bluuebunny/crossref_metadata_2025_split huggingface dataset:
Antitumor effects of two polyamine antimetabolites combined with mitomycin C on human stomach cancer cells xenotransplanted into nude mice
Authors: Fujimoto Shigeru , Igarashi Kazuei , Shrestha Ram Dhoj , Miyazaki Masaru , Okui Katsuji 
Published: February 2007

AbstractThe antitumor effects of alpha‐difluoromethylornithine (DFMO), methylglyoxal‐bis‐guanylhydrazone (MGBG) and mitomycin C (MMC), administered separately or in various combinations, on human stomach cancer cells xenotransplanted into BALB/c nude mice were studied using the protocol of Battelle's Columbus Laboratories (Ovejera et al., 1978). DFMO (1,000 mg/kg in 2 divided doses) and MGBG (50 mg/kg) were given Intraperitoneally (i. p.) for 7 consecutive days from the time when the tumor weighed about 100 mg. MMC (2 mg/kg) was given i. p. every other day from the same time. Animals treated with either DFMO or MGBG alone displayed tumor growth comparable to that seen in untreated controls. In mice treated with DFMO plus MGBG with or without MMC, or in mice treated only with MMC, tumor growth was significantly lower than in untreated mice. In the group which received only combined DFMO/MGBG there was a rapid regrowth of the tumor after termination of therapy. Tumor putrescine levels decreased within 4 days following the administration of DFMO; however, spermidine levels did not decline with either DFMO or MGBG treatment even after 7 days. When combined DFMO/MGBG was given, there was a significant decline in spermidine levels 7 days after the initiation of treatment. In contrast, when MMC alone was administered, putrescine and spermidine levels in the tumor did not differ from those in control mice. Spermine decreased markedly in tumor with the combined administration of DFMO/MGBG as well as with combined DFMO/MGBG/MMC, but decreased only slightly when MMC alone or MMC plus either DFMO or MGBG was administered. By the 7th treatment day, DNA biosynthesis in the tumor had dropped markedly in all groups except those receiving DFMO or MGBG alone.
The value of HLA phenotypes in the prognosis of Hodgkin's lymphoma
Authors: Hafez Mohamed M. , El‐Wehedy Gamal F. , El‐Kholy Nawal M. , El‐Shawaf Ibrahim M. , Gamil Tawakol M. , Mahmoud Mohamed Eissa A. 
Published: February 2007

AbstractThe study included 52 patients with Hodgkin's disease, 32 males and 20 females, whose ages ranged from 3 to 36 years (34 under and 18 over 15 years). All patients were carefully staged, and lymph‐node biopsies were taken for histopathological examination. HLA phenotype determinations were carried out, and the frequencies were statistically compared with those of normal Egyptian controls. We followed the patients for 3 years to monitor the effect of therapy. In order to determine the prognostic value of patients′ characteristics (age, stage, histologic pattern and HLA phenotypes), statistical analysis and retrospective stratification studies were performed. The frequency of HLA‐AI was significantly increased in our patients. The relative risk showed that persons carrying the Al antigen are 6 times more susceptible than those lacking it. There was no significant difference in the frequency of Al antigen in relation to the histopathologic subtypes. Furthermore, the results revealed a prognostic value of the HLA marker. In conclusion, we suggest that chemotherapy should be added to radiotherapy of marker‐positive patients at any stage.
The interaction of melanoma cells with fibroblasts and endothelial cells in three‐dimensional macromolecular matrices: A model for tumour cell invasion
Authors: Schor S. L. , Schor A. M. , Winn B. , Allen T. D. 
Published: February 2007

AbstractComparative quantitative data are presented concerning the adhesion, proliferation and invasive behaviour of RPMI‐3460 melanoma cells on (1) plain collagen gels, (2) monolayer cultures of fibroblasts and endothelial cells growing on the gel surface, and (3) the exposed endothelial and fibroblast extracellular matrices (ECMs). Both types of ECMs enhanced melanoma cell adhesion and proliferation (compared with plain gels) and had marked, but distinctive, effects on melanoma morphology. The thickness and composition of the ECMs was altered by treatment of the matrices with enzymes (trypsin, elastase and chondroitinase ABC) or by using ECMs produced by endothelial cells at various times after confluence. Variations in the thickness and composition of the ECMs had no effect on the behaviour of melanoma cells growing on these matrices; our results suggest that the glycoproteins and glycosaminoglycan ECM constituents removed by digestion with the enzymes do not play an important role in melanoma cell attachment, proliferation and migration. Melanoma cells plated on the surface of a plain collagen gel rapidly migrated down into the collagen matrix, with approximately 30% of the cells found within the gel after 6 days of incubation. Fibroblast and endothelial ECMs significantly and distinctively inhibited melanoma invasion into the underlying collagen gel. The extensive invasion of melanoma cells into the gel was not accompanied by hydrolysis of the collagen fibres. Conversely, fibroblast and endothelial ECMs, which acted as effective barriers, were extensively hydrolysed by the melanoma cells. The possible use of ECMs deposited on collagen in the study of melanoma local invasion (on fibroblast ECMs) and extravasation (on endothelial ECMs) is discussed.
Survey of a population with a high incidence of oral and oesophageal cancer
Authors: Zaridze David G. , Blettner Maria , Trapeznikov Nikolai N. , Kuvshinov Juri P. , Matiakin Eugene G. , Poljakov Boris P. , Poddubni Boris K. , Parshikova Svetlana M. , Rottenberg Vera I. , Chamrakulov Farchad S. , Chodjaeva Mamlakat C. , Stich Hans F. , Rosin Miriam P. , Thurnham David I. , Hoffmann Dietrich , Brunnemann Klaus D. 
Published: February 2007

AbstractThe results of a survey of a population with a high incidence of oral and oesophageal cancer are presented. The population under study appears to have several epidemiologic characteristics, some of which may be associated with a high incidence of oral and oesophageal cancer. A remarkably high proportion (41%) of the men surveyed were nass users and this habit, like the use of other types of tobacco mixtures, has been related to oral cancer. Oral leukoplakia and chronic oesophagitis (conditions thought to be precursors of oral and oesophageal cancer) have been diagnosed in 11% and 60%, respectively, of the persons examined. Analysis of the relationship between nass use, cigarette smoking, oral leukoplakia and oesophagitis revealed that the prevalence of oral leukoplakia is highest among cigarette smokers who use nass. It appears that nass use does not affect the frequency of occurrence of chronic oesophagitis. However, a slight elevation of the prevalence odds ratio was observed for current smokers and drinkers. Biochemical analysis of the blood of a random sample of the surveyed population revealed low levels of riboflavin, vitamin A and carotenoids—vitamins that most probably have a protective effect against the development of cancer. The mutagenicity test has shown that nass contains a chemical or chemicals that exert a genotoxic effect. Chemical analysis revealed the presence in nass of tobacco‐specific N‐nitroso compounds.
Differential responsiveness of cloned mammary carcinoma cell populations to the human recombinant leukocyte interferon enhancement of tumor antigen expression
Authors: Greiner John W. , Tobi Martin , Fisher Paul B. , Lancer Jerome A. , Pestka Sidney 
Published: February 2007

AbstractWe have previously shown that a recombinant human leukocyte interferon (IFN‐αA)5 can mediate an increase in cell surface tumor antigen expression in human carcinoma cells but not normal cells (Greiner et al., 1984). Such a biological response modifier may prove useful in circumventing the problem of antigenic heterogeneity and could increase the effectiveness of monoclonal antibodies (MAbs) for detection and/or therapy of human carcinoma lesions. These studies also revealed that, within populations of human carcinoma cells, there exist subpopulations which are unresponsive to the antigen‐enhancing properties of IFN‐αA. Utilizing cloned cell populations from the MCF‐7 human breast carcinoma cell line, we now report the differential responsiveness to the tumor antigen enhancing and antiproliferative actions of IFN‐αA. Binding of MAb B72.3 to the 220‐400 kd tumor antigen, TAG‐72, is increased by IFN‐αA treatment on the surface of the parental MCF‐7 cell line and 2 cloned cell populations. A third MCF‐7 clone does not express this antigen either before or after IFN‐αA treatment, but does express a 90 kd tumor antigen and carcinoembryonic antigen which bind MAbs B6.2 and BI. I, respectively. The level of expression of these 2 surface tumor antigens remained unchanged upon interferon treatment. The growth of the parental MCF‐7 cells and the 3 cloned cell lines was, however, inhibited IFN‐αA. These cell lines also exhibited approximately the same number of interferon receptors with similar binding affinities for IFN‐αA. The results demonstrate a dissociation of two biological actions of IFN‐αA‐antiproliferative activity and enhancement of tumor antigen expression within a cloned human carcinoma cell line. Our studies also indicate that the differential response of cloned MCF‐7 cells to tumor antigen modulation by interferon involves alterations in the transduction of signals occurring distal to receptor occupancy within the biochemical pathways responsible for the actions of this biological response modifier. In addition, the clonal cell lines we have isolated which differ in their responsiveness to interferon should prove valuable in analyzing the molecular basis of interferon actions and may provide insights into the mechanism by which this compound confers its anti‐tumor activity.
Elevated expression of the cellular SRC gene in tumors of differing etiologies in xiphophorus
Authors: Schartl Manfred , Schmidt Carl‐Rudolf , Anders Annerose , Barnekow Angelika 
Published: February 2007

AbstractIn the fish Xiphophorus we have detected elevated levels of pp60c‐src kinase activity in a variety of tumors (n = 34) of neurogenic, epithelial, and mesenchymal origin either of hereditary etiology or induced by carcinogens. This elevation ranged from 2‐fold up to 50‐fold compared to the corresponding non‐tumorous tissue and up to 6‐fold compared to the highest activities found in any of the normal organs. The level of elevation parallels the degree of malignancy in melanoma and in tumors of mesenchymal origin. In fish bearing tumors of hereditary etiology kinase activity was also elevated in the non‐tumorous brain, while in fish bearing induced tumors, kinase activity was elevated only in the cells of the neoplasia.
Humoral response against murine lymphoma cells xenogenized by drug treatment in vivo
Authors: Romani L. , Mage M. G. , Puccetti P. , Fioretti M. C. 
Published: February 2007

AbstractTreatment of murine lymphomas with triazene derivatives may lead to the appearance of novel drugmediated tumor antigens, a phenomenon known as chemical xenogenization. Such antigens, which are capable of eliciting specific transplantation resistance in histocompatible mice, have been previously detected by in vivo and in vitro cell‐mediated immune responses. In the present report we address the question of the humoral antibody response to a chemically xenogenized lymphoma. Histocompatible mice were given several injections of live cells of the xenogenized tumor. Ten days after each immunization, pooled sera from different animals were analyzed for Ab content by means of flow microfluorometry analysis and CELISA assay. The results reveal that antibodies of both IgG and IgM classes capable of binding the xenogenized tumor can already be detected after one single sensitization. However, the Ab titer gradually increases through subsequent immunizations, reaching a peak level after 3–4 injections at a time when most of the humoral response is made up of antibodies of IgG class. The specificity of the anti‐xenogenized tumor hyperimmune sera was subsequently investigated by its reaction with the parental, nonxenogenized line and with normal tissue cells of the same or allogeneic haplotypes. The data obtained point out that cross‐reactivity with the parental line could be completely removed by absorption of the hyperimmune sera on parental cells, which removed most of the IgM antibodies. Moreover, the presence of an excess of anti‐parental antibodies on the xenogenized tumor cells does not prevent the subsequent binding of the hyperimmune absorbed serum, thus indicating that the novel determinant(s) recognized on xenogenized cells are not spatially related to those shared with the original parental tumor. In addition, the hyperimmune absorbed serum does not crossreact with normal hemopoietic or lymphoid cells of the same (H‐r, or allogeneic H‐t> and H‐r haplotypes. Furthermore, no alien histocompatibility antigens of H‐t> or H‐r haplotypes could be detected on the xenogenized tumor cell surface. Taken together, these data provide evidence that chemical xenogenization of a murine lymphoma leads to the appearance of novel determinant(s) detectable by specific antibodies.
Differentiation of abelson murine leukemia virus‐infected promonocytic leukemia cells
Authors: Hines David L. 
Published: February 2007

AbstractVirus‐producing, tumorigenic, promonocytic leukemia cell lines were derived from Abelson murine leukemia virus‐infected mice. This study shows that, of these 25 cloned lines, 22 were capable of extensive differentiation. It also shows that granulocyte‐macrophage colony‐stimulating activity increased the proportion of differentiating cells in 17/22 lines. Cells from agar colonies with a diffuse colony morphology had an increased expression of mature macrophage phenotypic characteristics, and a reduced proliferative capacity in vitro, compared to cells from agar colonies with a compact colony morphology. Cells from diffuse colonies also produced less Abelson virus, and were less tumorigenic in vivo than cells from compact colonies. Together, these results suggest some Abelson virus‐producing leukemic cells are not blocked in their capacity to differentiate and are capable of reversing the transformed phenotype.
Two distinct human myeloma cell lines originating from one patient with myeloma
Authors: Katagiri Shuichi , Yonezawa Takeshi , Kuyama Jun , Kanayama Yoshio , Tamakl Toshiharu , Ohnishi Mitsunobu , Tarui Seiichiro , Nishida Kazuhiro , Abe Tatsuo 
Published: February 2007

AbstractTwo distinct cell lines (OPM‐l and OPM‐2) were established from the peripheral blood of a 56‐year‐old female myeloma patient at the stage of terminal leukemic evolution associated with loss of cytoplasmic immunoglobulin heavy chain (Gλ ± λ). The lines grew in suspension with a doubling time of 36‐42 hr and 30‐36 hr, respectively. EBNA was absent from both lines. The lines synthesized cytoplasmic λ‐chain, but had no detectable surface immunoglobulins. Fc receptors and complement receptors could not be detected in either line. The lines had very complex chromosomal abnormalities, but the patterns of chromosomes differed greatly between the two lines. The two lines, together with the RPMI 8226 line established by Matsuoka et al. (1967), were analyzed for phenotypic expression as defined by a panel of monoclonal antibodies to B cells (B1, BA‐1, BA‐2, BA‐3, OKla‐1 and OKT10/BMA0100). Neither OPM‐I nor OPM‐2 reacted with any of the antibodies tested except OKT10. OPM‐l cells reacted weakly ( < 30%) with OKT10/BMA0100, while OPM‐2 cells showed a fluctuating reactivity, ranging from 40 to 80%, with OKT10/BMA0100. In contrast, RPMI 8226 reacted strongly with OKT10 and BA‐2. These results demonstrate the presence of phenotypic heterogeneity in all 3 myeloma cell lines, suggesting that the lines might represent different stages of terminal B‐cell development.
An immunohistological study of leukocyte localization in benign and malignant breast tissue
Authors: Lwin Khin Y. , Sloane John P. , Zuccarini Ombretta , Beverley Peter C. L. 
Published: February 2007

AbstractUsing morphometric ana immunohistological techniques, we investigated the distribution of T lymphocytes and subsets, B lymphocytes, macrophages and plasma cells in sections of human breast tissue. In normal lobules and ducts, leukocytes were found in greater density in the epithelium than in the stroma. The intra‐epithelial cells consisted largely of suppressor/cytotoxic T lymphocytes with a smaller number of macrophages; inducer T cells were seen in only 1 out of 10 subjects and were present in very low numbers. In the stroma, there were roughly equal numbers of suppressor/cytotoxic cells, macrophages and plasma cells containing IgA or IgM. Small numbers of stromal inducer lymphocytes were seen in only 2 cases. Although the density of suppressor/cytotoxic cells in the epithelium was considerably greater than in the stroma, macrophages were present in roughly similar density in both locations. In carcinoma, the ratio of epithelial to stromal leukocyte density was reversed, due to a marked reduction in intra‐epithelial cells and to an increase in those in the stroma. Between 10% and 30% of lymphocytes expressed activation markers in contrast to the normal breast in which virtually all were negative. Inducer lymphocytes were identified in 9/10 carcinomas. The possible relationship of inducer cells to breast carcinoma and pre‐neoplasia is discussed and warrants further investigation. No alteration in stromal plasma cell numbers was observed.
Induction of cell differentiation in burkitt lymphoma lines. BLA: A glycolipid marker of B‐cell differentiation
Authors: Balana Anne , Wiels Joëlle , Tetaud Cécile , Tursz Thomas , Mishal Zohar 
Published: February 2007

AbstractWe have previously described an MAb referred to as 38.13 which reacts with a glycolipid membrane antigen (named BLA) on Burkitt lymphoma (BL) lines. The BLA antigen and other B‐cell differentiation markers have been studied on BL lines treated with sodium butyrate, agents from the phorbol‐diester series (with or without differentiating properties) and teleocidin. With all differentiation inducers tested, expression of BLA as well as of surface IgM decreased on the induced cells whereas that of B1 increased and that of HLA DR remained stable. No BL cells studied reacted with anti‐IgD, with B2 or with LBI MAbs, either before or after induction. An EBV‐negative line (BJAB) was compared to its Epstein‐Barr virus (EBV)‐converted subline (BJAB/B95). Both EBV‐positive and EBV‐negative lines gave comparable results. These data demonstrate that BL cells could be moved along their differentiation pathway by chemical inducers and suggest that BLA represents a new glycolipid marker of early B‐cell differentiation.
Phorbol myristate acetate (PMA) suppresses polarization and locomotion and alters F‐actin content of walker carcinosarcoma cells
Authors: Keller H. D. , Zimmermann A. , Cottier H. 
Published: February 2007

AbstractThis study demonstrates a novel feature of PMA, its ability to suppress chemokinetic polarization and locomotion of tumor cells. Walker carcinosarcoma cells exhibit two distinct types of polarization and locomotion, i.e. spontaneous polarization characterized by ruffles at the front and stimulated polarization and locomotion in response to the microtubule‐disassembling agents colchicine, vinblastine and nocodazole, which are characterized by bleb bing at the front. The tumor promotor phorbol myristate acetate (PMA), but not phorbol, was found to suppress both types of polarization and random locomotion at concentrations between 10−8 and 10−6M. The effect of 10−6M PMA was virtually complete within 5 min. Inhibition of locomotion was due to both a reduction in the speed of migrating cells and the proportion of migrating cells. Changes in shape and chemokinesis of Walker carcinosarcoma cells were associated with alterations in the relative amount and the topographical distribution of F‐actin as determined by NBD‐phallacidin binding. Suppression by PMA was associated with loss of the polar topographical distribution of F‐actin visualized by NBD‐phallacidin binding. In the presence of PMA, the relative amount of F‐actin was higher than in unstimulated controls and lower in cells exposed to microtubule‐disassembling agents.
Induction and maintenance of flattened morphology in highly adhesive friend leukemia clones depends on the time‐ and space‐specific assembly of microtubular networks
Authors: Benedetto A. , Amici C. , Djaczenko W. , Zaniratti S. , Elia G. 
Published: February 2007

AbstractIndirect immunofluorescent staining with anti‐tubulin antibodies, SEM and TEM were applied to study microtubule (MT) assembly in clones isolated from Friend leukemia cells (FLC, 745 A strain) on the basis of their sensitivity to exogenous fibronedin (FN). Kinetics of cell spreading and elongation were studied using computerized image analysis and SEM. In contrast to 745 A cells, FN‐sensitive clones (referred to as FF clones) showed elaborate MT networks when observed by immunofluorescent staining as well as by TEM. A good correlation was found between the degree of spreading and elongation of FF cells and the degree and cellular distribution of their MT. The highest concentration of MT networks oriented parallel to the main cellular axis was observed in very elongated FF cells. The majority of MT in interphase FF cells radiated from the centrosomes; some MT apparently originated from the nuclear membranes. TEM showed the existence of morphological differences between centrosomes of 745 A and FF cells. The characteristic ultrastructure of the centrosomes of FF cells was maintained in trypsinized cells, even if such FF cells lost MT's and acquired a spherical morphology. FF cells, treated with a wide spectrum of MT ‐ disrupting agents, promptly acquired a rounded morphology with rapid dissolution of polymerized tubulin. Removal of MT‐disrupting agents from the culture medium rapidly restored a flattened morphology with concurrent regeneration of MT's. During recovery from MT‐disrupting agents, FF cells showed increased numbers of centrosomes per cell. We conclude that MT networks cooperate in the attachment, spreading and elongation of FF cells isolated from FLC. Moreover, we hypothesize the existence in FF cells of a variant form of centrosomes as compared with those of 745 A cells.
DBA/2‐like minor histocompatibility antigens on a BALB/c lymphoma. A balb/c anti‐DBA/2 serum which lyses the tumor and blocks balb/c anti‐tumor and anti‐DBA/2 effectors
Authors: Ballinari Dario , Grazioli Laura , Sensi Maria Luisa , Parmiani Giorgio , Borrello Maria Grazia 
Published: February 2007

AbstractWe have previously shown that BALB/c anti‐DBA/2 T cells can lyse the Moloney virus‐induced BALB/c lymphoma YC8. In order to determine whether serologically defined minor histocompatibility antigens (MiHA) cross‐reacting with those of DBA/2 tissues are present on YC8, we produced an antiserum directed against non‐H‐2 antigens by immunizing BALB/c mice with DBA/2 Con A and lipopolysaccharide (LPS)‐induced lymphoblasts. In a direct complement‐dependent cytotoxicity assay, the antiserum (OR‐I) lysed DBA/2 and YC8 but not BALB/c lymphocytes and blasts. No reactions against viral antigens were detected in the antisera as shown by the lack of cytotoxicity on a panel of lymphomas expressing a variety of viral antigens. In addition, OR‐I was able to specifically block a cytotoxic T lymphocyte (CTL), H‐2‐restricted BALB/c anti‐DBA/2 cytotoxic response when bound to DBA/2 or to YC8 target cells. These results indicate that antigens cross‐reacting between YC8 lymphoma and DBA/2 tissues are serologically defined MiHA of DBA/2 background and that OR‐I serum can block a CTL reaction by binding to target antigen rather than to major histocompatibility complex products.