bluuebunny/crossref_metadata_2025_split huggingface dataset:
Establishment of a new human myeloma cell line (u‐2030) and selection of a hat‐sensitive subline
Authors: Jernberg H. , Björklund G. , Nilsson K. 
Published: February 2007

AbstractWe have established a new human myeloma cell line from the pleural effusion of a patient with an IgAλ myeloma, using special tissue culture conditions and selection procedures to prevent the outgrowth of contaminating Epstein‐Barr virus (EBV)‐carrying normal B‐lymphoblastoid cells present in the explant. The myeloma cell line, U‐2030, is aneuploid and EBNA‐negative and has morphological features, reactivity with cytochemical markers and cell‐surface antigen expression typical of plasmablasts. The cell line thus appears to be representative of the malignant clone in vivo. However, functionally the line is a non‐lg‐producer and must therefore be derived from a non‐secretory variant cell present within the highly aneuploid myeloma cell clone in vivo. The U‐2030 differs from previously established human myeloma cell lines in that it has a comparatively high growth rate, is clonable and can be made HAT‐sensitive relatively easily. This, together with the facts that it is a non‐lg‐producer and mycoplasma‐free, suggests that the 6‐thioguanine‐resistant, HAT‐sensitive subline, U‐2030 TG, derived from this cell line may be used as a malignant fusion partner for the production of human‐human hybridomas. An EBV‐carrying lymphoblastoid cell line (U‐2031) was also established. This line was diploid and had all the phenotypic properties of lymphoblastoid lines established from normal individuals.
Influence of some dietary chemopreventive agents on the expression of functional differentiation of the mouse mammary gland in vitro
Authors: Chakraborty Sarbani , Menon Ravi , Banerjee Mihir R. 
Published: February 2007

AbstractThe purpose of the present studies was to determine the influence of the chemopreventive agents selenium, 4‐(hydroxyphenyl)‐retinamide (4‐HPR) and β‐carotene, on functional differentiation (lactogenesis) of the mouse mammary gland cells. The hormone‐induced expression of the milk‐protein genes, β‐casein, ϵ‐casein and the whey acidic protein (WAP) was used as molecular marker of differentiation of the mammary cells in organ culture medium containing insulin, prolactin, aldosterone and hydrocortisone. Quantitative determination of the cellular concentration of the respective mRNA was ascertained by molecular hybridization of RNA to the specific cloned cDNA probes using both the solution and the filter hybridization methods. Selenium at 100 nm concentration caused a pronounced inhibition of accumulation of the respective mRNAs. The retinoid, 4‐HPR, also caused a dose‐dependent inhibition of expression of these mRNA sequences. In contrast, concentrations of the 3 mRNAs in β‐carotene‐treated glands remained similar to those observed in glands cultured in medium containing the hormones and hexane (the latter being the solvent for β‐carotene). The significant antagonistic action of selenium and 4‐HPR, however, was reversible after removal of the chemicals from the culture medium. Thus, among the 3 chemicals tested, selenium and retinoid can cause an adverse effect on functional differentiation (lactogenesis) of the mammary cells. This inhibitory effect, however, was reversible. β‐Carotene, on the other hand, caused no apparent antagonistic effect on expression of the milk‐protein genes in the isolated whole mammary organ in culture.
Tumor‐cell‐induced platelet aggregation is a glycoprotein‐dependent and lipoxygenase‐associated process
Authors: Bastida Eva , Almirall Lourdes , Ordinas Antonio 
Published: February 2007

AbstractTo characterize the platelet receptor sites and the platelet metabolic pathways involved in tumor‐cell‐induced platelet aggregation, we have used a homologous system consisting of human platelets and 2 tumor cell lines of human origin, which activate platelets through different mechanisms. Preincubation of platelets with an MAb against platelet glycoprotein Ib partially blocked tumor‐cell‐induced platelet aggregation, and preincubation of platelets with an MAb against the glycoprotein complex GPIIbIIIa, totally blocked the aggregation induced by the 2 tumor‐cell lines. No inhibitory effect was found when platelets were treated with PAF‐receptor antagonists or with specific peptides which block the platelet sites involved in bacterially induced platelet aggregation. Compounds which raised intra‐platelet cAMP levels inhibited tumor‐cell‐induced platelet aggregation in a dose‐related manner. Inhibition of cyclo‐oxygenase by aspirin which blocked TxB2 formation by platelets did not inhibit platelet aggregation induced by tumor cells whereas the BW755 compound which inhibits cyclo‐ and lipoxygenase blocked platelet aggregation. These results demonstrate that tumor‐cell‐induced platelet aggregation is a glycoprotein‐dependent and a lipoxygenase‐associated phenomenon.
Inhibition of mannose incorporation into glycoproteins and dolichol‐linked intermediates of sarcoma 180 cells by 6‐methylmercaptopurine ribonucleoside
Authors: Sokoloski John A. , Sartorelli Alan C. 
Published: February 2007

Abstract6‐Methylmercaptopurine ribonucleoside (6‐MMPR), an inhibitor of purine nucleotide biosynthesis de novo, was used as a model compound to evaluate the relationship between the levels of intracellular guanosine triphosphate (GTP) and the formation of cellular glycoproteins and their dolichol‐oligosaccharide precursors in Sarcoma 180 cells. Previous studies using the purine antimetabolite, 6‐thioguanine (6‐TG), demonstrated a relationship between the drug‐induced decrease in GTP levels and the incorporation of radiolabelled mannose and fucose into cellular glycoproteins; estimation of the importance of these cell‐surface alterations to the cytotoxicity produced by this agent was complicated by the incorporation of 6‐TG nucleotides into cellular DNA and RNA. In this report, evidence is presented to show that the toxicity of 6‐MMPR to Sarcoma 180 cells is associated with the effects of this agent on the intracellular pools of purine nucleotides. GTP functions in part in the activation of the sugar mannose, a step necessary for the biosynthesis of glycoproteins from nucleotide sugar precursors. Thus, 6‐MMPR, which blocks the de novo pathway of purine nucleotide biosynthesis, caused a pronounced decrease in the intracellular pools of GTP in Sarcoma 180 cells; this phenomenon was accompanied by a marked reduction in the incorporation of radiolabelled mannose into cellular glycoproteins and their dolichol‐linked oligosaccharide precursors. In contrast, the incorporation of glucosamine, a sugar not metabolically activated by GTP, into glycoproteins, and of leucine into protein, were depressed only after prolonged incubation with either 6‐MMPR or 6‐TG. Adenine restored purine nucleotide pools depleted by 6‐MMPR and partially prevented both the reduction in mannose incorporation into glycoprotein and the cytotoxic effects of this antimetabolite. Guanosine partially reversed the effects of 6‐MMPR on intracellular GTP pools and mannose incorporation but not the depression of ATP pools produced by this antimetabolite. However, guanosine did not reverse the cytotoxicity of 6‐MMPR but instead enhanced its toxicity. The findings are consistent with the possibility of membrane changes being involved in the cytotoxicity of 6‐MMPR, but clearly other factors are involved as well.
Several murine metastasizing tumors possess a cysteine proteinase with cancer procoagulant characteristics
Authors: Falanga Anna , Dalessandro Anna Paola Bolognese , Casali Bruno , Roncaglioni Maria Carla , Donati Maria Benedetta 
Published: February 2007

AbstractCancer Procoagulant (CP), a cysteine proteinase which triggers blood coagulation by directly activating Factor X (FX) in the absence of Factor VII (F VII), has recently been isolated from rabbit V2 carcinoma and biochemically characterized. We have studied the procoagulant activity of tissue extracts from 4 murine experimental tumors in order to define whether or not a F VII‐independent activity with cysteine proteinase characteristics was present. The tumors studied were: Lewis lung carcinoma (3LL), B16 melanoma (B16), JW sarcoma (JWS) and the M4 variant of the mFS6 fibrosarcoma (M4). Extracts from 3LL, B16 and JWS tumor initiated coagulation in both the presence and absence of F VII, their procoagulant activity was sensitive to iodoacetamide (1 mm) and mercury chloride (0.1 mm). The procoagulant of M4 extract was dependent on the presence of F VII and was not significantly affected by the cysteine proteinase inhibitors. An Ouchterlony double immunodiffusion study showed immunological cross‐reactivity of all but M4 extracts to a polyclonal antibody to purified CP. The present study suggests that the procoagulant(s) present in the murine tumors 3LL, B16 and JWS are enzymatically and immunologically indistinguishable from cancer procoagulant of the rabbit V2 carcinoma.
c‐yes and bc1‐2 genes located on 18q21.3 in a follicular lymphoma cell line carrying a t(14;18) chromosomal translocation
Authors: Ohno Hitoshi , Fukuhara Shirou , Takahashi Rei , Mihara Koh‐Ichirou , Sugiyama Taketoshi , Doi Shoichi , Uchino Haruto , Toyoshima Kumao 
Published: February 2007

AbstractThe c‐yes‐1 and bc1‐2 genes have been independently mapped at the same position of the chromosome band, 18q21.3, which is a breakpoint in the t(14; 18) chromosomal translocation. High‐molecular‐weight genomic DNAs and mRNA isolated from a follicular lymphoma cell line FL‐18 and an Epstein‐Barr virus harboring FL‐18EB cell line, which carried the t(14;18), were analyzed. Although there was no detectable c‐yes rearrangement, the chromosome 18‐specific probe b (bc1‐2) revealed one rearranged fragment after EcoRI, BamHI, PstI and SstI digestion. Therefore, breakage of chromosome 18 in the t(14;18) occurred at the SstI fragment containing the probe b sequence on the bc1‐2 gene. The transcript of c‐yes was undetectable, whereas active transcription of bc1‐2 was observed in the FL‐18 and FL‐18EB cell lines at a higher level than in other types of lymphoma cell line. These data suggest that the c‐yes‐1 is not involved in the t(14;18), and the 2 genes located at 18q21.3 are independent sequences.
Anti‐tumor effects of interferon in mice injected with interferonsensitive and interferon‐resistant friend leukemia cells. VI. Adjuvant therapy after surgery in the inhibition of liver and spleen metastases
Authors: Gresser Ion , Maury Chantal , Belardelli Filippo 
Published: February 2007

AbstractAdult DBA/2 mice were injected s.c. with the highly malignant, interferon‐resistant 3C18 line of Friend erythroleukemia cells (FLC). Eight or 9 days after established s.c. tumors had developed, the primary tumor was excised and mice were treated i.p. with either mouse interferon α/β or a control preparation. At the time of surgery, mice already had tumor cells in the liver. All control‐treated mice died in the ensuing 2 weeks with extensive tumor metastases in the liver and spleen. Interferon treatment resulted in an inhibition of the development of liver and spleen metastases and a markedly increased survival time. We conclude that interferon α/β is effective as adjuvant therapy after surgery for metastatic disease in mice.
Immunohistological analysis of lymphocyte subpopulations infiltrating breast carcinomas and benign lesions
Authors: Von Kleist S. , Berling J. , Bohle W. , Wittekind C H. 
Published: February 2007

AbstractWe characterized different subpopulations of infiltrating mononuclear cells using 8 monoclonal antibodies (MAbs) on serial cryosections of breast tissue from 85 cancer patients and 32 samples of benign lesions, and the ABC technique. In general, lymphocytes were found more frequently and more abundantly in cancerous lesions. The infiltrates consisted mainly of T‐cells in close contact with malignant cell‐nests. T‐helper/inducer cells clearly predominated over T‐suppressor/ cytotoxic cells in neoplastic tissues, whereas in benign tissues the T‐helper/suppressor ratios seemed to be well balanced. While a few MAb Leu‐7 (HNK‐l)‐reactive NK cells were found in the stroma of the breast tumors, none could be identified in the noncancerous lesions. The correlation of these data with histology and tumor stage of patients has been evaluated by a quantitative approach using planimetry in an interactive registration system.
Defective expression of MHC class I antigens is frequent in B‐cell lymphomas of high‐grade malignancy
Authors: Möller P. , Herrmann B. , Moldenhauer G. , Momburg F. 
Published: February 2007

AbstractAn unselected series of 66 immunohistologically proven B‐cell lymphomas was examined for the expression of MHC class I antigens with monoclonal antibodies directed against non‐polymorphic determinants of HLA‐A,B,C heavy chain and β2‐microglobulin. The tumors were classified according to the Kiel classification. No significant differences were observed in the reaction for HLA‐A,B,C and β2m which may be indicative of a coordinate expression in our lymphoma series. In 37 cases (56%), all tumor cells exhibited strong staining for class I antigens as observed in normal B cells. The remaining 29 cases (44%) showed abnormally low or undetectable class I expression in varying tumor cell subsets; 13 cases were completely devoid of HLA‐A,B,C. Twenty‐two out of 30 lymphomas of high‐grade malignancy but only 7/36 lymphomas of low‐grade malignancy presented defective class I expression. This difference in proportion is highly significant (p < 0.00002). Eleven of the 13 class l‐negative lymphomas belonged to the group of high‐grade malignancy. Centrocytic lymphoma, which has the poorest prognosis among the B‐cell lymphomas of low‐grade malignancy, was defective in 40% of the cases examined. The lymphoblastic type represented an exception within the lymphomas of high‐grade malignancy as no defective expression was observed. In addition to the correlation between the high‐grade malignancy and defective class I expression, defects occurred more frequently in lymphomas with an extra‐nodal primary manifestation (p < 0.05). The grade of malignancy, however, was not correlated with the primary site of the lymphoma.
Anti‐proliferative effects of interferons on Daudiburkitt Lymphoma cells: Induction of cell differentiation and loss of response to autocrine growth factors
Authors: Exley Ruth , Gordon John , Nathan Paul , Walker Leonie , Clemens Michael J. 
Published: February 2007

AbstractTreatment of Oaudi B‐lymphoblastoid cells with low concentrations of either natural or recombinant human α‐inter‐ferons inhibits cell proliferation and modulates the expression of a number of cell‐surface antigens. Using a panel of monoclonal antibodies (MAbs) identifying determinants expressed at the surface of normal plasma cells, and polyclonal antibodies against surface and cytoplasmic immunoglobulin, we have found that growth inhibition is accompanied by plasmacytoid differentiation. Assays of growth stimulation of heterologous cells indicate that the culture medium from interferon‐treated Daudi cells contains substantially more B‐cell growth factor activity than that from control cells. However, the interferon‐treated cells exhibit an impaired ability to respond to both these autocrine factors and exogenous factors produced by another Burkitt lymphoma line. These findings show that, in the case of Daudi cells, growth inhibition by interferons is closely associated with both terminal differentiation and a refractoriness to growth factors. In this system IFN‐α may therefore be considered to be a B‐cell differentiation factor, suggesting a possible basis for the anti‐proliferative effects observed with certain human B‐cell malignancies.
Influences of diethylnitrosamine on longevity of surrounding hepatocytes and progression of transplanted persistent nodules during phenobarbital promotion of hepatocarcinogenesis
Authors: Hayes M. Anthony , Lee George , Tatematsu Masae , Farber Emmanuel 
Published: February 2007

AbstractThe possibility that phenobarbital (PB) selectively promotes liver nodule development by decreasing survival of surrounding hepatocytes previously exposed to diethylnitrosamine (DENA) was evaluated. Livers of F‐344 rats were labelled with [3H‐methyl]‐thymidine (3H‐TdR) during developmental or regenerative growth. Neonatal rats given 3H‐TdR between days 3 and 12 were subjected at 12 weeks of age to partial hepatectomy (PH) followed 24 hr later by DENA (10 mg/kg) or saline. Subsequent administration of PB (0.1 % in drinking water) for 28 weeks reduced total liver label to 46 ± 10% (saline group) or 40 ± 4% (DENA group). Adult male rats initiated with DENA (200 mg/kg) and later labelled with 3H‐TdR after PH also lost total liver label during 28 weeks' promotion with PB (0.05% in water) at rates similar to those exhibited by non‐ initiated rats given PB, and by DENA‐treated or control rats not given PB. Large persistent (12 weeks) liver nodules generated by DENA in the Solt‐Farber model were transplanted as small fragments into the spleens of syngeneic rats previously given 0, 100 or 200 mg/kg of DENA. Subsequent exposure to PB (0.05% in drinking water for 40 weeks) or Aroclor 1254 (6 ± 300 mg/kg per month) promoted nodule and cancer development only in livers of DENA‐initiated recipients. Surviving transplanted nodules remained as small microscopic clusters even after 40 weeks of promotion. However, PB increased transplant survival (50% vs. 21% in controls) whereas Aroclor reduced it to 8%. These findings indicate that promotion of liver nodules by PB occurs without enhanced mortality of surrounding hepatocytes previously damaged by DENA. They further suggest that promoters such as PB and PCBs do not directly influence the progression of established persistent nodules.
Interrelationships among X‐ray‐induced anchorage independence, mutagenesis and chromosomal rearrangements in human diploid fibroblasts
Authors: Kano Yoshio , Grosovsky Andrew J. , Little John B. 
Published: February 2007

AbstractThe changes in the frequencies of X‐ray‐induced mutations to 6‐thioguanine resistance, chromosomal abnormalities and transformation to anchorage‐independent growth were examined during confluent holding recovery in density‐inhibited cultures of human diploid fibroblasts. Chromosomal abnormalities studied included non‐stable aberrations, deletions, and reciprocal translocations measured up to 20 mean population doublings post‐irradiation. Complex recovery kinetics were observed. A comparison of these kinetics suggests that reciprocal translocations are associated with the induction of both transformation and mutations. Mutagenesis correlated with deletions and translocations, whereas transformation correlated with translocations only.
The biological activity of hydrogen peroxide. III. Induction of Epstein‐Barr virus via indirect action, as compared with TPA and teleocidin
Authors: Oya Yukiko , Tonomura Akira , Yamamoto Kohtaro 
Published: February 2007

AbstractHydrogen peroxide (H2O2 ) was found to be a potent inducer of the production of the early antigen complex (EA) and/or virus capsid antigen (VCA), determined by Epstein‐Barr virus (EBV). Maximum synthesis of EBV antigens was induced by 0.2 mm H2O2, 5 days after a single 10‐min treatment, in both B95‐8 cells (30.2%) and P3HR‐1 cells (17.4%). These induction frequencies by H2O2 of proteins encoded by the EBV genome were almost the same as those obtained by 10 min treatment with the potent inducers, 12‐O‐tetradecanoylphorbol‐13‐acetate (TPA) and teleocidin. In combination with n‐butyrate (4mm), H2O2 showed an additive induction of EBV antigens (1.9‐ and 1.7‐fold in B95‐8 and P3HR‐1 cells, respectively) and was as efficient as TPA and teleocidin. H2O2 induced EBV antigens at a very low level (less than 1 %) in Raji cells by itself, but it induced EBV antigens synergistically in combination with n‐butyrate (about 25‐fold). In combined treatments using H2O2, TPA and teleocidin, the combination of H2O2 and TPA or H2O2 and teleocidin showed additive effects on the induction of synthesis of EBV antigens, but the combination of TPA and teleocidin showed almost the same induction level as that produced by H2O2, TPA or teleocidin alone. The inducing activities of H2O2, TPA and teleocidin were suppressed completely, in the case of H2O2, and slightly, in the cases of TPA and teleocidin, by treatment with catalase. Moreover, the effects of H2O2 were largely suppressed by scavengers of hydroxyl radical (‐OH) and singlet oxygen (1O2), but not by superoxide dismutase (SOD), whereas the induction of EBV proteins by TPA and teleocidin was largely suppressed by SOD, but only slightly by scavengers of ‐OH and 1O2. Thus, the biological actions of H2O2 on the activation of the EBV genome seem to be essentially different from those of TPA and teleocidin, though the biological actions of TPA and teleocidin may be partially ascribed to those of H2O2.
Studies on the polyoma tumor‐specific transplantation antigen (TSTA): Selection and characterization of TSTA‐negative segregants from somatic hybrids
Authors: Ramqvist Torbjörn , Reinholdsson Git , Szigeti Robert , Klein George , Dalianis Tina 
Published: February 2007

AbstractTwo polyoma‐TSTA‐negative variants were selected independently from a polyoma fibrosarcoma/Moloney lymphoma somatic hybrid, by repeated passages in polyoma‐virus‐preimmunized mice. One of the variants had lost all its polyoma DNA, while the other only retained a deleted piece of its integrated polyoma DNA. In contrast to the parental hybrid clone, none of the variants produced detectable amounts of T‐antigens. This finding indicates that a detectable expression of the products of the polyoma virus early genome, the T‐antigens, is important either directly or indirectly for the expression of TSTA.
An immunohistological study of cells infiltrating progressive and regressive tumors induced by two variant subpopulations of a rat colon cancer cell line
Authors: Martin M. S. , Caignard A. , Hammann A. , Pelletier H. , Martin F. 
Published: February 2007

AbstractIn order to understand the mechanisms leading up to progression or regression, tumors resulting from the s.c. inoculation of progressive or regressive variants of a cell culture established from a chemically‐induced rat colonic carcinoma were subjected to sequential histological study. As immune‐ logical factors have been previously described in this system of progressive or regressive tumors, special interest was given to inflammatory cells, T and B lymphocytes and macro‐phages, located inside and outside the tumor. Immunohisto‐ logical methods using monoclonal or polyclonal antibodies and enzyme histology were performed to identify different populations of infiltrative cells. In both variants of tumors an accumulation of these cells were seen at the periphery of the tumor, surrounding the nodules. In contrast, very few inflammatory cells, macrophages or T lymphocytes were seen inside the clumps of tumor cells where cytolytic cells could have a contact‐dependent tumoricidal effect. Only small differences were found between progressive and regressive tumors in the density of the various populations of T helper, T cytotoxic/suppressor, B lymphocytes or macrophages inside or around the tumor nodules. On the other hand, progressive and regressive tumors clearly differ in the relationship between tumor cells and the fibroblastic reaction they induce. Regressive tumors were rapidly encircled by a fibroblastic reaction isolating them from the peripheral tissues. The fibroblastic reaction was less dense around the progressive tumor cells which were able to migrate and invade the periphery. This suggests that immunological factors leading to tumor progression or regression could act indirectly through a control of the fibroblastic reaction, rather than through a direct cytotoxic effect on the tumor cells.