bluuebunny/crossref_metadata_2025_split huggingface dataset:
Characterization of a species of non‐specific cross‐reacting antigen (NCA) exressed by human monocytic cell lines: Structure and expression during cell differentiation
Authors: Kuroki Motomu , Yamanaka Takahiko , Matsuo Yoshino , Ohtani Takeshi , Matsuo Yoshinobu , Minowada Jun , Misumi Yoshio , Oikawa Shinzo , Nakazato Hiroshi , Matsuoka Yuji 
Published: February 2007

AbstractIt has been documented that human monocytes/macro‐phages are reactive with antibodies directed to carcinoembryonic antigen (CEA) and non‐specific cross‐reacting antigens (NCAs), a group of glycoproteins antigenically cross‐reactive with CEA, yet the molecules responsible for this antigenic activity have not been fully clarified. In the present study, among 7 myelomonocytic cell lines tested, 2 monoblastoid lines, U‐937 and THP‐I, were found to express NCA‐50/90, a glycosyl‐phosphatidylinositol‐anchored cell‐adhesion molecule chiefly expressed on granulocytes. The 2 cell lines showed a reaction pattern with 5 distinct anti‐CEA and anti‐NCA monoclonal antibodies, similar to that of CHO transfectants expressing recombinant NCA‐50/90. Immunoprecipitation and SDS‐PAGE analyses identified glycoproteins of about 95 and 55 kDa in U‐937 and THP‐1 cells, respectively. Deglycosylation of the 2 antigens with N‐glycanase gave the same apparent molecular mass of about 45,000, which was also the same as that of the deglycosylated form of the recombinant NCA‐50/90. Upon Northern‐blot analysis, only one band of approximately 2.5 kb was detected in both cell lines with a cDNA probe for NCA‐50/ 90, which has a broad specificity to the CEA gene family members. cDNA cloning demonstrated that the 2.5‐kb clones encode the peptide of NCA‐50/90. The expression of NCA‐50/90 by U‐937 and THP‐1 was down‐regulated at both the protein and mRNA levels during cell differentiation from monoblastoid to monocyte/macrophage‐like cells induced by stimulation with phorbol 12‐myristate 13‐acetate. Our observations suggest that NCA‐50/90 is a differentiation antigen of cells of the monocyte/macrophage lineage as well as of the granulocyte lineage.
Comparison between the effect of butyric acid and its prodrug pivaloyloxymethylbutyrate on histones hyperacetylation in an HL‐60 leukemic cell line
Authors: Aviram Adina , Zimrah Yael , Shaklai Mali , Nudelman Abraham , Rephaeli Ada 
Published: February 2007

AbstractA butyric acid pro‐drug, pivaloyioxymethyl butyrate, AN‐9, developed in our laboratory, was previously shown to act as a differentiation‐inducing and an anti‐cancer agent. In this study we have shown that both AN‐9 and butyric acid caused a transient hyperacetylation of histones, which returned to basal levels after 6 and 12 hr, respectively. This activity precedes the induction of differentiation elicited by both agents. AN‐9 induced acetylation of histones at a concentration one order of magnitude lower than butyric acid. Pre‐treatment of the cells with esterase(s) inhibitors diminished the ability of AN‐9 to inhibit proliferation and induce differentiation. The above suggests that the intracellular release of butyric acid fragment, from the pro‐drug, is catalyzed by cellular esterase(s).
Tobacco, alcohol and the risk of gastric cancer. A population‐based case‐control study in Sweden
Authors: Hansson Lars‐Erik , Baron John , Nyrén Olof , Bergström Reinhold , Wolk Alicja , Adami Hans‐Olov 
Published: February 2007

AbstractPrevious studies have provided conflicting information on the role of tobacco and alcohol in gastric carcinogenesis. A population‐based case‐control study with 338 histologically confirmed gastric‐cancer cases and 679 control subjects was conducted. Information relating to life‐time tobacco consumption, alcohol intake and diet during adolescence and 20 years before interview, and to socio‐economic conditions was obtained through face‐to‐face interviews. Current cigarette smokers were found to have a greater risk than non‐users of tobacco. The duration of cigarette or pipe smoking was positively associated with gastric‐cancer risk. There was significant interaction between tobacco use and fruit consumption. High fruit intake was more protective among users of tobacco than among non‐users, and the risk estimates associated with cigarette smoking were higher among those with low fruit consumption than among frequent fruit‐eaters. Likewise, though to a lesser extent, vegetable intake interacted with tobacco use. Snuff dipping and alcohol intake was not associated with gastric‐cancer risk. However, high alcohol intake tended to increase the risk associated with tobacco use. This study adds further support to the role of tobacco smoking in gastric carcinogenesis, and demonstrates that high intake of fruits and vegetables may be particularly beneficial in smokers. © Wiley‐Liss, Inc.
Non‐involvement ofrasmutations in flat colorectal adenomas and carcinomas
Authors: Fujimori Takahiro , Satonaka Kazuhiro , Yamamura‐Idei Yuka , Nagasako Kou , Maeda Sakan 
Published: February 2007

AbstractRas gene mutations occur relatively early during colorectal tumor development and have been observed in 40‐50% of malignant colorectal tumors. Advances in endoscopic techniques have made it possible to detect small, flat colorectal tumors that could not be detected by standard examinations. To determine whether ras gene mutations are also involved in the genesis of small, flat colorectal tumors, we examined ras point mutations in 34 cases of small polypoid or flat elevated colorectal tumors (32 adenomas, 2 carcinomas) and in 26 cases of small, flat colorectal tumors (13 adenomas, 13 carcinomas) by means of the polymerase chain reaction (PCR) and dot‐blot hybridization. Ras gene point mutations were observed in 16 of the 34 tumors of the former type (47%), but in none of the 26 tumors of the latter type, even though the grade of dysplasia was severe in the flat tumors. Our results suggest that different genetic pathways for tumor progression may exist for polypoid and for flat colorectal carcinomas. © Wiley‐Liss, Inc.
Micro‐encapsulation of MDCK‐ras‐e cells prevents loss of E‐cadherin invasion‐suppressor function in vivo
Authors: Vandenbossche Geert M. R. , De Bruyne Georges K. , Bruyneel Erik A. , Clemminck Guy , Vleminckx Kris , van Roy Frans M. , Mareel Marc M. 
Published: February 2007

AbstractThe invasion‐suppressor molecule E‐cadherin mediates Cal2+‐dependent cell aggregation and prevents invasion. E‐cadherin‐positive Madin‐Darby canine kidney (MDCK) cells that were non‐invasive in vitro formed, upon i.p. injection, tumors that were invasive. Differentiated tubular tumor areas showed an intense immuno‐signal for E‐cadherin at intercellular contacts, whereas undefferentiated structures did not. Cell lines derived from such tumors turned out to be invasive in vitro and showed decreased Ca2+‐dependent cell aggregation but no change in E‐cadherin immunopositivitv. This combination of phenotypes indicated a loss of the E‐cadherin invasion‐suppressor function‐Mi cro‐en capsulation of i.p.‐injected cells prevented the loss of the E‐cadherin invasion‐suppressor function. We concluded that this loss in vivo was dependent upon immediate contacts between tumor cells and host cells or upon host factors that could not cross the capsule membrane. © Wiley‐Liss, Inc.
Molecular cloning and expression of a cDNA encoding a protein detected by the ki antibody from an ovarian carcinoma (OVCAR‐3) cell line
Authors: Chang Kai , Pastan Ira 
Published: February 2007

AbstractMAb Kl recognizes a cell‐surface glycoprotein (MW ∼40 kDa) present in ovarian carcinomas, malignant mesotheliomas, squamous‐cell carcinomas and normal mesothelial cells. In this study, expression screening was used to isolate cDNA clones encoding an antigen recognized by MAb 0Kl from a cDNA library made from a human ovarian carcinoma cell line (OVCAR‐3). Subsequently, other clones were isolated by DNA hybridization using a cDNA probe derived from one of the initial clones. The sequence of all the clones was similar. The longest cDNA contains 2,444 base pairs, and encodes a polypeptide of 263 amino acids with a calculated molecular weight of 30,511 daltons. The nudeotide sequence and deduced ami no‐acid sequence of the protein show no homology to other sequences in current data bases. In vitro translation of RNA transcripts from the cDNA inserts yielded polypeptides of 29 and 30 kDa. Similar‐sized proteins were obtained upon expression of the cDNA in Escherich'm coti, and these proteins were reactive with MAb Kl. The protein(s) expressed in E. coli were purified and used to make rabbit or mouse anttsera. These antisera reacted strongly with a soluble cytosolk protein in OVCAR‐3 cells, but not with the membrane‐bound antigen. Soluble cytosolk proteins of a similar size, recognized with MAb Kl, were found in OVCAR‐3 and N87 (gastric cancer) cells but not in 10 other cancer cell lines. These data indicate that the cloned cDNA encodes a cytosolk protein that reacted with MAb Kl. This soluble protein is expressed only in cells containing the CAKI surface glvcoprotein, suggesting that the 2 proteins could be structurally related. © Wiley‐Liss, Inc.
Comparison of retinoic acid and phorbol myristate acetate as inducers of monocytic differentiation
Authors: Matikainln Sampsa , Hurme Mikko 
Published: February 2007

AbstractSeveral human myeloid leukemia cell lines growing in vitro can be induced to differentiate to more mature monocyteJ. macrophage‐like cells by treatment with protein kinase C‐activating phorbol esters, such as PMA. In addition to PMA, cells of the THP‐I myeloid leukemia cell line acquire macro‐phage‐like characteristics after treatment with all‐trans retinoic acid (RA). To analyze the signal transduction mechanisms induced by RA, we first compared the effects of PMA and RA on the expression of genes which are known to be regulated during monocytic differentiation. Both RA and PMA effectively down‐regulated c‐myc expression, while c‐myb expression decreased only after PMA treatment. Expression of the β2‐integrin genes. CDIIa and CDIIb, was clearly increased after both of these treatments. Their effects on the src‐family tyrosine kinase genes were different: hck expression was similarly induced by these agents but lyn expression was stronger and more rapid after RA treatment. RA also enhanced lyn mRNA production rapidly in HL‐60, indicating that the activation of lyn gene expression is common in monocytic and granulocytic maturation of myeloid leukemia cells. To examine whether the AP‐1 enhancer activity is involved in RA‐induced monocytic differentiation, THP‐1 cells were transiently transfected with a chloramphenicol acetyi transferase (CAT)‐reporter gene containing S copies of the AP‐1 binding sites. In contrast to PMA, RA did not induce any CAT activity in these cells, thus suggesting that the RA‐induced changes in the expression of those genes described above were not dependent on the AP‐1 enhancer activity. © Wiley‐Liss, Inc.
The protein kinase C inhibitor CGP 41251, a staurosporine derivative with antitumor activity, reverses multidrug resistance
Authors: Utz Irene , Hofer Susanne , Regenass Urs , Hilbe Wolfgang , Thaler Josef , Grunicke Hans , Hofmann Johann 
Published: February 2007

AbstractMultidrug resistance (MDR) is frequently associated with overexpression of a 170‐kDa P‐glycoprotein (Pgp). Data suggest altered protein kinase C (PKC) activity in cells expressing the multidrug‐resistant phenotype. The staurosporine derivative CCP A1251, an experimental anticancer drug, has been shown to exert selectivity for inhibition of protein kinase C activity and to exhibit antitumor activity in Wtro and in vivo. Here we show that CGP A1251 is also able to reverse MDR. After treatment of the mult id rug‐resistant human lymphoblastoid cell line CCRF‐VCR1000 with 500 nM Adriamydn, cell proliferation was reduced to 81% of untreated controls. A combination of 500 nM Adriamydn with a non‐toxic concentration of 150 nM CGP 41251 (IC50 for inhibition of cell proliferation 420 nM CGP 41251) inhibits cell proliferation of CCRF‐VCR1000 cells to 29% of untreated controls. In sensitive CCRF‐CEM cells no enhancement of Adriamycin‐induced cytotoxicity was observed upon addition of 150 nM CGP 41251. Strong synergism of the inhibition of cell proliferation was also observed after concomitant treatment of KB‐851 I cells with CGP 41251 and Vinblas‐tine or Adriamydn. Drug‐sensitive KB‐31 cells could not be further sensitized to Adriamycin or Vinblastine with CGP 41251 doses above 100 nM. Pretreatment with 50‐1000 nM CGP 41251 for 30 min led to a dose‐dependent increase in the intracellular accumulation of rhodamine 123, a substrate of P‐glycoprotein. Treatment of multidrug‐resistant CCRF‐VCR1000 cells with CGP 41251 for 10 min was sufficient to inhibit the efflux of rhodamine 123. Preincubation with CGP 41251 for 12 or 24 hr did not alter multidrug resistance gene (mdrl)‐mRNA levels. CGP 41251, a drug with antitumor efficacy in experimental systems, might offer an attractive combination partner for the treatment of tumors expressing the MDR phenotype. © Wiley‐Liss, Inc.
Pancreatic cancer in europe: Ki‐ras gene mutation pattern shows geographical differences
Authors: Scakpa Aldo , Capelli Paola , Villanueva Alberto , Zamboni Giuseppe , Lluì Felix , Accolla Roberto , Mariuzzi Gianmario , Capellà Gabriel 
Published: February 2007

AbstractSeventy‐seven pancreatic ado no carcinomas (60 Spanish and 17 Italian) were tested for Ki‐ras gene mutations by analysis of polymerase chain reaction amplified sequences. Mutations involving codon 12 (GGT; gly) were detected in 16 Italian and 46 Spanish cases (80.5%in total). All Italian mutations involved the second base and were G to A transitions (GAT; asp) in 8 cases and G to T transversiorrs (GTT; val) in the remaining 8. Forty‐two Spanish mutations were characterized. Thirty‐eight were at the second and 4 at the first base: asp in 24 cancers, val in 14, arg (CGT) in 2 and cvs (TGT) in 2. Previous European studies and our present data show that 149 of the 186 pancreatic cancers harbored a codon 12 Ki‐ras mutation (80%), the large majority affecting the second base (73%), with a transitions/trans versions ratio of 1.3:1. However, the mutational pattern of cancers of the different European countries shows remarkable differences, both in the site of the mutation (first or second base) and in the ratio of transitions over transversions. Moreover, a significant subgroup of pancreatic carcinomas do not harbor Ki‐ras mutations. The classification of pancreatic cancers, according to the presence or absence, and type of Ki‐ras mutation, may be of importance in epidemiological studies. A critical reappraisal of existing epidemiological data, through a retrospective genotypic study using paraffin‐embedded cancer samples, may reveal significant correlations with specific genotoxic agents. © 1994 Wiley‐Liss, Inc.
Arachidonic acid metabolism in benign and malignant prostatic tissue in vitro: Effects of fatty acids and cyclooxygenase inhibitors
Authors: Chaudry Aziz A. , Wahle K. W. J. , McClinton S. , Moffat L. E. F. 
Published: February 2007

AbstractConcentrations of fatty acids (FA) in prostatic tissue of patients with either benign or malignant prostatic disease have previously been shown to be significantly different. In particular, there was a significant reduction in arachidonic acid (AA, C20:4n‐6) and docosapentaenoic acid (DPA, C22:5n‐6) concentrations in malignant prostatic tissue (PCa) phospholipids (PL). It was suggested that the decreased AA concentration in PCa may be due to its increased metabolism via the cyclooxygenase (CO) and/or lipoxygenase (LO) pathways to produce eicosanoids such as prostaglandins (PGs) and/or leucotrienes (LTs) rather than an impairment in desaturase activity in situ. The eicosanoid production in benign prostatic tissue (BPH) and PCa was determined using [3H]AA. The only eicosanoid produced in significant amounts by either tissue was PGE2 and PCa converted radiolabelled AA to PGE2 at an almost 10‐fold higher rate than BPH. PGE2 production from [3H]AA by PCa was investigated in the presence of oleic acid (OA, C18:In‐9), eicosapentaenoic acid (EPA, C20:5n‐3), docosahexaenoic acid (DHA, C22:6n‐3), dihomo‐gamma‐linolenic acid (DGLA, C20:3n‐6), eicosatetraynoic acid (FTYA) and ketoprofen (KPN) respectively. OA was found to be the most effective inhibitor of PGE2 production by PCa compared with DHA. EPA, ETYA and KPN, while DGLA was the least effective. Diacyiglycerol (DAG) formation from labelled AA by PCa was about 4‐fold greater than in BPH. Such high levels of DAG may be a means of promoting tumorigenesis through activation of protein kinase C as found with phorbol esters which can be regarded as DAG analogues. © 1994 Wiley‐Liss, Inc.
The anti‐tumor arotinoid RO 40‐8757 protects bone marrow from the toxic effects of 5‐fluorouracil
Authors: Eliason James F. , Inoue Tomoaki , Kubota Akiko , Horii Ikuo , Hartmann Diethelm 
Published: February 2007

AbstractCombination therapy with 5‐Fluorouracil (5‐FU) and the arotinoid Ro 40‐8757 (mofarotene) of established chemically induced mammary tumors in rats was examined. The cytotoxic drug was administered weekly and Ro 40‐8757 was given daily. The dose of Ro 40‐8757 used in this study did not have an effect on tumor burden but, in combination with 5‐FU, significantly enhanced the reduction in tumor burden and tumor number. In order to determine if Ro 40‐8757 had a protective effect on 5‐FU‐treated animals, several studies were performed with non‐tumor‐bearing mice. The 5‐FU was given once a week for 3 weeks at a dose that was lethal only after the third administration. When this treatment was combined with Ro 40‐8757 given 5 times/week, approximately 50% of the mice survived. Examination of the progenitor cell contents of femura and spleens of treated mice indicated that the protective effect of Ro 40‐8757 was manifested at the primitive hemopoietic progenitor cell level. Studies with murine bone marrow cells and human breast‐cancer cell lines in vitro demonstrated that there was no interaction between the 2 drugs at the cellular level, indicating that the arotinoid does not enhance the ability of cells to metabolize 5‐FU. This protective effect of the arotinoid makes it a useful potential partner for combination therapy with 5‐FU. © 1994 Wiley‐Liss, Inc.
Characterization of monoclonal antibody PAM4 reactive with a pancreatic cancer mucin
Authors: Gold David V. , Lew Karen , Maliniak Richard , Hernandez Marisol , Cardillo Thomas 
Published: February 2007

AbstractA monoclonal antibody (MAb), PAM4, having reactivity with pancreatic carcinoma has been developed. PAM4 is an IgG, immunoglobulin produced by immunization of mice with mucin purified from the xenografted RIPI human pancreatic carcinoma. An immunohistochemical study of normal adult tissues showed the PAM4 reactive epitope to be restricted to the gastrointestinal tract and absent from normal pancreas. In neoplastic tissue, PAM4 was reactive with 85% of the pancreatic carcinomas, approximately half of the colon cancers and none of the breast, ovarian, prostate, renal and liver cancers. PAM4 was, in general, non‐reactive with pancreatitis specimens whereas CAI 9.9 and DUPAN2 were strongly reactive with each one. Treatment of the mucin antigen by heating, reduction of disulfide bonds, or protease digestion abolished immunoreactivity with PAM4. Treatment of the mucin by neuraminidase or period ate oxidation reduced immunoreactivity but did not completely abolish it. Our data are consistent with the proposal that the PAM4 epitope is a conformation ally dependent peptide epitope and that certain carbohydrate structures are necessary in order to maintain the correct peptide conformation. The high specificity and intense reactivity of PAM4 with pancreatic carcinoma tissue suggests that the antibody may prove useful for in vitro diagnostic assays as well as in vivo targeting of diagnostic and therapeutic agents. © 1994 Wiley‐Liss, Inc.
Acquisition of immunogenicity by AKR leukemic cells following DNA‐mediated gene transfer is associated with the reduction of constitutive reactive superoxide radicals
Authors: Qua Kwok Y. , Lim Siew P. , Oei Audrey A. , Sabapathy Tr. Kanaga , Hui Kam M. 
Published: February 2007

AbstractWe have employed the DNA‐mediated gene transfer method to introduce the allogeneic major‐histocompatibility‐complex(MHC)‐class‐1 gene H‐2Kb into the K36.16 tumor cells, H‐2k, in order to generate tumor‐specific immunity. The acquisition of immunogenicity by the H‐2Kb‐transformed clones following gene transfer is associated with the reduction of constitutive reactive superoxide radicals. When the levels of cellular superoxide for the H‐2Kb‐positive immunogenic clones were determined, they were significantly lower (30 to 60%) than that of the parental K36.16 tumor cells. This reduction of superoxide in the H‐2Kb‐transformed cells was associated with a significant increase in the level of Cu‐Zn superoxide dismutase (SOD) and GPX I, together with a reduction in the DNA‐binding form of the NF‐kB transcription factor. The K36.16 parental tumor cells were also found to be relatively more resistant to the cytotoxic effects of hydrogen peroxide in vitro. To further support the role of superoxide anion radicals in tumorigenesis, in vivo depletion of glutathione promoted the tumorigenicity of the H‐2Kb‐transformed clones in (AKR/J X C57BL/6/J) F1 mice, whereas SOD was able to reduce their tumorigenicity. In addition, the presence of R‐sulfoxine (BSO) in spleen‐cell cultures in vitro abolished the ability of the immune lymphocytes to develop into tumor‐specific cytotoxic T lymphocytes (CTL). These observations support the concept that oxidative processes in tumor cells may have a strong influence on the host response against tumors. © 1994 Wiley‐Liss, Inc.
The epstein‐barr virus latent membrane protein‐1 (LMP1) induces interleukin‐10 production in burkitt lymphoma lines
Authors: Nakagomi Hiroshi , Dolcetti Riccardo , Bejarano Maria Teresa , Pisa Pavel , Kiessling Rolf , Masucci Maria G. 
Published: February 2007

AbstractHuman interleukin‐10 (h‐IL‐10) is a pleiotropic cytokine with stimulatory activity on B‐Iymphocytes. Recent evidence indicates that infection with Epstein‐Barr virus (EBV) induces h‐IL‐10 production in B‐cells and that this cytokine may contribute to EBV‐induced B‐cell transformation. It is not known whether h‐IL‐10 induction by EBV correlates with distinct phenotypic features of the infected cells or with the expression of particular viral genes. We have approached these questions by investigating the expression of h‐IL‐10 mRNA in a panel of B‐cell lines including: in vitro EBV‐transformed lymphoblastoid cell lines (LCLs), EBV‐carrying Burkitt lymphoma (BL) lines, EBV‐negative BL lines and their sublines infected with different EBV strains, or transfected with the transformation‐associated viral gene. h‐IL‐10 mRNA was detected by reverse‐transcriptase‐assisted (RT)‐PCR in a subset of EBV‐negative BLs and in all FBV‐positive BL lines and LCLs investigated except Daudi. This cell line carries an EBV nuclear antigen (EBNA)‐2 gene‐defective virus strain. h‐IL‐10 mRNA was induced by conversion of 3 EBV‐negative and h‐IL‐10‐negative BL lines (BL41, BL47 and BL49) with the transforming, B95.8‐derived EBV strain. P3HR‐1 virus convertants that do not express the viral EBNA‐2 and the EBV latent membrane protein (LMP)‐1, and fail to progress towards a LCL‐like cell phenotype, showed no evidence of h‐IL‐10 up‐regulation. Expression of LMP1 was sufficient to induce h‐IL‐10 mRNA in transfected sublines of the EBV‐negative DG75 and BL41 cell lines, whereas expression of EBNA1, 2, 5 or 6 had no effect. h‐IL‐10 was detected in the culture supernatants of the LMP1 transfectants by specific ELISA assays. The present findings confirm the role of LMP1 in the transactivation of a wide variety of cellular genes which may be involved in EBV‐induced B‐cell transformation. © 1994 Wiley‐Liss, Inc.