosed patients with nasopharyngeal carcinoma was obtained from population‐based registries in the United States. Age‐adjusted incidence rates were similar for whites and blacks and both were significantly lower than for Chinese Americans. Age‐related differences in cell type were observed in white NPC patients, lymphoepithelial carcinomas having a younger age distribution than either squamous‐cell or transitional‐cell carcinomas. Mortality rates for nasopharyngeal cancer were substantially lower than incidence rates for nasopharyngeal carcinoma, but both indices revealed a minor peak in rates among teenaged whites and blacks. The five‐year survival rate for nasopharyngeal carcinoma was less than 25% and has not changed in recent years. Prognosis was better for females and for young patients. Despite the difficulties in obtaining uniform pathologic classification in such a large study, the interrelationship between pathologic subtype of nasopharyngeal carcinoma and demographic features emphasizes the need for adherence to a more uniform histologic classification.
A possible correlation between the degree of karyotype aberrations and the rate of sister chromatid exchanges in lymphoma lines
Authors: Fonatsch Christa , Schaadt Michael , Kirchner Hartmut , Diehl Volker 
Published: February 2007

AbstractThe sister chromatid exchange (SCE) frequencies of six freshly established and two old cell lines derived from patients with lymphatic tumors or leukemia were compared to the SCE rates of lymphoblastoid cell lines of normal controls. All cell lines from malignant tumors displayed significantly higher SCE values than the control lines. In general, the SCE rates seem to be correlated to the number of chromosomal markers and the degree of karyotypic instability of each line.
Malignant bone tumours induced by a local injection of colloidal radioactive 144cerium in rats as a model for human osteosarcomasl
Authors: Allouche Michele , Delbrück Hermann G. , Klein Bernard , Masse Roland , Matar Abdou , Morin Michele , Lafuma Jacques , Jasmin Claude 
Published: February 2007

AbstractLung metastases were observed in 80% to 85% of rats bearing advanced malignant bone tumours (osteogenic osteosarcomas and angiosarcomas). These tumours were induced in 2‐month‐old Sprague‐Dawley rats by inoculation of a colloidal suspension of radioactive cerium (144Ce) into the hind leg, in close contact to the bones of the knee joint. Twenty‐eight rats were killed or died spontaneously shortly after detection of palpable tumours at the site of injection: the incidence of lung metastases was 73.3% and 53.8%, respectively, for osteogenic sarcomas and angiosarcomas, showing that most lung metastases are present at the time of diagnosis of the primary tumour. Tumour‐cell kinetic parameters were studied in 49 rats bearing tumours following intraperitoneal injection of [3H]thymidine. The labelling index (LI) of the primary tumours was significantly lower in advanced tumours (7.2% for osteosarcomas and 10.1% for angiosarcomas) than in tumours examined at the time of detection (12.2% and 13.5%, respectively). Mitotic indices (MI) of all tumours were less than 1%. From the curve of the percentage of labelled mitoses (PLM) at different times after [3H]thymidine injection, Ts (6.5 h) and TG2 (1.75 h) were determined. Tc and TG1, were also evaluated (18 h and 9.25 h, respectively). These results show that malignant bone tumours induced in rats with 144Ce may be a good model for human osteosarcomas and may be useful in studying the numerous problems in the therapy of malignant bone tumours in man.
Tumorigenicity of friend murine erythroleukemia cell lines differing in spontaneous differentiation rates
Authors: Axelrod David E. , Majumdar Shyamal K. , Wivell Judith A. , Terry Robert W. 
Published: February 2007

AbstractThe relationship between tumorigenicity and in vitro differentiation was studied in four Friend erythro‐leukemia cell lines. The cell lines were isolated by repeated subcloning of an unmutagenized population (sib selection). The cell lines differed in their ability to form tumors when 103 cells were injected subcutaneously into syngeneic mice (8 to 56% animals with tumors). The ability of cell lines to form tumors was not proportional to their ability to be induced to differentiate by dimethylsulfoxide. The cell lines had indistinguishable chromosome numbers, plating efficiencies, number of cycling cells, population doubling times and spontaneous mutation rates to drug resistance. However, the cell lines had different spontaneous differentiation rates in the absence of dimethylsulfoxide (0.87 to 16.0 × 10−4 per cell per generation). The ability of cell lines to form tumors was inversely proportional to their spontaneous differentiation rate. Apparently cells which are most efficiently blocked in differentiation have the highest probability of forming tumors.
Presensitization of human cells with extrinsic signals to induced chemical carcinogenesis
Authors: Milo G. E. , Dipaolo J. A. 
Published: February 2007

AbstractForeskin‐derived low‐passage human cell populations were reproducibly transformed with chemical carcinogens when the cells were blocked in G1, released from the block, and treated with either the carcinogen N‐methyl‐N‐nitro‐N‐nitrosoguanidine (MNNG) or with Aflatoxin BI in the S period of the cell cycle. Arginine‐and glutamine‐deficient medium was required to effectively block the cells in the G1 period. Estradiol, insulin, anthralin or phorbol myristate acetate sensitized the cell population to carcinogen treatment when added 10 h before the carcinogen in early S period. Presensitized cells kept blocked in G1 period for 48 h or longer, released and treated in S period with MNNG or Aflatoxin BI were not transformed; nor did transformation occur in presensitized cell populations treated in G2 (4.5 h), M (1.5 h) or G1 (8.2 h). Cells derived from carcinogen‐treated presensitized cells grew as colonies in soft agar at 16‐20 PDL. When cells derived from colonies isolated from the soft agar were injected subcutaneously into nude mice, tumors developed.
Transplantation resistance of drug‐treated hybrid or allogeneic mice against murine lymphomas. I. Immunopharmacology studies
Authors: Bonmassar Anna , Riccardi Carlo , Rivosecchi‐Merletti Paola , Goldin Abraham , Bonmassar Enzo 
Published: February 2007

AbstractSequential treatment of mice with non‐lethal doses of 5(3,3′‐dimethyl‐I‐triazeno)‐imidazole‐4‐carboxamide (DTIC) and cyclophosphamide (Cy) was found to produce long‐term inhibition of endogenous cell proliferation in the spleen and profound impairment of classical allograft responses, similar to that detectable in lethally irradiated mice. Studies were carried out with drug‐treated (i.e. treated with DTIC + Cy) conventional or nude mice inoculated with lymphoma cells homozygous for the H‐2b or H‐2d haplotype. Transplantation resistance in various tumor‐host combinations was studied in terms of survival times after tumor challenge or lymphoma cell proliferation in spleen and liver, measured by the uptake of DNA precursor 125I‐labelled 5‐iodo‐2′‐deoxyuridine ([125I]dUrd). The results of in vivo transplantation immunity tests or in vitro tests of generation of cytotoxic lymphocytes confirmed that classical T‐dependent allograft responses were abrogated by drug treatment of H‐2‐incompatible hosts. However, localized resistance against lymphoma graft, mainly at spleen level, was found in drug‐treated hybrid mice, or conventional and “nude” allogeneic recipients, as judged by [125I]dUrd uptake inhibition. Resistance presumably regulated, at least in part by the Hh (hemopoietic histocompatibility) system, was abrogated by pretreatment with carrageenan, an antimacrophage agent. In addition, treatment with DTIC + Cy did not abrogate NK activity of mice when the in vitro cytotoxicity test was conducted 5h after Cy administration, i.e. at the time used for tumor challenge in vivo. It was concluded that selected immunological functions (i.e., antilymphoma natural resistance insensitive to DTIC + Cy, called drug‐resistant inhibition of tumors, DRIT) possibly of non‐T origin, similar to those detectable in lethally‐irradiated mice, can be retained by hosts subjected to high doses of certain anti‐tumor agents.
Suppression of activity of mouse natural killer (NK) cells by activated macrophages from mice treated with pyran copolymer
Authors: Santoni Angela , Riccardi Carlo , Barlozzari Teresa , Herberman Ronald B. 
Published: February 2007

AbstractTreatment of young mice with pyran copolmyer caused a substantial decrease in natural killer (NK) cell activity at 7 days. The decrease in cytotoxicity was associated with the presence of splenic suppressor cells, capable of inhibiting in vitro the NK activity of spleen cells from normal mice. The suppressor cells appeared to be macrophages, being plastic‐adherent, phagocytic and radioresistant, and lacking demonstrable Thy 1.2 antigen. Sonicates or culture supernatants of adherent spleen cells from pyran‐treated mice were also able to inhibit NK activity, suggesting that suppressor cells act by release of soluble factors.
Chemotherapy of human colorectal tumor xenografts in athymic mice with clinically active drugs: 5‐fluorouracile and 1‐3‐bis‐(‐2‐chloroethyl)‐1‐nitrosourea (bcnu). Comparison with doxorubicin derivatives: 4′deoxydoxorubicin and 4′‐0‐methyldoxorubicin
Authors: Giuliani Fernando C. , Zirvi Karimullah A. , Kaplan Nathan O. , Goldin Abraham 
Published: February 2007

AbstractThe effects of single‐agent therapy with two clinically useful drugs, 5‐fluorouracil (5‐FU) and 1‐3‐bis‐(2‐chloro‐ethyl)‐1‐nitrosourea (BCNU) against nine human colorectal tumors (rectum T 157 and T 348, lung metastasis T 84, lymph‐node metastasis T 245, colon, T 183, T 219, T 347, T 362 and T 380) transplanted and passed serially in athymic (nude) mice were studied. In addition, chemosensitivity of the tumors to 5‐FU and BCNU was compared with the chemosensitivity of the tumors to two new doxorubicin analogues, 4′‐deoxydoxorubicin and 4′‐O‐methyldoxorubicin. BALB/c nude mice were treated intravenously on a weekly basis for 3–4 weeks, starting when the tumor volume became relatively large (advanced stage of tumor treatment). All the tumors showed a 90–100% take rate and stable growth. In these experiments, 77% (5/9) of the colorectal tumors were biologically sensitive to the treatment with 5‐FU but the percentage of statistically significant sensitive tumors was 22%, which is in good agreement with the clinical data reported in the literature (21%). In patients, BCNU has been reported to give up to 13% response. In contrast, we have found a 33% statistically significant response rate in our panel of colorectal tumors. The difference could be related to the higher tolerance of nude mice to certain drugs, including BCNU. The results suggest that the two new doxorubicin derivatives, 4′‐deoxydoxorubicin and 4′‐O‐methyl‐doxorubicin, should be more active in the patient than both of the clinically used drugs, 5‐FU and BCNU. Furthermore, there is a good correlation between the results obtained in the experimental system (human tumor/nude mouse) and in human patients with the active drugs, 5‐FU and BCNU.
Early changes in the glycopeptides of human B‐lymphocytes after epstein‐barr virus infection in vitro
Authors: Van Beek Wim , Breekveldt Jan , De Bakker Ellen , Hilgers Jo , Hilgers Frans , Nilsson Kenneth 
Published: February 2007

AbstractHuman B lymphocytes obtained from healthy donors were infected with Epstein‐Barr virus in vitro. From the initiation of infection to the final establishment of a permanent lymphoblastoid cell line, fucosyl glycopeptides of the cell surface were investigated. In order of appearance the following events took place: expression of Epstein‐Barr virus‐determined nuclear antigen, mitotic activity of the cells and specific glycopeptide alterations on the cell surface. This specific alteration in glycopeptides, as determined by gel filtration, is manifested by the appearance of fast‐eluting glycopeptides and was similar to that found on Burkitt lymphoma cells. Neither pokeweed‐mitogen‐stimulated B lymphocytes nor exponentially growing normal T lymphocytes exposed fast‐eluting glycopeptides on their surfaces. Therefore, it is concluded that the appearance of these fast‐eluting glycopeptides on the surface of lymphoblastoid cells after EBV infection is not the result of culture conditions or conditions of growth as such. The similarity with glycopeptides derived from Burkitt lymphoma cells, and the observation that a considerable proportion of the B cells becomes immortalized, are discussed.
Chromosome 15 trisomy in spontaneous and carcinogen‐induced murine lymphomas of B‐cell origin
Authors: Wiener F. , Babonits M. , Spira J. , Bregula U. , Klein G. , Merwin R. M. , Asofsky R. , Lynes M. , Haughton G. 
Published: February 2007

AbstractG‐banding analyses of 14 independently derived B‐cell lymphomas showed the frequent occurrence of chromosome 15 trisomy. It was present in seven of nine spontaneous B‐cell lymphomas, but in company with other trisomies, monosomies and marker chromosomes. In five carcinogen‐induced primary B‐cell leukemias, trisomy 15 was the dominating change. Taken together with the previously demonstrated importance of chromosome 15 trisomy for T‐cell leukemogenesis and of the 12;15 translocation in plasmacytogenesis in the mouse, it appears likely that the distal part of chromosome 15 carries a cluster of genes, perhaps a supergene region, that may play an important role in the differentiation and/or the normal responsiveness of various lymphoreticular cell types to growth control.
Induction of type‐C retrovirus by the tumor promoter TPA
Authors: Hellman Kiki B. , Hellman Alfred 
Published: February 2007

AbstractThe tumor promoter 12‐0‐tetradecanoyl‐phorbol‐13‐acetate (TPA) induced endogenous murine xenotropic type‐C retrovirus from A1‐2 cells, derived from the BALB/c mouse, as determined by infectious center focus‐forming assay on permissive normal rat kidney (NRK) cells. Kinetic dose‐response studies showed that the number of cells induced to release virus was dependent on TPA concentration and the time of assay following TPA exposure. Maximal induction occurred when cells were treated with 80 ng/ml of TPA for 24 h and assayed at 24 or 48 h. A 30‐min pulsed TPA exposure of 200 ng/ml induced virus levels approximating those observed after a continous 24‐h exposure to 80 ng/ml. The combination of TPA at concentrations of 10 and 20 ng/ml and a suboptimal level of 5‐iodo‐2‐deoxyuridine (IdUrd) enhanced retrovirus induction threefold above that seen by the optimum IdUrd concentration alone. The protease inhibitors, antipain and leupeptin, decreased virus induction by TPA, a protease inducer. The capacity of TPA to induce type‐C retrovirus complements results demonstrating the enhancement of Epstein‐Barr virus (EBV) and murine mammary tumor virus (MMTV) synthesis by TPA.
Epstein‐barr virus‐induced malignant lymphoma in a white‐lipped marmoset
Authors: Sundar Syam K. , Levine Paul H. , Ablashi Dharam V. , Leiseca Sergio A. , Armstrong Gary R. , Cicmanec John L. , Parker George A. , Nonoyama Meihan 
Published: February 2007

AbstractOne of six white‐lipped marmosets inoculated with cell‐free B95‐8 virus developed diffuse malignant lymphoma. Epstein‐Barr virus (EBV) DNA was detected in a pathologically enlarged mandibular lymph node by DNA‐DNA hybridization. The affected animal at the time of killing had EBV antibody titers of 1:320 for viral capsid antigen (VCA) and 1:20 for early antigen (EA) while all non‐diseased animals had ≦1:80 VCA antibody and no detectable EA antibody. This is the first report of lymphoma development in a white‐lipped marmoset following EBV inoculation.