bluuebunny/crossref_metadata_2025_split huggingface dataset:
Ca 72‐4 radioimmunoassay in the diagnosis of malignant effusions. Comparison of various tumor markers
Authors: Ferroni P. , Szpak C. , Greiner J. W. , Simpson J. F. , Guadagni F. , Johnston W. W. , Colcher D. 
Published: February 2007

AbstractWe evaluated the utility of the CA 72‐4, CEA, CA 125, CA 19‐9 and CA 15‐3 radioimmunoassays for the detection of tumor‐associated antigens (TAAs) in effusions of malignant vs. benign origin. Fluids were obtained from 51 patients with adenocarcinomas, 27 with non‐epithelial malignancies, and 68 with benign disorders. The CA 72‐4 radioimmunoassay (cut‐off value 8.5 U/ml) detected the TAG‐72 antigen in 51% of adenocarcinoma patients′ effusions, while only 1 of 68 benign specimens had an elevated TAG‐72 level. Similarly, CEA levels above 5 ng/ml were found in 55% of the fluids from patients with adenocarcinoma and 3.2% of effusions from patients with benign disease. CA 19‐9 (cut‐off value 37 U/ml) exhibited a lower degree of sensitivity, with positive values in 23.5% of the effusions due to adenocarcinomas and in 4.5% of the effusions due to benign disease. At a cut‐off value of 29 U/ml, CA 15‐3 was positive in 49% of fluids from patients with adenocarcinoma and in 3.0% of the benign fluids. The CA 125 RIA failed to show any specificity using the established cut‐off value of 35 U/ml, with approximately 80% of all the effusions giving positive results. The specificity of the assay was increased by using a cut‐off value of 3000 U/ml, but with a substantial loss in sensitivity (23.5%). Using a combination of the CA 72‐4 and CEA RIAs the sensitivity for malignant effusions was increased to 73.5%. No additional improvement in the overall sensitivity was observed when using the CA 72‐4 assay in combination with assays for the other markers, except in the case of I effusion. We conclude that the CA 72‐4 RIA, possibly in combination with other assays such as CEA, may be useful in distinguishing between adenocarcinomatous and benign effusions.
Icam ‐ melanoma cells are relatively resistant to cd3‐mediated t‐cell lysis
Authors: Braakman Eric , Goedegebuure Peter S. , Vreugdenhil Rea J. , Segal David M. , Shaw Stephen , Bolhuis Reinder L. H. 
Published: February 2007

AbstractThe primary activation pathway of T cells is via the T‐cell receptor (TCR)/CD3 complex, which is functionally interrelated with various accessory molecules. We examined the contribution of the lymphocyte‐function‐associated antigenI/intercellular adhesion molecule I (LFA‐I/ICAM‐I) interaction to CD3/TCR‐mediated lysis by cytotoxic T lymphocytes (CTL). We used ICAM‐I‐or+ tumor cell lines as target cells and anti‐CD3‐ or anti‐LFA‐I containing hetero‐cross‐linked monoclonal antibody (MAb) to bridge CTL and target cells and simultaneously to activate CTL. The ICAM‐I‐ melanoma‐derived cell line lgR39 was relatively resistant to CD3‐mediated lysis by both TCRαβ+ and TCRγdL+ CTL, when compared with ICAM‐I+ cell lines. Induction of ICAM‐I on the membrane of lgR39 cells by tumor necrosis factor (TNF) rendered these cells more susceptible to CD3‐mediated lysis. Anti‐ICAM‐I MAb inhibited this TNF‐enhanced susceptibility to lysis, directly demonstrating that the induction of ICAM‐I was critical in the TNF‐induced increase in susceptibility to lysis of lgR39 cells. CTL formed less efficient conjugates with the ICAM‐I‐ cells as compared to ICAM‐I+ cells. Both spontaneous and CD3‐induced conjugate formation as well as CD3‐mediated lysis of ICAM‐I‐ tumor cells by CTL were enhanced by the addition of anti‐LFA‐I containing heterocross‐linked MAb, thereby mimicking the LFA‐I/ICAM‐I interaction between CTL and target cells. Soluble anti‐CD18 MAb inhibited CD3‐mediated lysis of ICAM‐I‐ target cells by CTL without affecting their conjugate formation. Anti‐LFA‐I MAb added after conjugate formation still inhibited lysis of both ICAM‐I+or‐ tumor cells. Taken together, these findings suggest that the LFA‐I/ICAM‐I interaction co‐activates CD3/TCR‐mediated lysis by CTL through both an enhanced CTL‐target cell binding and the delivery of post‐conjugate costimulatory signals.
Analysis of cell‐surface sugar receptor expression by neoglycoenzyme binding and adhesion to plastic‐immobilized neoglycoproteins for related weakly and strongly metastatic cell lines of murine tumor model systems
Authors: Gabius Sigrun , Schirrmacher Volker , Franz Holger , Joshi Shantaram S. , Gabius Hans‐Joachim 
Published: February 2007

AbstractRecognition of the carbohydrate part of cellular glycoconjugates by cell‐surface sugar receptors may contribute to interactions, essential to the establishment of metastases. Comparison of the properties of strongly metastatic variants to their related, less metastatic counterparts offers a generally accepted approach to the discovery of metastasisassociated characteristics. The chemically induced murine lymphoma line Eb and its spontaneously arising variant ESb with increased potential for lung and liver colonization, the virally induced lymphosarcoma cell line RAW 117‐P and its in vivo selected variant H 10 with increased potential for liver colonization, and the B16‐FI melanoma line and its in vivo selected variant F 10 with increased potential for lung colonization, were chosen. A panel of 12 types of chemically glycosylated E. coli β‐galactosidase, exposing the pivotal carbohydrate residues for specific carbohydrate‐dependent cell binding, was employed to study the expression of respective cellsurface sugar receptors on these cell lines. Specific binding occurred in a non‐uniform manner for the individual probes. Systematic measurements at a non‐saturating ligand concentration revealed quantitative differences between the 2 cell lines of each system. However, there were no consistent changes associated with the metastatic phenotype. A similar result was obtained employing Scatchard analyses for quantitative evaluation of binding characteristics in several cases. Surface receptor expression was responsive to chemical induction of differentiation in the lymphosarcoma model. Analyses of sugar‐inhibitable cell adhesion to neoglycoproteincoated plastic wells for the lymphoma and lymphosarcoma cells revealed that the presence of cell‐surface sugar receptors, even at similar densities to those defined by neoglycoenzyme binding, will not necessarily translate into an identical adhesive response. Several carbohydrates, especially N‐acetyl‐D‐galactosamine, can differentially affect this interaction at a non‐toxic concentration in both model systems.
Degradation of immobilized soluble elastin by tumor cells in culture: Quantitation by elisa
Authors: Caenazzo C. , Spina M. , Onisto M. , Fastelli G. , Gotte L. , Agostini C. , Semenzato G. , Garbisa S. 
Published: February 2007

AbstractA new, sensitive assay based on the enzyme‐linked immunosorbent assay has been developed for measuring elastolytic activity produced by invasive and/or metastatic tumor cells in culture. Elastin peptides, obtained by treating the insoluble protein with either oxalic acid, KOH, or chymotrypsin, are adsorbed onto the surface of cell culture microtiter plastic wells, and incubated with dilution of standard proteinases or viable normal or tumor cells. The total amount of immobilized elastin peptides is revealed by the mean of specific antibodies, and detected by a microplate reader, while dose‐ and time‐dependent reduction of bound antibodies after incubation with proteases or cells is taken as a measure of elastin degradation. Adsorbed elastin has been found to be available as a substrate for purified enzymes, as well as for living melanoma cells (A2058 and B 16‐B16), c‐Ha‐ras transformed rat embryo fibroblasts, and human pulmonary macrophages, as demonstrated by the release into the culture medium of lower molecular weight digestion products. No degradation was achieved by BALB/3T3 and rat embryo control fibroblasts, and no inhibition was produced by the presence of fetal calf serum which, on the contrary, potentiated the degradation by active cells. This new method, revealing degradation of only a few nanograms of soluble elastin peptides, can be used for studying the importance in tissue invasion and metastasis of elastolytic proteinases produced by cells in culture.
Influence of cigarette smoking on the levels of DNA adducts in human bronchial epithelium and white blood cells
Authors: Phillips David H. , Schoket Bemadette , Hewer Alan , Bailey Eric , Kostic Szilárd , Vincze István 
Published: February 2007

AbstractThe presence of carcinogen‐DNA adducts in human tissues is evidence of exposure to carcinogens and may be an indicator of cancer risk. DNA was isolated from non‐tumorous bronchial tissue of 37 cigarette smokers, 8 former smokers and 8 non‐smokers and analyzed for the presence of aromatic and/or hydrophobic DNA adducts in the32P‐post‐labelling assay. Adducts were detected as bands of radioactive material when 5′‐32P‐labelled deoxyribonucleoside 3′, 5′‐bisphosphates were chromatographed on polyethyleneimine‐cellulose tic plates, and the patterns indicated the formation of adducts by a large number of compounds. Adduct levels detected in DNA from non‐smokers, former smokers and current smokers were 3.45 ± 1.62, 3.93 ± 1.92 and 5.53 ± 2.13 adducts/108nucleotides, respectively. The differences in adduct levels be tween smokers and former and non‐smokers were statistically significant (p< 0.01); and among the smokers, significant correlations were found between adduct levels and both daily cigarette consumption and total cigarette consumption (daily consumption × number of years smoked). DNA was also isolated from the peripheral‐blood leukocytes of 31 heavy smokers (>20 cigarettes/day) and 20 non‐smokers and analyzed by32P‐post‐labelling. Adduct levels in the smokers' samples were not significantly different from levels in the nonsmokers' samples (2.53 ± 1.31 and 2.12 ± 1.44 adducts/108nucleotides, respectively). Thus, evidence for carcinogen exposure was found in human bronchial epithelium, a target tissue for tobacco‐induced tumour formation, but not in peripheral‐blood cells, indicating possible limitations in the use of the latter as a surrogate, non‐target tissue source of DNA for monitoring human exposure to inhaled carcinogens.
Asbestos exposure and histologic cell types of lung cancer in surgical and autopsy series
Authors: Mollo F. , Piolatto G. , Bellis D. , Andrion A. , Delsedime L. , Bernardi P. , Pira E. , Ardissone F. 
Published: February 2007

AbstractA case‐control study was carried out on 411 surgical and 106 autopsy histological tissue samples of lung cancer in men, in order to investigate the relationships between asbestos expo sure and cell type of pulmonary carcinoma. Both occupational history (obtained by interviews of surgical patients or of the next‐of‐kin for deceased subjects) and lung asbestos body con tent (determined by optical count after hypochlorite diges tion and membrane filtration of lung tissues) were considered as asbestos exposure indicators. No significant relationships were found in the surgical series after adjustment for smok ing. The autopsy series showed a trend towards an association between lung adenocarcinoma and asbestos exposure indicators and a markedly higher agreement between the 2 kinds of indicators than that observed in the surgical series.
High frequency of Epstein‐Barr virus genome detection in Hodgkin's disease of HIV‐positive patients
Authors: Uccini Stefania , Monardo Francesca , Stoppacciaro Antonella , Gradilone Angela , Aglianò Anna M. , Faggioni Alberto , Manzari Vittorio , Vago Luca , Cosianzi Giulio , Ruco Luigi P. , Baroni Carlo D. 
Published: February 2007

AbstractLymph nodes obtained from 7 HIV‐positive and 20 HIV‐negative patients with Hodgkin's disease were examined for the presence of Epstein‐Barr virus antigens and genome. EBV antigens were observed in only 2 out of 20 HIV‐negative patients, whereas lymph nodes of HIV‐positive patients did not reveal evidence of EBV antigens. By In situ hybridization and Southern blot analysis, EBV genome was found in 5 out of 7 HIV‐positive patients; the EBV genome was detected in the nucleus of Reed‐Sternberg and Hodgkin's cells. EBV DNA was observed by in situ hybridization and Southern blot analysis in only out of 20 HIV‐negative patients with Hodgkin's disease. In both groups, Reed‐Sternberg and Hodgkin's cells were neg ative for C3d EBV receptor. Our results show a statistically significant increased expression of EBV DNA in HIV‐positive patients with Hodgkin's disease, as compared with HIV‐negative patients with HD.
Expression and production of tenascin in benign and malignant lesions of melanocyte lineage
Authors: Natali Pier Giorgio , Nicotra Maria Rita , Bartolazzi Armando , Mottolese Marcella , Coscia Nadia , Bigotti Aldo , Zardi Luciano 
Published: February 2007

AbstractThe distribution of the extracellular matrix (ECM) glycoprotein tenascin (TN) has been evaluated immunohistochemically in benign and malignant lesions of the melanocytic lineage. Results of our study show that TN is detectable in a variety of benign and malignant lesions. In primary melanomas, TN displays a heterogeneous distribution, and a higher degree of expression of this glycoprotein is seen in lesions of greater dermal invasiveness. TN expression does not correlate with that of other ECM glycoproteins such as fibronectin. In vivo and in vitro experiments have also demonstrated that melanoma cells are capable of producing and releasing TN in the extracellular milieu.
Geographic association of Helicobacter pylori antibody prevalence and gastric cancer mortality in rural China
Authors: Forman D. , Sitas F. , Newell D. G. , Stacey A. R. , Boreham J. , Peto R. , Campbell T. C. , Li J. , Chen J. 
Published: February 2007

AbstractTo examine the geographic association between Helicobacter pylori infection and gastric cancer, we have assessed the prevalence of IgG antibodies to H. pylori in plasma samples taken in 1983 from 1882 men, aged 35‐64 years, in 46 rural counties of the People's Republic of China. The gastric cancer mortality rates in these counties in 1973‐75 varied from 3 per 1,000 (cumulative rate, 0‐64 years) to 69 per 1, 000. while the proportions of the population positive for H. pylori antibodies (based on an average of about 41 men per county) varied from 28% to 96%. After correction for the limited number of blood samples per county, the estimated correlation between H. pyori antibody prevalence and gastric cancer mortality was 40% (p = 0.02). No other type of cancer showed a significant association with H. pylori.
F11C antigen: A membrane marker able to distinguish two regressive and progressive variants from a rat colon adenocarcinoma
Authors: Caignard Anne , Genne Philippe , Olsson Nils‐Olivier , Oriol Rafael , Martin François 
Published: February 2007

AbstractCell variants that differ in their tumorigenicity and immunogenicity have been isolated from a BDIX rat colon adenocarcinoma cell line, DHD/K12. One variant, PRO, and the clones derived from it, are poorly immunogenic and induce progressive and metastatic tumors; the other one, REG, and its clones, are highly immunogenic and induce regressive tumors. When looking for a membrane marker distinguishing between PRO and REG lines, we obtained monoclonal hybridomas by immunizing BALB/c mice with PROb or REGb cell clones. Hybridoma FI IC, producing an IgM monoclonal antibody (MAb) was able to distinguish between the cell variants on membrane immunofluorescence. All REGb cells strongly express FI IC membrane antigen. On PROb cells, FI IC antigen expression is weak, as demonstrated by cytofluorimetric analysis, and limited to a fraction of the cell population. The FI IC membrane antigen is highly specific for the DHD/K12 cell line and the variants derived from it, but is not expressed on cells dissociated from the DHD transplanted tumor, from which DHD/K12 was established, suggesting that FI IC antigen emerged during cell culture. Fluorescence absorption on synthetic oligosaccharides demonstrated that FI IC antibody cross‐reacts with A type 3, A type 4 and A type 5 chain blood group tetrasaccharides.
Modulation of cellular gene expression in B lymphoma cells following in vitro infection by Epstein‐Barr virus (EBV)
Authors: Calender Alain , Cordier Martine , Billaud Marc , Lenoir Gilbert M. 
Published: February 2007

AbstractIn vitro infection of EBV‐negative lymphoma cell lines with immortalizing strains of Epstein‐Barr virus induces the cellsurface expression of B‐cell markers, such as the EBV receptor/CR2 (CD21) and the CD23 antigen. The non‐immortalizing EBV variant, P3HRI, which carries a deletion encompassing the EBV nuclear antigen 2 (EBNA2) gene, fails to induce any such expression. We show here that the EBV‐mediated up‐regulation of cell‐surface expression of these molecules is associated with an increased level of the specific steady‐state RNA corresponding to these 2 genes. These results suggest that the role of EBNA2 in B‐cell growth and immortalization may be related to its role in transactivation of cellular genes. In order to identify other cellular genes whose expression may be modulated by EBV, we analyzed the level of transcription of a set of genes possibly involved in Burkitt's lymphoma pathogenesis. The level of the c‐myc oncogene transcript was not significantly affected by in vitro EBV infection. The c‐fgr oncogene, thought to be specifically activated in EBV‐infected cells, was found to be expressed in some EBV‐negative lymphoma cells and also to be activated by both non‐immortalizing and immortalizing strains of EBV. The expression of vimentin, the major 56‐kDa polypeptide of mesenchymal cell intermediate filaments, was altered by all EBV isolates, in either a negative or a positive way, depending on the cell line. Expression of lymphocyte‐function‐associated antigens, LFA‐I α/β (CDI la/18) and LFA‐3 (CD58), involved in intercellular adhesion and the T‐cytotoxic pathway, were differentially regulated by EBV; a crucial observation was the activation by immortalizing EBV isolates of LFA‐1 β chain (CD18) and of LFA‐3 (CD58). The EBV‐ and possibly EBNA2‐associated modulation of cellular genes, such as CR2 (CD21), CD23 and LFAs, probably represents key events for EBV‐induced B‐cell proliferation, and also for in vivo immune control of EBV‐infected B cells.
A single dose‐response effect of aflatoxin B1 on rapid liver cancer induction in two strains of rats
Authors: Angsubhakorn Subhkij , Get‐Ngern Panisa , Miyamoto Makoto , Bhamarapravati Natth 
Published: February 2007

AbstractTo investigate rapid liver cancer induction in rats by aflatoxin B1 (AFB1), different single oral doses of AFB1 were given to 3 groups of I‐year‐old Buffalo and Wistar rats. The animals were treated once and all survivors were killed 6 weeks later. Control animals received an equal volume of solvent (DMSO), and both groups of animals were maintained under identical conditions throughout the period of experiment. The survival rates were 40% with low and medium doses in AFB1‐treated Buffalo and Wistar rats, and 0% in the high‐dose Buffalo rats. Slight ante‐mortem elevations in serum concentrations of glutamic pyruvic transaminase (SGOT) and glutamic oxaloacetic transaminase (SGPT) were indicative of the persistent damage effect of AFB1 at week 6. Total protein and albumin concentrations were not altered. The percent incidence of altered cell foci (areas) and neoplastic nodules was higher in Wistar than in Buffalo rats given a similar low dose. Various stages of well differentiated hepatocellular carcinomas (0.1‐0.2 cm in diameter) developed in 3 of 8 Wistar rats. It thus appears that Wistar rats are more susceptible to hepatocarcinogenesis following a single oral dose of AFB1 than Buffalo rats.
Relationships among tumor responsiveness, cell sensitivity, doxorubicin cellular pharmacokinetics and drug‐induced DNA alterations in two human small‐cell lung cancer xenografts
Authors: Pratesi G. , Capranico G. , Binaschi M. , De Isabella P. , Pilotti S. , Supino R. , Zunino F. 
Published: February 2007

AbstractIn an attempt to understand the underlying cellular/biochemical factors of sensitivity/resistance in human small‐cell lung cancer (SCLC), 2 SCLC tumor lines were compared with respect to tumor responsiveness to drug treatment, cell sensitivity, cellular doxorubicin accumulation, and DNA topoisomerase‐II‐mediated DNA cleavage. The tumor lines growing in nude mice with simillar growth characteristics (doubling time around 10 days) were selected since one (POCI tumor) was found to be hypersensitive and the other (POSG tumor) resistant to doxorubicin treatment. The pattern of anti‐tumor, drug response of the doxorubicin‐resistant tumor was atypical (i. e., non‐adherent to the well‐characterized multi‐drug‐resistant phenotype), since it responded to vincristine. The markedly different in vivo tumor response reflected the intrinsic cellular sensitivity to doxorubicin. No correlation was found between cellular drug accumulation and doxorubicin sensitivity following in vitro exposure to the drug. In agreement with this observation, the expression of mdr‐I gene was undetectable in these tumors. Thus, in the POSG tumor, resistance to doxorubicin occurred without expression of the P‐glycoprotein and reduction of cellular drug accumulation. In contrast, the extent of DNA cleavage produced by doxorubicin was markedly higher in the doxorubicin‐hypersensitive than in the doxorubicin‐resistant tumor. These results, taken together with previous observations in SCLC cell lines, support the important role of DNA topoisomerase‐mediated effects in the sensitivity of SCLC to doxorubicin.
Generation and characterization of monoclonal antibodies against multiple epitopes on the C‐terminal half of envelope gp46 of human T‐cell leukemia virus type‐I (HTLV‐I)
Authors: Tanaka Yuetsu , Yasumoto Masazumi , Nyunoya Hiroshi , Ogura Tsutomu , Kikuchi Masayoshi , Shimotohno Kunitada , Shiraki Hiroshi , Kuroda Naotaka , Shida Hisatoshi , Tozawa Hideki 
Published: February 2007

AbstractIn order to study the antigenicity of envelope 46 kDa glycoprotein (gp46) of human T‐cell leukemia virus type‐l (HTLV‐I), we have generated monoclonal anti‐gp46 antibodies (MAbs), REY‐7, REY‐11, REY‐16, REY‐30, MET‐2 and MET‐3 from rats and mice. Immunoblot and immunofluorescence assays showed that these MAbs recognize gp46 and its related antigens, and specifically stained HTLV‐I‐bearing cells. All MAbs reacted with a recombinant gp46 antigen, NI47, expressing the 147 amino acids in the C‐terminal half of gp46. By using various synthetic peptides corresponding to the gp46 sequence, epitopes recognized by REY‐7 and MET‐3, REY‐11 and RE Y‐16, and REY‐30 were mapped to regions corresponding to the amino acids 175‐199, 253‐282 and 288‐312, respectively. MET‐2 did not react with any of the peptides used. These results indicate that the present MAbs are directed against at least 4 distinct epitopes expressed on the C‐terminal half of gp46. The binding of these MAbs to gp46 was specifically inhibited by sera from HTLV‐I‐infected individuals, but none of these MAbs inhibited the cell fusion activity of HTLV‐I.