bluuebunny/crossref_metadata_2025_split huggingface dataset:
Blood group abh‐related antigens in normal and malignant bladder urothelium: Possible structural basis for the deletion of type‐2 chain abh antigens in invasive carcinomas
Authors: Ørntoft Torben F. , Wolf Hans , Clausen Henrik , Dabelsteen Erik , Hakomori Sen‐Itiroh 
Published: February 2007

AbstractA complete panel of mouse monoclonal antibodies (MAbs) against Type‐2 chain (Galβ1‐4GlcNAc‐R) blood‐group antigens (N‐acetyl‐lactosamine, Lex, H, Ley, A monofucosylated, ALey, repetitive A) was used in a detailed immunohistological study of the modulation of these carbohydrate antigens in transitional‐cell carcinomas. The histological and cellular locations of these antigens were studied in 19 normal bladder biopsies and 53 transitional‐cell carcinomas with as well as without neuraminidase treatment of tissue sections in order to uncover potential sialylated antigens. The antigen expression was correlated to individual A1A2BO, Lewis, and secretor status. Several alterations of blood group expression were found: (1) loss of A and H antigens with accumulation of Ley antigens; (2) loss of correlation between antigen expression and secretor status; (3) disruption of the orderly stratification of blood‐group antigen expression in relation to cell layers; and (4) changes in subcellular location of antigen expression. The present data indicate that deletion of Type‐2 chain ABH antigens in transitional‐cell carcinomas is associated with α1‐3 fucosylation of the H antigen leading to accumulation of Ley antigens.
Tumor‐associated glycoprotein (TAG‐72) expression in ulcerative colitis
Authors: Thor A. , Itzkowitz S. H. , Schlom J. , Kim Y. S. , Hanauer S. 
Published: February 2007

AbstractMonoclonal antibody (MAb) B72.3 reactive with the high‐molecular‐weight (Mr > 106) tumor‐associated glycoprotein (TAG)‐72 is being increasingly utilized in vivo and in vitro for a variety of purposes in colon cancer patients. Recent evidence has suggested that the TAG‐72 antigen expression may be enhanced in inflammatory bowel disease, particularly ulcerative colitis (Thor et al., 1986a: Cancer Res., 46, 3118–3124). We have utilized 117 paraffin‐embedded formalin‐fixed colonic specimens from 56 ulcerative colitis patients which demonstrate a spectrum of epithelial abnormalities (reactive atypia, dysplasia, and carcinoma) as well as 11 inflammatory controls to evaluate TAG‐72 expression. Our selected patient population all had pan‐colitis and demonstrated a generally increasing incidence of dysplasia or carcinoma with duration of disease (20% at 0 to 10 years, 50% at 11 to 20 years, 59% at 21 to 30 years, and 100% at more than 31 years). TAG‐72 expression was similar in the control and non‐dysplastic colonic epithelia, and increased with low‐ or high‐grade dysplasia as well as carcinomatous lesions (mean cellular reactivities 23.7%, 26.5%, 36.7%, 70% and 84.3%, respectively). Epithelium with low‐grade dysplasia exhibited a focal perinuclear, superficial crypt staining (when present). High‐grade dysplastic epithelium showed pancytoplasmic, pan‐cryptic reactivity. Invasive disease showed cytoplasmic as well as extracellular mucin staining. Biopsies from patients with active disease showed significantly more immunoreactive cells for TAG‐72 than patients with quiescent disease. For any given biopsy specimen the percentage of cells reactive did not always correlate with the degree of dysplasia. TAG‐72 expression in quiescent disease generally increased with duration of disease, in contrast to active disease which showed no correlation between MAb B72.3 staining and duration of disease. The frequent expression of TAG‐72 in actively inflamed colonic mucosa (ulcerative colitis and other colitides) may limit the clinical utility of this antigen for detecting colon cancer in ulcerative colitis patients by serological assay or in vivo radiolocalization techniques. The tendency for TAG‐72 expression to correlate with disease duration in patients with quiescent disease and to increase with more severe degrees of dysplasia suggests that the expression of this gene product correlates with the dysplasia‐to‐carcinoma sequence.
Urokinase‐type plasminogen activator biosynthesis is induced by the EJ‐Ha‐ras oncogene in CL26 mouse colon carcinoma cells
Authors: Testa J. E. , Medcalf R. L. , Cajot J.‐F. , Schleuning W.‐D. , Sordat B. 
Published: February 2007

AbstractCL26 murine colon carcinoma cells express urokinase‐type plasminogen activator (u‐PA) mRNA and activity after transfection with the activated c‐Ha‐ras‐1 (EJ‐ras) oncogene cloned from the EJ bladder carcinoma. PA activity and mRNA in control cells transfected with the non‐mutated c‐Ha‐ras‐1 (CO‐ras) gene remained negative. Ras mRNA was detected in EJ‐ras‐ and CO‐ras‐transfected cells, but not in untransfected or pSV2‐neo‐transfected cells. These results indicate that u‐PA biosynthesis can be modulated by EJ‐Ha‐ras‐dependent pathways of signal transduction.
Differential response of adherent and unanchored melanoma cells to bromodeoxyuridine evidenced by specific lectin‐binding protein changes
Authors: Rieber Manuel , Rieber Mary S. , Urbina Cecilia , Lira Renée 
Published: February 2007

AbstractThe possible differential response of adherent and nonadherent cells of the same tumor type to pyrimidine analogues has been investigated. We show that bromodeoxyuridine (BUdR) increases interactions of attached cells with their substrate without markedly affecting the cell adhesion properties of the same cells when these are not anchored. However, evidence for an adhesion‐independent response of both cell types to BUdR has been obtained with lectin binding assays using 125I‐labelled Lens culinaris agglutinin (LCA). This revealed a greatly increased binding of LCA to a large glycoconjugate in all cultures exposed to the halogenated pyrimidine. Attachment‐dependent effects of BUdR were manifested in flattened cells by a greater LCA‐binding to a 240‐kDa protein and by increased interaction of 125labelled wheat‐germ agglutinin (WGA) with a 200‐kDa protein and a large glycoconjugate sharply defined in electrophoresis. Although both tumor cell aggregates and anchored cells exhibit detectable responses to pyrimidine analogues such as BUdR, the corresponding effects are thus manifested unequally in cells with different adhesion properties.
A derivative of staurosporine (CGP 41 251) shows selectivity for protein kinase C inhibition and In vitro anti‐proliferative as well as In vivo anti‐tumor activity
Authors: Meyer Thomas , Regenass Urs , Fabbro Doriano , Alteri Enrica , Röusel Johannes , Möller Marcel , Caravatti Giorgio , Matter Alex 
Published: February 2007

AbstractAnalogues of staurosporine were synthesized and their ability to inhibit protein kinases was examined. Staurosporine is a potent but non‐selective inhibitor of in vitro protein kinase C (PKC) activity (IC50 6.0 nm). The derivative CGP 41 251 had reduced PKC activity with an IC50 of 50 nm but showed a high degree of selectivity when assayed for inhibition of cyclic AMP‐dependent protein kinase (IC50, 2.4 μm). 56 kinase (IC50 5.0 μm). and tyrosine‐kinase‐specific activity of epidermal growth factor receptor (IC50 3.0 μm). Staurosporine and CGP 41 251 exerted growth inhibition in the human bladder carcinoma line T‐24, human promyelocytic leukemia line HL‐60 and bovine corneal endothelial cells at concentrations which correlated well with in vitro PKC inhibition. In addition, both compounds inhibited the release of H2O2 from human monocytes pre‐treated with 12‐O‐tetradecanoyl‐phorbol‐13‐acetate at non‐toxic concentrations. In vivo anti‐tumor activity was examined in T‐24 human bladder carcinoma xenografts in athymic nude mice. Tumor growth inhibition tests revealed significant anti‐tumor activity (2p < 0.001) at 1/10 of the maximum tolerated doses for both compounds. By contrast, a closely related derivative of staurosporine (CGP 42 700) was inactive at concentrations of over 100 μm in all in vitro enzyme and anti‐proliferative assays as well as in animal tumor models. Our data suggest an association between PKC inhibition and anti‐proliferative and anti‐tumor activity.
Ganglioside GM2 expression on human melanoma cells correlates with sensitivity to lymphokine‐activated killer cells
Authors: Hoon Dave S. B. , Ando Iwao , Sviland Greg , Tsuchida Tetsuya , Okun Edward , Morton Donald L. , Irie Reiko F. 
Published: February 2007

AbstractGanglioside GM2 is expressed on cell surface membranes of a variety of human malignant cells and has been demonstrated to be immunogenic in humans. We have assessed the role of the antigen GM2 on melanoma cells as a recognition structure for lymphokine‐activated killer (LAK) cells. LAK cells were generated by stimulation of non‐adherent peripheral blood lymphocytes (PBL) from human donors with recombinant interleukin‐2 (IL‐2). The selection of target cells was based on GM2 content and included II human melanoma cell lines and 2 human leukemia lines. Using a single‐cell binding assay, LAK cell binding to target lines expressing high levels of GM2 was significantly greater than to those expressing minimum GM2. This cell‐binding was specifically inhibited by addition of purified GM2 but not by other gangliosides. LAK‐melanoma cell‐binding was also specifically inhibited by anti‐GM2 monoclonal antibody (MAb). For further analysis LAK cell lysis of melanoma target cells expressing various amounts of GM2 was assessed. A significant correlation occurred with GM2 expression and LAK cell lysis (p < 0.025; r = 0.623). Three other gangliosides commonly expressed on human melanoma, GM3, GD3 and GD2, had no correlation with LAK cell lysis. These studies suggest that GM2 on melanoma cells is a marker for LAK cell sensitivity, as well as indicate that GM2 is a potential target recognition structure for human LAK cells.
Effect of retinyl acetate on cAMP‐dependent protein kinase in transformed mouse 10t1/2 cells
Authors: Hohmann Philip 
Published: February 2007

AbstractThe effect of retinyl acetate (RAC) on the activity of cAMP‐dependent protein kinase (PKA) was studied in mouse 10T1/2 cells. The studies revealed that normal 10T1/2 cells had about 13‐fold more PKA activity than did methylcholanthrene‐transformed cells (MCA cells). The addition of RAC to MCA cells increased the activity of PKA about 3‐fold as measured by the in vitro phosphorylation of a specific site in H1 histone (site A) or Kemptide. The increased PKA activity coincided with a reduction in the rate of cell replication of MCA cells, about 24 hr after exposure to the retinoid. Addition of forskolin to RAC‐treated MCA cells resulted in a further reduction in the rate of cell replication, and this suggested that the enhanced PKA activity was also capable of action in vivo. To test this notion, MCA cells were grown with and without RAC, and the phosphorylation of the H1 histone at site A, a site known to be phosphorylated by PKA in cells treated with hormones or other agonists which activate PKA, was studied in vivo. RAC, by itself, was capable of causing an increase in the phosphorylation of the H1 histone at site A, demonstrating that the retinoid‐mediated increase in PKA activity was sufficient to cause the enhanced phosphorylation of a known substrate.
Growth stimulation of human breast epithelial cells by basic fibroblast growth factor in serum‐free medium
Authors: Takahashi K. , Suzuki K. , Kawahara S. , Ono T. 
Published: February 2007

AbstractGrowth‐stimulating activities of basic and acidic fibroblast growth factors (FGFs) toward human breast epithelial cells were examined and compared with the mitogenic activity of bovine pituitary extract (BPE) by the use of a serum‐free medium which contained epidermal growth factor, insulin, transferrin, hydrocortisone, ethanolamine, phosphoethanolamine, prolactin and prostaglandin. Addition of 1 ng/ml of basic FGF (bFGF) to the serum‐free medium significantly enhanced the growth potential of epithelial cells derived from human breast carcinoma, and the number of cells grown for 7 days with bFGF was more than 1 1/2 times higher than that in the serum‐free medium containing BPE instead of prolactin and prostaglandin. Growth responsiveness toward bFGF of epithelial cells derived from histologically non‐malignant breast tissues was lower than that of carcinoma‐derived cells, and the growth‐stimulating activity of bFGF was lower than that of BPE, which could significantly enhance the growth potential of the cells. Contrary to bFGF, acidic FGF at 1 ng/ml had no significant effect on the growth potential of breast epithelial cells which had grown out from either carcinoma or non‐malignant tissues. The present results suggest that bFGF is a putative growth‐stimulating factor for human breast epithelial cells, especially for carcinoma‐derived cells, and can substitute at least in part for BPE in serum‐free monolayer culture of the cells.
Effects of low‐ and high‐density lipoproteins on the proliferation of human breast cancer cells In vitro: Differences between hormone‐dependent and hormone‐independent cell lines
Authors: Rotheneder Martina , Kostner Gerhard M. 
Published: February 2007

AbstractThe influence of low‐ and high‐density lipoproteins on the proliferation of human breast cancer cells in culture was studied. We compared total cell number after incubation for 48 hr in culture medium containing or lacking plasma lipoproteins. Marked differences were found between hormone‐dependent (MCF‐7, T‐47‐D, ZR‐75) and hormone‐independent (MDA‐MB‐231, HBL‐100) mammary tumor cell lines. The cells also reacted differently on the different lipoproteins offered in the medium. Human low‐density lipoproteins (LDL) exhibited a marked stimulation of the growth of hormone‐independent cell lines but no or only toxic effects upon the hormone‐sensitive lines. Human high‐density lipoproteins (HDL) stimulated the proliferation of all cell lines in a dose‐dependent manner but hormone‐independent cells showed a higher response. These findings point towards different utilizations of nutrients in hormone‐dependent and hormone‐independent cells.
Role of glucose‐6‐phosphate dehydrogenase on enhanced proliferation of pre‐neoplastic and neoplastic cells in rat liver induced by n‐nitrosomorpholine
Authors: Baba Miyako , Yamamoto Reiko , Iishi Hiroyasu , Tatsuta Masaharu , Wada Akira 
Published: February 2007

AbstractThe relationship between G6PD and the number and size of pre‐neoplastic and neoplastic lesions in rat liver was examined. Male Sprague‐Dawley rats were given drinking water containing 250 mg/l of NNM for 8 weeks. Pre‐neoplastic and neoplastic lesions with positive staining of GT were classified histochemically into G6PD‐positive and G6PD‐negative lesions. At week 24, quantitative analysis showed that the incidence and number of G6PD‐positive lesions were significantly higher than those of G6PD‐negative lesions. Histologically, hepatocellular carcinomas were more frequent and larger in G6PD‐positive lesions than in G6PD‐negative ones. Statistical analysis of the quantitative data also showed that the number and volume of G6PD‐positive hepatocellular carcinomas were significantly higher than in G6PD‐negative carcinomas. The G6PD‐positive pre‐neoplastic lesions had a significantly higher labelling index than G6PD‐negative ones. These findings revealed a considerable difference in the growth of these 2 populations of the lesions, and indicate that G6PD activity may be closely related to proliferation of the pre‐neoplastic and neoplastic cells in the liver.
Correlations of dihydropyrimidine dehydrogenase, thymidine phosphorylase and thymidine kinase activities in strongly and weakly malignant cultured murine neuroblastoma cells
Authors: Williams Christopher S. , Tuchman Mendel 
Published: February 2007

AbstractThe C‐1300 neuroblastoma tumor which arises spontaneously in the A/J mouse has been maintained in this mouse strain. Two different cell populations have been recognized in cultured C‐1300 mouse neuroblastoma (MNB): (1) round, “neuroblast‐like” cells, growing in suspension (poorly attached), that have a highly malignant behavior when injected into the A/J mouse (T1 cells); and (2) flat, “epithelioid” cells that attach well to surfaces and show low malignancy towards the inoculated animals (T2 cells). The specific activities of the pyrimidine metabolizing enzymes thymidine phosphorylase (TP), dihydropyrimidine dehydrogenase (DPD) and thymidine kinase (TK) were examined in both MNB cell lines by a new radiochromatographic method. Enzymatic activities of TP and DPD in the cytosols of T2 (weakly malignant) cells were up to 15 times higher than those of T1 (strongly malignant) cells, whereas the mean TP/DPD activity ratio was 16 in either cell line. TP and DPD activity levels increased with time of growth in culture in T2 cells while no such increase was seen in the T1 cells. Maximal TK activity was similar in both cell lines but dropped more rapidly in the T2 cells as cell densities increased. The enzymatic activity levels of TP and DPD but not of TK correlated inversely with neoplastic expression of MNB cells. The observed patterns of pyrimidine metabolizing enzymes in MNB cells could result in an increased thymidine pool in T1 cells whenever TK activity is suppressed, whereas such conditions would favor the generation of thymine in the T2 cells.
A survey of in vivo growth characteristics and spontaneous metastasizing potentials of C3H mouse mammary tumors
Authors: Vaage Jan 
Published: February 2007

AbstractThis investigation examined the relationship between spontaneous metastasizing potential, immunogenicity and growth rate in 34 C3H/He mammary carcinomas. The main purpose of our studies was to examine the hypothesis that a tumor's metastasizing potential is affected by its immunogenicity. The tumors were studied during serial intra‐mammary transplantations, starting with tissue from autochthonous, spontaneous pulmonary metastases. The results show that there was no correlation between metastasizing potential and tumor immunogenicity, and no correlation between metastasizing potential and tumor growth rate. Moreover, metastasizing potential was not related to invasive behavior, because histological examination showed that all of the metastases grew extensively within pulmonary vessels and displayed no tendency to active extravasation.
Inhibition of dmba‐induced mammary tumorigenesis by caloric restriction in rats fed high‐fat diets
Authors: Klurfeld David M. , Welch Carrie B. , Lloyd Lisa M. , Kritchevsky David 
Published: February 2007

AbstractMost previous studies on the inhibiting effect of caloric restriction during promotion of DMBA‐induced mammary carcinogenesis have used low to moderate levels of dietary fat, i.e., about 4 to 14% by weight. The current study was designed to test whether a moderate degree of caloric restriction, 25%, would inhibit tumor growth in rats fed the equivalent of 20% dietary fat which approximates human consumption in affluent countries. Rats were fed diets ad libitum that contained 5, 15 or 20% corn oil. Groups of rats were pair‐fed to the last 2 groups, but subjected to a 25% caloric restriction. These groups were fed 20 or 26.7% corn oil so that absolute fat intake in the paired groups was identical. Significant inhibition of tumor incidence, tumor weight, tumor burden, body fat deposition, and fasting serum insulin were observed in the 2 calorically restricted groups. We conclude that moderate caloric restriction is significantly more effective in inhibiting tumor growth than is the promoting effect of diets high in fat. Total body weight, body fat and serum insulin concentrations may be better correlates of risk of developing mammary tumors than is dietary fat.
Presence of nerve growth factor‐like immunoreactivity in carcinoid tumour cells and induction of a neuronal phenotype in long‐term culture
Authors: Ahlman Håkan , Wigander Anneli , Möulne Johan , Nilsson Ola , Karlsson Jan Erik , Theodorsson Elvar , Dahlström Annica 
Published: February 2007

AbstractMid‐gut carcinoid tumour cells expressed a neuronal phenotype, observed and characterized immunocytochemically in long‐term culture. Initially the culture contained a main population of spherical tumour cells with granules immuno‐positive for serotonin (5‐HT) and tachykinins (TK). Production and secretion of these substances into media was verified biochemically. Cytoplasmic granules with 5‐HT‐like immuno‐reactivity (5‐HT‐LI) were markedly reduced during culture, while granules with TK‐LI were unchanged in number, corresponding to the biochemical findings. After a few days in culture, tumour cells were flattened and fine neurite‐like processes extended. After 2‐3 weeks many endocrine tumour cells had converted to neuron‐like cells with slender cell processes containing granules with TK‐LI. Varicose enlargements and apparent growth cones were observed. When neurites were extended, 50‐80% of the neuron‐like cells were positive with antisera against the neurofilament triplet. Cells of both endocrine and neuronal phenotypes were positive with antisera against tetanustoxin, Thy I‐antigen, neuron‐specific enolase, synapsin and a synaptic vesicle protein (p 38) supporting the concept of these tumour cells as para‐neurons. Intermediate filaments, studied with monoclonal anti‐vimentin, were found in all cells. Filaments were also observed ultrastructurally. Initially, nerve growth factor (NGF)‐LI was found in granules of all spherical tumour cells. When neuritic processes were extended, the cells appeared to lose these granules. After 40 days in culture, NGF‐LI was absent or very sparse. The studies indicate autocrine secretion of a growth factor, reacting with the NGF antiserum, by cultured midgut carcinoid tumour cells inducing a neuronal phenotype with enhanced NF and TK synthesis and suppressed 5‐HT synthesis. In bioassay systems the culture media caused a delayed neurite reaction on PC12 cells, but no reaction on chick ciliary ganglion cells, indicating that the factor is not authentic NGF.
Risk factors for oral cancer in Brazil: A case‐control study
Authors: Franco Eduardo L. , Kowalski Luiz P. , Oliveira Benedito V. , Curado M. Paula , Pereira Raimunda N. , Silva M. Estela , Fava Antonio S. , Torloni Humberto 
Published: February 2007

AbstractA case‐control study of risk factors for carcinomas of the tongue, gum, floor, and other specified parts of the mouth was conducted in 3 metropolitan areas in Brazil: São Paulo (South‐east), Curitiba (South), and Goiãnia (Central‐West). We analyzed information on demographics, occupational history, environmental exposures, tobacco smoking and alcohol drinking habits, as well as diet, oral and other health characteristics obtained from interviews with 232 cases and 464 hospital non‐cancer controls matched for 5‐year age‐group, sex, hospital catchment area and trimester of admission. Tobacco and alcohol consumption were the strongest risk factors irrespective of the anatomical site. The adjusted relative risks (RR) for ever vs. never smokers were: 6.3, 13.9, and 7.0, for industrial‐brand cigarettes, pipe, and hand‐rolled cigarettes, respectively. A strong correlation was seen between number of pack‐years and risk. The RR for the heaviest vs. the lowest consumption categories (>100 vs. <1 pack‐years) was 14.8. Risk levels generally decreased to those of never smokers after 10 years had elapsed since stopping smoking. The risk associated with alcohol was mostly evident for wine (cancer of the tongue) and “cachaça” (all sites), a hard liquor distilled from sugar cane. Other important risk factors were drinking “chimarrão” (a type of maté), use of a wood stove for cooking, and frequent consumption of charcoal‐grilled meat and manioc. Oral hygiene characteristics represented correlates of disease risk. A significant protective effect was observed for consumption of carotene‐rich vegetables and citric fruits, but not for green vegetables in general.