bluuebunny/crossref_metadata_2025_split huggingface dataset:
Insulin‐like growth factor‐I has a biphasic effect on colon carcinoma cells through transient inactivation of forkhead1, initially mitogenic, then mediating growth arrest and differentiation
Authors: Ewton Daina Z. , Kansra Sanjay , Lim Seunghwan , Friedman Eileen 
Published: August 2002

AbstractIGF‐I stimulates intestinal cell differentiation after initiating a short proliferative burst, similar to its effect on muscle cell differentiation. Levels of IGF‐I attainable in serum (10–20 ng/ml) induced transient growth stimulation of colon carcinoma cells, then growth arrest. When IGF‐I functioned as a mitogen, it blocked differentiation. Intestinal cell differentiation occurred once cells had undergone the IGF‐I–initiated growth arrest and IGF‐I and butyrate acted synergistically to induce maturation markers. IGF‐I induces NIH‐3T3 cell proliferation and survival by activating the kinase akt, which in turn inhibits various apoptotic mediators and the forkhead family of transcription factors, which mediate expression of p27kip1. Promoter reporter assays demonstrated that forkhead1 mediates transcription of p27kip1 in colon carcinoma cells. The mitogenic effects of IGF‐I on 4 colon carcinoma cell lines were transient because the inactivating phosphorylation of forkhead1 by akt was short‐lived. This allowed transcriptional upregulation of the cdk inhibitor p27kip1, with a resulting growth arrest. In contrast, in NIH‐3T3 cells treated in parallel with identical IGF‐I levels, forkhead phosphorylation levels were sustained; thus, no increase in p27kip1 levels was seen and cells continued to proliferate. Intestinal epithelial cells in vivo undergo a limited number of divisions, then growth arrest and completion of their maturation. IGFs found in intestinal tissue may control the timing of this process. In addition, colon cancers may have developed strategies to overcome IGF‐I–mediated growth arrest. Earlier (Kansra et al., Int J Cancer 2000;87:373–8), we found that levels of IGFBP‐3 were elevated at least 2‐fold in 70% of resected colon cancers compared with adjacent normal tissue. In the current study, growth inhibition by IGF‐I and IGF‐II was blocked by concurrent addition of IGFBP‐3, implying that colon cancers with elevated IGFBP‐3 levels would be selected for in vivo because they could bind and inactivate high serum IGF‐I levels and continue to proliferate. © 2002 Wiley‐Liss, Inc.
Peripheral γδ T‐cell deficit in nasopharyngeal carcinoma
Authors: Zheng Bo Jian , Ng Sze Park , Chua Daniel T.T. , Sham Jonathan S.T. , Kwong Dora L.W. , Lam Clarence K. , Ng Mun Hon 
Published: August 2002

AbstractPrevious studies identified CD56+ and CD56− subsets of peripheral γδ T cells from healthy donors. Both subsets responded to stimulation by a myeloma cell line, XG‐7 and undergo vigorous ex vivo expansion in the presence of exogenous IL‐2. They are cytotoxic for different tumor targets including nasopharyngeal carcinoma, but they differ from one another in that the CD56− subset has an additional growth requirement for IL‐7 and exhibited greater cytotoxicity against nasopharyngeal carcinoma (NPC) targets. These immune cells were further shown to retard tumor growth in a nude mice NPC model. To assess if these immune cells might contribute to host defense against NPC, we compared γδ T‐cell status of NPC patients with healthy donors and survivors who had been in clinical remission of the cancer. It was found that peripheral γδ T cells of patients were impaired in their response to the stimulatory effects of XG‐7 and exhibited weak or essentially no cytotoxicity for the NPC targets. The deficits were present in early and advanced stages of the cancer but were restored among survivors after successful treatment of the cancer. These findings support a role for peripheral γδ T cells in host defense against NPC. It was noted that these immune cells comprise less than 5% of peripheral blood monocytic cells and hence it was not surprising that this component of host defense was breached early in the development of the cancer. © 2002 Wiley‐Liss, Inc.
Mapping of two new epitopes on the apomucin encoded by MUC5AC gene: Expression in normal GI tract and colon tumors
Authors: Nollet Séverine , Forgue‐Lafitte Marie‐Elisabeth , Kirkham Paul , Bara Jacques 
Published: August 2002

AbstractThree hybridomas secreting monoclonal antibodies (MAbs) against human (62M MAb) or rat (463M and 589M MAbs) gastric mucins were isolated. These MAbs immunoreacted against a human recombinant protein encoded by the 3′ region of the MUC5AC gene. We have mapped 2 new gastric mucin epitopes and the M1‐f epitope previously characterized by the 19/21M1 MAbs on MUC5AC‐encoded apomucin. The M1‐f, 463/589M and 62M epitopes are located in the MUC11p15/von Willebrand factor (vWF)‐A3uD4 domain, in the D4‐(vWF)‐like domain and in the C‐ and CK‐vWF‐like domains of MUC5AC, respectively. The 463/589M and 62M MAbs stained the surface epithelium of human gastric mucosae, but not the normal colon mucosae (except 463/589M MAbs, which immunoreacted with 5 of 49 cases). All hyperplastic polyps are stained strongly with the 463/589M MAbs and faintly with the 62M MAb. In addition, 463/589M epitope was detected in 64% of the adenomas and in 93% of the mucosae adjacent to adenocarcinomas; in contrast, only 9% of the adenomas and 29% of the mucosae adjacent to adenocarcinomas expressed the 62M epitope. The expression pattern of the 463/589M epitope in colonic carcinogenesis is different from that of the 19/21M1 epitope, although the 2 epitopes are encoded by MUC5AC gene. © 2002 Wiley‐Liss, Inc.
Chemotherapeutic agents sensitize osteogenic sarcoma cells, but not normal human bone cells, to apo2l/trail‐induced apoptosis
Authors: Evdokiou Andreas , Bouralexis Stelios , Atkins Gerald J. , Chai Fugui , Hay Shelley , Clayer Mark , Findlay David M. 
Published: August 2002

AbstractApo2L/TRAIL is a member of the tumor necrosis factor (TNF) family of cytokines that induces death of cancer cells but not normal cells. Its potent apoptotic activity is mediated through its cell surface death domain‐containing receptors, DR4 and DR5. Apo2L/TRAIL interacts also with 3 “decoy” receptors that do not induce apoptosis, DcR1, DcR2, which lack functional death domains, and osteoprotegerin (OPG). The aim of our study was to investigate the cytotoxic activity of Apo2L/TRAIL on established osteogenic sarcoma cell lines (BTK‐143, HOS, MG‐63, SJSA‐1, G‐292 and SAOS2) and in primary cultures of normal human bone (NHB) cells. When used alone, Apo2L/TRAIL at 100 ng/ml for 24 hr induced greater than 80% cell death in only 1 (BTK‐143) of the 6 osteogenic sarcoma cell lines. In contrast, Apo2L/TRAIL‐resistant cells were susceptible to Apo2L/TRAIL‐mediated apoptosis in the presence of the anticancer drugs, Doxorubicin (DOX), Cisplatin (CDDP) and Etoposide (ETP) but not Methotrexate (MTX) or Cyclophosphamide (CPM). Importantly, neither Apo2L/TRAIL alone nor in combination with any of these drugs affected primary normal human bone cells under equivalent conditions. Apo2L/TRAIL‐induced apoptosis, and its augmentation by chemotherapy in the resistant cell lines was mediated through caspase‐8 and caspase‐3 activation. Furthermore, Apo2L/TRAIL‐induced apoptosis and its augmentation by chemotherapy was effectively inhibited by caspase‐8 zIETD‐fmk and caspase‐3 zDEVD‐fmk protease inhibitors and by the pan‐caspase inhibitor zVAD‐fmk. The pattern of basal Apo2L/TRAIL receptor mRNA expression, or expression of the intracellular caspase inhibitor FLICE‐inhibitory protein, FLIP, could not be readily correlated with resistance or sensitivity to Apo2L/TRAIL‐induced apoptosis. However, the augmentation of Apo2L/TRAIL effects by chemotherapy was associated with drug‐induced up‐regulation of death receptors DR4 and DR5 mRNA and protein. No obvious correlation was seen between the expression of OPG mRNA or protein and susceptibility of cells to Apo2L/TRAIL‐induced apoptosis. Stable over‐expression of a dominant negative form of the Fas‐associated death domain protein (FADD) in the Apo2L/TRAIL‐sensitive BTK‐143 cells completely inhibited Apo2L/TRAIL‐induced cell death. Our results indicate that chemotherapy and Apo2L/TRAIL act synergistically to kill cancer cells but not normal bone‐derived osteoblast‐like cells, which has implications for future therapy of osteosarcoma. © 2002 Wiley‐Liss, Inc.
Cleavage and polyadenylation specificity factor (CPSF)‐derived peptides can induce HLA‐A2‐restricted and tumor‐specific CTLs in the majority of gastrointestinal cancer patients
Authors: Maeda Yoshiaki , Ito Masaaki , Harashima Nanae , Nakatsura Tetsuya , Hida Naoya , Imai Nobue , Sato Yuuji , Shichijo Shigeki , Todo Satoru , Itoh Kyogo 
Published: August 2002

AbstractTo identify CTL‐directed antigens in gastrointestinal cancer, we have investigated antigens recognized by the HLA‐A2‐restricted CTL line established from T cells infiltrating into colon cancer and report herein cleavage and polyadenylation specificity factor (CPSF) as a potent antigen holding peptides capable of inducing CTLs. Five peptides at amino acid positions 250–258, 392–400, 534–542, 1296–1304 and 1359–1368 of CPSF, which were recognized by the CTL line, were found to have the ability to induce HLA‐A2‐restricted and tumor‐specific CTLs in peripheral blood mononuclear cells of the majority (69%, 11/16) of gastrointestinal cancer patients with different HLA‐A2 subtypes. Thus, these peptides might be appropriate molecules for use in the peptide‐based specific immunotherapy of HLA‐A2+ patients with gastrointestinal cancers. © 2002 Wiley‐Liss, Inc.
A variant of the DNA repair gene XRCC3 and risk of squamous cell carcinoma of the head and neck: A case‐control analysis
Authors: Shen Hongbing , Sturgis Erich M. , Dahlstrom Kristina R. , Zheng Yuxin , Spitz Margaret R. , Wei Qingyi 
Published: August 2002

AbstractIndividuals differ in their ability to repair DNA damage induced by carcinogens. Studies have shown that polymorphisms in DNA repair genes contribute to individual variation in DNA repair capacity and cancer risk. In a hospital‐based case‐control study, we tested the hypothesis that a C to T variant (Thr241Met) of DNA repair gene X‐ray repair cross‐complementing group 3 (XRCC3) is associated with risk of developing squamous cell carcinoma of the head and neck (SCCHN). We genotyped for this variant in 367 non‐Hispanic white patients newly diagnosed with SCCHN and 354 frequency‐matched cancer‐free controls. Compared with the XRCC3 18067CC and 18607CT genotypes, the variant XRCC3 18067TT genotype was associated with a non‐statistically significantly increased risk of SCCHN (adjusted odds ratio [ORadj], 1.36; 95% confidence interval [CI], 0.89–2.08), but this risk was significantly increased among female subjects (ORadj 2.23, 95% CI, 1.00–4.98) and current smokers (ORadj, 2.26; 95% CI, 1.02–4.99). These findings suggest that the variant XRCC3 18067TT genotype may not play a major role in the etiology of SCCHN but may contribute to a subset of SCCHN. Larger studies are needed to verify these findings. © 2002 Wiley‐Liss, Inc.
Time trends incidence of both major histologic types of esophageal carcinomas in selected countries, 1973–1995
Authors: Vizcaino A. Paloma , Moreno Victor , Lambert Rene , Parkin D. Maxwell 
Published: August 2002

AbstractThe purpose of our study was to examine the incidence patterns of 2 major histologic types of esophageal cancer, in selected countries world‐wide and to identify components of birth cohort, period and age as determinants of observed time trends using regression modeling. The roles of temporal changes in specification of histology of tumors and of classification of cancers at the gastroesophageal junction as esophageal or gastric in origin were taken into consideration. In all, 56,426 esophageal cancer cases were included. The results indicate that the incidence rate of squamous cell carcinoma of the esophagus has been relatively stable in most of the countries analyzed, although increasing trends were observed in Denmark and the Netherlands (Eindhoven) among men and in Canada, Scotland and Switzerland among women. There was a significant increase in the incidence of esophageal adenocarcinomas in both sexes in the United States (among whites and blacks), Canada and South Australia and in 6 European countries (Scotland, Denmark, Iceland, Finland, Sweden and Norway). In France the increase was limited to men and in Switzerland the increase was observed only in women. Modeling was unable to distinguish which trends were the results of changes in risk between generations (as cohort effects), or changes in all age groups simultaneously (as a period effect). © 2002 Wiley‐Liss, Inc.
Y‐box factor YB‐1 predicts drug resistance and patient outcome in breast cancer independent of clinically relevant tumor biologic factors HER2, uPA and PAI‐1
Authors: Janz Martin , Harbeck Nadia , Dettmar Peer , Berger Ursula , Schmidt Anja , Jürchott Karsten , Schmitt Manfred , Royer Hans‐Dieter 
Published: August 2002

AbstractIntrinsic or acquired resistance to chemotherapy is responsible for failure of current treatment regimens in breast cancer patients. The Y‐box protein YB‐1 regulates expression of the P‐glycoprotein gene mdr1, which plays a major role in the development of a multidrug‐resistant tumor phenotype. In human breast cancer, overexpression and nuclear localization of YB‐1 is associated with upregulation of P‐glycoprotein. In our pilot study, we analyzed the clinical relevance of YB‐1 expression in breast cancer (n = 83) after a median follow‐up of 61 months and compared it with tumor‐biologic factors already used for clinical risk‐group discrimination, i.e., HER2, urokinase‐type plasminogen activator (uPA) and plasminogen activator inhibitor type 1 (PAI‐1). High YB‐1 expression in tumor tissue and surrounding benign breast epithelial cells was significantly associated with poor patient outcome. In patients who received postoperative chemotherapy, the 5‐year relapse rate was 66% in patients with high YB‐1 expression. In contrast, in patients with low YB‐1 expressions, no relapse has been observed so far. YB‐1 expression thus indicates clinical drug resistance in breast cancer. Moreover, YB‐1 correlates with breast cancer aggressiveness: in patients not treated with postoperative chemotherapy, those with low YB‐1 expression are still free of disease, whereas the 5‐year relapse rate in those with high YB‐1 was 30%. There was no significant correlation between YB‐1 expression and either HER2 expression or uPA and PAI‐1 levels. Risk‐group assessment achieved by YB‐1 differed significantly from that by HER2 or uPA/PAI‐1. In conclusion, YB‐1 demonstrated prognostic and predictive significance in breast cancer by identifying high‐risk patients in both the presence and absence of postoperative chemotherapy, independent of tumor‐biologic factors currently available for clinical decision making. © 2001 Wiley‐Liss, Inc.
Why is the business‐cycle behaviour of fundamentals alike across exchange‐rate regimes?
Authors: Dedola Luca , Leduc Sylvain 
Published: August 2002

AbstractSince the adoption of flexible exchange rates, real exchange rates have been much more volatile than they were under Bretton Woods. However, the volatilities of most other macroeconomic variables have remained approximately unchanged. This poses a puzzle for standard international business cycle models. This paper develops a two‐country, two‐sector model with nominal rigidities featuring deviations from the law of one price due to firms setting prices in buyers' currencies. By partially insulating goods markets across countries and thus mitigating the international expenditure‐switching effect, this pricing behaviour is found to considerably dampen the responses of quantities to shocks hitting the economies therefore helping to account for the puzzle. Copyright © 2001 John Wiley & Sons, Ltd.
Parametric and semiparametric estimation of sample selection models: an empirical application to the female labour force in Portugal
Authors: Martins Maria Fraga O. 
Published: August 2002

AbstractThis paper applies both parametric and semiparametric methods to the estimation of wage and participation equations for married women in Portugal. The semiparametric estimators considered are the two‐stage estimators proposed by Newey (1991) and Andrews and Schafgans (1998). The selection equation results are compared using the specification tests proposed by Horowitz (1993), Horowitz and Härdle (1994), and the wage equation results are compared using a Hausman test. Significant differences between the two approaches indicate the inappropriateness of the standard parametric methods to the estimation of the model and for the purpose of policy simulations. The greater departure seems to occur in the range of the low values of the index corresponding to a specific group of women. Copyright © 2001 John Wiley & Sons, Ltd.
Polarized light scattering as a rapid and sensitive assay for metal toxicity to bacteria
Authors: Bronk B. V. , Li Z. Z. , Czégé Jozsef 
Published: August 2002

AbstractA new method that utilizes the scattering of polarized light from a suspension of bacteria to assay the effect of toxins is evaluated. The method compares the time dependence of changes in an angular scattering pattern obtained from a suspension of Escherichia coli bacteria with no toxin exposure to the corresponding, but reduced, changes that occur when there is exposure to a small concentration of certain toxicants. The changes are due to growth of a specially prepared population of these bacteria. The changes in the pattern normally reflect a change in average bacterial size due to growth, whereas the reduction of the change in pattern occurs when there is rapid cessation of bacterial growth. The method was tested with varying concentrations of the ions of five different heavy metals. The results using this method during the first few minutes after exposure to the toxicant were compared to the relative survival of colony‐forming units of the bacteria. The graphs for the two methods were found to be approximately parallel for each of the five metals examined. This result indicates that the toxic effect of these metals takes place relatively quickly for these bacteria. These results were compared with results available from the literature for the same metals but using other methods for measuring the toxicity to bacteria. Published in 2001 by John Wiley & Sons Ltd.
Effects of trivalent chromium on hepatic CYP‐linked monooxygenases in laying hens
Authors: Guerra M. C. , Renzulli C. , Antelli A. , Pozzetti L. , Paolini M. , Speroni E. 
Published: August 2002

AbstractChromium is an essential nutrient required for the metabolism of carbohydrates and lipids in humans and many animal species. We evaluated whether feeding laying hens with high levels of different chemical forms of trivalent chromium may affect hepatic metabolizing cytochrome P‐450 (CYP)‐linked enzymes. Modulation of CYP‐dependent monooxygenases (which play a pivotal role in the endogenous metabolism) by Cr(III) was tested using either specific substrates as probes of different CYPs or testosterone as a multi‐bioprobe. The CYP‐supported oxidases were studied in liver microsomes from laying hens fed with diet supplemented with either 25 or 50 ppm chromium chloride as a yeast or as aminoniacinate. Although at 25 ppm no appreciable effects were observed, at 50 ppm a general inactivation of the recorded monooxygenases (ranging from 34% loss for ethoxycoumarin O‐deethylase with chromium chloride to 85% loss for O‐deethylation of ethoxyresorufin with either chromium yeast or aminoniacinate) were achieved in the supplemented groups vs controls. The only exception was the O‐dealkylation of pentoxyresorufin, which was significantly boosted by both chromium yeast (up to 65% increase) and chromium aminoniacinate (up to 141%). Measurements of the regio‐ and stereoselective hydroxylation of testosterone used as a multi‐bioprobe corroborated the inactivating properties of Cr(III) at the higher dose. Taken as a whole, these findings seem to indicate that high levels of Cr(III) supplementation can substantially impair CYP‐catalysed drug metabolism in laying hens. Copyright © 2002 John Wiley & Sons, Ltd.
Characterization of angiogenesis and inflammation surrounding ePTFE implanted on the epicardium
Authors: Kellar Robert S. , Kleinert Leigh B. , Williams Stuart K. 
Published: August 2002

AbstractThe response of epicardial tissue to the implantation of expanded polytetrafluoroethylene (ePTFE) was evaluated and compared with identical material implanted within subcutaneous and adipose tissues. These two tissue environments were selected for comparison with epicardial implants because they represent tissue often involved in device implantation. Discs of ePTFE (6 mm) were implanted into three different tissue sites in Sprague‐Dawley rats. At 5 weeks, polymers and surrounding tissues were harvested and processed for light microscopy. General histology and histochemistry data indicated all polymers to be well incorporated with new tissue. Subcutaneous implants were covered by a dense fibrous capsule (55–70 μm). Epicardial and adipose implants had no fibrous capsule and a significantly greater number of microvessels (arterioles, capillaries, and venules) within the surrounding tissues compared with subcutaneous implants. An increased level of inflammation was also observed around epicardial implants compared with the other implants. Additionally, the new vasculature surrounding epicardially implanted ePTFE revealed an altered microvessel density and vessel type distribution compared with normal (control) epicardium. These results suggest that epicardial tissue responds to implanted ePTFE with a robust inflammatory response that may support the formation of a new microvasculature that is uniquely different from the native epicardial microvasculature. © 2002 Wiley Periodicals, Inc. J Biomed Mater Res 61: 226–233, 2002
Bonelike apatite growth on hydroxyapatite–gelatin sponges from simulated body fluid
Authors: Bigi A. , Boanini E. , Panzavolta S. , Roveri N. , Rubini K. 
Published: August 2002

AbstractIn vitro bioactivity of gelatin sponges and hydroxyapatite‐enriched gelatin sponges was tested through evaluation of the variations in their composition and morphology after soaking in simulated body fluid (1.5) for periods up to 21 days at 37°C. The presence of hydroxyapatite inside the sponges promotes the deposition of bonelike apatite crystals. The deposits are laid down as spherical aggregates, with mean diameters increasing from about 1–2 μm, after 4 days of soaking in simulated body fluid solution, up to about 3.5 μm in the samples soaked for 21 days. Simultaneously, the relative amount of inorganic phase increases up to about 56% wt, leading to a composite material with a composition quite close to that of bone tissue. The inorganic phase is a poor crystalline carbonated apatite similar to trabecular bone apatite. © 2001 Wiley Periodicals, Inc. J Biomed Mater Res 59: 709–714, 2002