bluuebunny/crossref_metadata_2025_split huggingface dataset:
CD26 (dipeptidyl peptidase IV/DPP IV) as a novel molecular marker for differentiated thyroid carcinoma
Authors: Tanaka Tetsuji , Umeki Kazumi , Yamamoto Ikuo , Sakamoto Fujio , Noguchi Shiro , Ohtaki Sachiya 
Published: February 2007

AbstractIn this report we show that CD26 (dipeptidyl peptidase IV/DPP IV) is a novel molecular marker for differentiated thyroid carcinoma. Northern‐blot analysis of 22 various thyroid tissues revealed that CD26 is a more specific marker of differentiated thyroid carcinoma than 3 proto‐oncogenes previously reported to increase mRNA expression in thyroid carcinomas: c‐met, c‐erbB‐2 and EGF‐R. A comparative study of 3 CD26 assays, Northern blotting, immunohistochemical staining and activity staining clearly showed that CD26 enzyme activity staining is the most specific assay for differentiated thyroid carcinoma, yet the easiest to perform. Activity staining of 216 thyroid tissues detected CD26 in all 52 papillary carcinomas and all 5 follicular carcinomas, while all 58 cases of Graves' disease were CD26‐negative. Among benign neoplasms, 54 of 55 adenomatous goiters and 29 of 33 follicular adenomas were CD26‐negative. Staining intensity of the enzyme activity was relative to the degree of CD26 mRNA expression. Southern‐blot study showed no gene amplification or major translocation of the CD26 gene in 7 papillary carcinomas examined. Based on this study, ectopic expression of CD26 in differentiated thyroid carcinomas is thought to be mainly caused by increased CD26 mRNA expression. In conclusion, CD26 activity staining is a simple, specific assay which should be added to the usual pathological examinations in order to distinguish differentiated thyroid carcinomas from benign thyroid diseases. © 1995 Wiley‐Liss, Inc.
Frequency and prognostic evaluation of 3p21‐22 allelic losses in non‐small‐cell lung cancer
Authors: Thiberville Luc , Bourguignon Jeannette , Metayer Josette , Bost Frederic , Diarra‐Mehrpour Maryam , Bignon Jean , Lam Stephen , Martin Jean‐Pierre , Nouvet Georges 
Published: February 2007

AbstractPrevious loss of heterozygosity (LOH) studies of chromosome 3p loci have displayed a 60% deletion frequency in non‐small‐cell lung cancers (NSCLC), as opposed to small‐cell lung cancers, in which the 3p deletion is consistently found. However, the high stromal‐cell admixture found in NSCLC and the use of the Southern‐blot method lead to under‐evaluation of this frequency. In this study, we used a very precise microdissection technique followed by PCR amplification of 6 3p21‐22 polymorphic genomic sequences to analyze LOH in 86 NSCLC and in normal adjacent tissue. We found the sensitivity of the microdissection‐PCR‐based LOH technique higher than the sensitivity of the Southern‐blot technique: 87% of the squamous‐cell carcinomas and 84% of the large‐cell undifferentiated carcinomas showed a clear LOH for a 3p21‐22 locus. All doubly informative cases but 4 showed concordant deletion at all 3p21‐22 loci. The analysis of 3p microsatellite sequences displayed only 2 cases of genomic instability, one of them also displaying features of tumoral heterogeneity as regards the instability genotype. Four carcinomas in situ adjacent to these NSCLC showed the same allelic profile as the invasive tumors. The only prognostic factors in this study were the disease stage and histology. The 3p21‐22 deletion was not related to the stage of the disease and did not appear to be a significant prognostic factor of survival. 3p21‐22 loss appears, so far, to be the most frequent and the earliest genetic alteration described in NSCLC, but does not seem to carry significant prognostic information in invasive tumors. © 1995 Wiley‐Liss, Inc.
Expression of MAGE‐1, MAGE‐2, MAGE‐3/‐6 and MAGE‐4A/‐4B genes in ovarian tumors
Authors: Yamada Akira , Kataoka Akio , Shichijo Shigeki , Kamura Toshiharu , Imai Yasuhisa , Nishida Takashi , Itoh Kyogo 
Published: February 2007

AbstractMAGE genes encoding tumor‐rejection antigens recognized by cytotoxic T lymphocytes are expressed at the mRNA level in various malignant tumors. We have investigated the expression of genes MAGE‐1, ‐2, ‐3/‐6 and ‐4a/‐4b at the mRNA level in malignant and non‐malignant ovarian tumors as well as in normal ovaries by reverse transcription‐polymerase chain reaction. MAGE‐1, ‐2, ‐3/‐6 and ‐4a/‐4b were expressed in 12, 5, 11 and 4 of 58 malignant tumors, respectively. The majority of these MAGE‐mRNA‐positive tumors were histologically surface‐epithelial‐stromal tumors, in particular serous adenocarcinomas. They mostly consisted of either advanced‐stage or recurrent tumors. In contrast, neither benign tumors nor normal ovaries expressed any of the MAGE genes investigated. A 46‐kDa MAGE‐1 protein was identified in MAGE‐1‐mRNA‐positive serous adenocarcinomas by immunoblot analysis with polyclonal anti‐MAGE‐1 antibody. These results provide important information for specific immunotherapy of ovarian serous adenocarcinomas with MAGE gene products. © 1995 Wiley‐Liss, Inc.
In vitro osteogenesis on a highly bioactive glass‐ceramic (Biosilicate®)
Authors: Moura João , Teixeira Lucas Novaes , Ravagnani Christian , Peitl Oscar , Zanotto Edgar Dutra , Beloti Márcio Mateus , Panzeri Heitor , Rosa Adalberto Luiz , de Oliveira Paulo Tambasco 
Published: February 2007

AbstractOne of the strategies to improve the mechanical performance of bioactive glasses for load‐bearing implant devices has been the development of glass‐ceramic materials. The present study aimed to evaluate the effect of a highly bioactive, fully‐crystallized glass‐ceramic (Biosilicate®) of the system P2O5–Na2O–CaO–SiO2 on various key parameters of in vitro osteogenesis. Surface characterization was carried out by scanning electron microscopy and Fourier transform infrared spectroscopy. Osteogenic cells were obtained by enzymatic digestion of newborn rat calvarial bone and by growing on Biosilicate® discs and on control bioactive glass surfaces (Biosilicate® parent glass and Bioglass® 45S5) for periods of up to 17 days. All materials developed an apatite layer in simulated body fluid for 24h. Additionally, as early as 12 h under culture conditions and in the absence of cells, all surfaces developed a layer of silica‐gel that was gradually covered by amorphous calcium phosphate deposits, which remained amorphous up to 72 h. During the proliferative phase of osteogenic cultures, the majority of cells exhibited disassembly of the actin cytoskeleton, whereas reassembly of actin stress fibers took place only in areas of cell multilayering by day 5. Although no significant differences were detected in terms of total protein content and alkaline phosphatase activity at days 11 and 17, Biosilicate® supported significantly larger areas of calcified matrix at day 17. The results indicate that full crystallization of bioactive glasses in a range of compositions of the system P2O5–Na2O–CaO–SiO2 may promote enhancement of in vitro bone‐like tissue formation in an osteogenic cell culture system. © 2007 Wiley Periodicals, Inc. J Biomed Mater Res, 2007
Tenascin cytotactin epidermal growth factor‐like repeat binds epidermal growth factor receptor with low affinity
Authors: Iyer Anand Krishnan V. , Tran Kien T. , Borysenko Christopher W. , Cascio Michael , Camacho Carlos J. , Blair Harry C. , Bahar Ivet , Wells Alan 
Published: February 2007

AbstractSelect epidermal growth factor (EGF)‐like (EGFL) repeats of human tenascin cytotactin (tenascin C) can stimulate EGF receptor (EGFR) signaling, but activation requires micromolar concentrations of soluble EGFL repeats in contrast to subnanomolar concentrations of classical growth factors such as EGF. Using in silico homology modeling techniques, we generated a structure for one such repeat, the 14th EGFL repeat (Ten14). Ten14 assumes a tight EGF‐like fold with truncated loops, consistent with circular dichroism studies. We generated bound structures for Ten14 with EGFR using two different approaches, resulting in two distinctly different conformations. Normal mode analysis of both structures indicated that the binding pocket of EGFR exhibits a significantly higher mobility in Ten14–EGFR complex compared to that of the EGF–EGFR complex; we hypothesized this may be attributed to loss of key high‐affinity interactions within the Ten14–EGFR complex. We proved the efficacy of our in silico models by in vitro experiments. Surface plasmon resonance measurements yielded equilibrium constant KD of 74 µM for Ten14, approximately three orders of magnitude weaker than that of EGF. In accordance with our predicted bound models, Ten14 in monomeric form does not bind EGFR with sufficient stability so as to induce degradation of receptor, or undergo EGFR‐mediated internalization over either the short (20 min) or long (48 h) term. This transient interaction with the receptor on the cell surface is in marked contrast to other EGFR ligands which cause EGFR transit through, and signaling from intracellular locales in addition to cell surface signaling. J. Cell. Physiol. 211: 748–758, 2007. © 2007 Wiley‐Liss, Inc.
Interleukin‐1β induces MMP‐9 expression via p42/p44 MAPK, p38 MAPK, JNK, and nuclear factor‐κB signaling pathways in human tracheal smooth muscle cells
Authors: Liang Kao‐Chih , Lee Chiang‐Wen , Lin Wei‐Ning , Lin Chih‐Chung , Wu Chou‐Bin , Luo Shue‐Fen , Yang Chuen‐Mao 
Published: February 2007

AbstractMatrix metalloproteinases (MMPs) are responsible for degradation of extracellular matrix and play important roles in cell migration, proliferation, and tissue remodeling related to airway inflammation. Interleukin‐1β (IL‐1β) has been shown to induce MMP‐9 production in many cell types and contribute to airway inflammatory responses. However, the mechanisms underlying MMP‐9 expression induced by IL‐1β in human tracheal smooth muscle cells (HTSMCs) remain unclear. Here, we investigated the roles of p42/p44 MAPK, p38 MAPK, JNK, and NF‐κB pathways for IL‐1β‐induced MMP‐9 production in HTSMCs. IL‐1β induced production of MMP‐9 protein and mRNA in a time‐ and concentration‐dependent manner determined by zymographic, Western blotting, and RT‐PCR analyses, which was attenuated by inhibitors of MEK1/2 (U0126), p38 MAPK (SB202190), JNK (SP600125), and NF‐κB (helenalin), and transfection with dominant negative mutants of MEK1/2, p38 and JNK, respectively. IL‐1β‐stimulated phosphorylation of p42/p44 MAPK, p38 MAPK, and JNK was attenuated by pretreatment with U0126, SB202190, SP600125, or transfection with these dominant negative mutants of MEK, ERK, p38 and JNK, respectively. Furthermore, IL‐1β‐stimulated translocation of NF‐κB into the nucleus and degradation of IκB‐α was blocked by helenalin. Finally, the reporter gene assay revealed that MAPKs and NF‐κB are required for IL‐1β‐induced MMP‐9 luciferase activity in HTSMCs. MMP‐9 promoter activity was enhanced by IL‐1β in HTSMCs transfected with MMP‐9‐Luc, which was inhibited by helenalin, U0126, SB202190, and SP600125. Taken together, the transcription factor NF‐κB, p42/p44 MAPK, p38 MAPK, and JNK that are involved in MMP‐9 expression in HTSMCs exposed to IL‐1β have now been identified. J. Cell. Physiol. 211: 759–770, 2007. © 2007 Wiley‐Liss, Inc.
Defining the involvement of proteinases in pemphigus vulgaris: Evidence of matrix metalloproteinase‐9 overexpression in experimental models of disease
Authors: Cirillo Nicola , Lanza Michele , Rossiello Luigi , Gombos Fernando , Lanza Alessandro 
Published: February 2007

AbstractPemphigus vulgaris (PV) acantholysis represents a complex phenomenon wherein a number of factors cooperates. PV serum is known to modulate important cellular events, including kinase activity, transcriptional regulation, and proteinase expression. Indeed, transduction of signals to the cell triggered by PV serum may induce proteinase up‐regulation potentially responsible for disruption of epidermal adhesion and, ultimately, blister formation. Here, we sought to investigate this hypothesis by using both in vivo and in vitro models of PV. Microarray analysis on mouse skin tissues suggested that the equilibrium between extracellular proteinases and their inhibitors moved towards enhanced proteolytic activity in PV neonatal mouse model, at least on the transcriptional level. Conversely, genes codifying cell adhesion proteins were dramatically down‐regulated. The effects of PV serum on the protein level were then studied in vitro both in keratinocyte monolayers and skin organ cultures focusing on matrix metalloproteinase (MMP) 9 expression and activity. By means of Western blotting, zymography, and living cell immunofluorescence studies, we showed that MMP‐9 was early overexpressed in keratinocytes exposed to PV serum, and subsequently secreted in the culture medium. However, we failed to demonstrate extracellular activation of MMP‐9, since it was found in its 92 kDa inactive form in serum‐free culture supernatants. Taken together, our data demonstrated that proteinase expression, particularly of MMP‐9, is modulated by PV serum and associated with PV acantholysis. J. Cell. Physiol. 212: 36–41, 2007. © 2007 Wiley‐Liss, Inc.
Fibroblast growth factor receptor‐induced phosphorylation of STAT1 at the golgi apparatus without translocation to the nucleus
Authors: Citores Lucía , Bai Ling , Sørensen Vigdis , Olsnes Sjur 
Published: February 2007

AbstractSTAT transcription factors signal from the plasma membrane to the nucleus in response to growth factors and cytokines, but little is known about activation of STAT1 from intracellular sites. Here we show that transient transfection of COS cells with fibroblast growth factor receptors (FGFRs) led to ligand‐independent phosphorylation of the receptors, including intracellular immature forms. FGF‐independent activation of STAT1 was demonstrated at the Golgi apparatus where it was colocalized with FGFRs. Both FGFR1 and FGFR2 induced strong phosphorylation of STAT1 causing redistribution of the Golgi apparatus, while FGFR3 and FGFR4 induced less phosphorylation of STAT1 and little or no redistribution of the Golgi apparatus. Upon expression of a cytosolic mutant of FGFR4 lacking the transmembrane as well as the extracellular region (CytR4), STAT1 was phosphorylated and transferred to the nucleus. The results indicate that immature forms of FGFRs form incomplete signaling complexes on Golgi membranes trapping phospho‐STAT1 on this organelle. J. Cell. Physiol. 212: 148–156, 2007. © 2007 Wiley‐Liss, Inc.
Growth factors improve gene expression after lentiviral transduction in human adult and fetal hepatocytes
Authors: Selden Clare , Mellor Neil , Rees Myrddin , Laurson Joanna , Kirwan Mike , Escors David , Collins Mary , Hodgson Humphrey 
Published: February 2007

AbstractBackgroundLentiviral vectors may be vectors of choice for transducing liver cells; they mediate integration in quiescent cells and offer potential for long‐term expression. In adult liver, hepatocytes are generally mitotically quiescent. There has been controversy as to the necessity for lentiviral vector target cells to be in the cell cycle; currently, there is consensus that effective transduction can be achieved in quiescent hepatocytes, by using virus at high titre. However, transduction approaches which reduce the multiplicities of infection (MOIs) required provide potential benefit of cost and safety for therapeutic use.MethodsWe used two late‐generation HIV‐based lentiviral vector systems (pHR‐SIN‐cppT SGW and pRRLSIN.cPPT.PGK.WPRE) encoding LacZ/GFP reporter genes to transduce adult and fetal human hepatocytes in vitro + /− growth factors, hepatocyte growth factor (HGF) and epidermal growth factor (EGF). Green fluorescent protein (GFP) expression was observed microscopically, and quantified by fluorescence spectrometry for protein expression, fluorescence‐activated cell sorting (FACS) analysis to identify the proportion of cells expressing GFP, and real‐time quantitative polymerase chain reaction (PCR) for number of integrations.ResultsGene expression following lentiviral transduction of human liver cells in vitro was markedly enhanced by the growth factors HGF and EGF. In adult cells growth factors led to a greater proportion of cells expressing more GFP per cell, from more integration events. In human fetal cells, the proportion of transduced hepatocytes remained identical, but cells expressed more GFP protein.ConclusionsThis has implications for the design of regimes for liver cell gene therapy, allowing marked reduction of MOIs, and reducing both cost and risk of viral‐mediated toxicity. Copyright © 2007 John Wiley & Sons, Ltd.
Genomic diversity of human papillomavirus genotype 53 in an ethnogeographically closed cohort of white European women
Authors: Kocjan Boštjan J. , Seme Katja , Močilnik Tina , Jančar Nina , Vrtačnik‐Bokal Eda , Poljak Mario 
Published: February 2007

AbstractHuman papillomavirus (HPV) genotype 53 is classified taxonomically in alpha HPV genus–species 6, together with HPV‐30, HPV‐56, and HPV‐66 and is considered to be one of three “probable high‐risk” HPV genotypes. Recent worldwide comparison of 44 isolates of HPV‐53 showed the existence of nine long control region (LCR) genomic variants, which formed a phylogenetic tree with two deep dichotomic branches. In order to investigate further the genomic diversity of HPV‐53, a total of 94 isolates of HPV‐53 obtained from an ethnogeographically closed cohort of 70 white European women was analyzed. The identification and characterization of HPV‐53 genomic variants was based on analysis of three different HPV genomic regions: LCR, E6 and E7. A higher genomic diversity of HPV‐53 was identified in the ethnogeographically closed cohort of white European women than has been reported previously on isolates collected worldwide. Altogether, 19 HPV‐53 genomic variants, composed of 13 LCR, 13 E6, and 5 E7 genomic variants, were identified. Eleven out of 13 LCR, all E6, and four out of five E7 genomic variants were described for the first time. The present study confirmed dichotomic phylogeny of HPV‐53 described previously and, in addition, showed for the first time that after a dichotomic split, both groups of HPV‐53 genomic variants formed star‐like phylogenetic clusters. In women with persistent HPV‐53 infection, HPV‐53 genomic variants remained unchanged for up to 51 months. In rare cases, infection with multiple HPV‐53 genomic variants is possible. Taking into account the results of this and previous studies, at least 26 different HPV‐53 genomic variants exist today. J. Med. Virol. 79:431–438, 2007. © 2007 Wiley‐Liss, Inc.
Distinctive distribution of HPV16 E6 D25E and E7 N29S intratypic Asian variants in Korean commercial sex workers
Authors: Choi Byeong‐Sun , Kim Sung Soon , Yun Haesun , Jang Dae Ho , Lee Joo‐Shil 
Published: February 2007

AbstractThe distribution of HPV16 sequence variations differs geographically and specific HPV16 E6 and E7 variants might carry a high risk for development of invasive cervical cancer and cervical intraepithelial neoplasia in a given population. To investigate the genetic variation of HPV 16 E6 and E7 genes, genomic DNAs from 56 HPV16‐infected commercial sex workers were extracted from their cervical swabs by using DNA isolation kit. The E6 and E7 coding region (34–880) with HPV16 E6/E7 specific PCR were amplified and analyzed by using the DNAstar software. At the nucleotide level, 26 variants of the HPV16 E6 and E7 genes were identified including 12 silent mutations. At the amino acid level, the isolates showed 14 variants including E6 Q14H, E6 D25E, E6 I27R, E6 H78Y, E6 L83V, and E7 N29S. The dominant HPV16 E6 and E7 variants were HPV16 E6 D25E (68%) and HPV16 E7 N29S (73%), respectively, which belong to Asian lineage. Although this study has some limitations such as a small sample size and not enough clinical data, these finding suggests that the distinctive distribution of HPV 16 As‐variant E6 D25E and E7 N29S might be associated with geographical dependence rather than disease progression. Further study is needed to determine the clinical and biological effects of these variants. J. Med. Virol. 79:426–430, 2007. © 2007 Wiley‐Liss, Inc.
Genetic characterization of hepatitis C virus strains in Estonia: Fluctuations in the predominating subtype with time
Authors: Tallo Tatjana , Norder Helene , Tefanova Valentina , Krispin Tõnu , Schmidt Jelena , Ilmoja Madis , Orgulas Karen , Pruunsild Kaije , Priimägi Ludmilla , Magnius Lars O. 
Published: February 2007

AbstractDuring the last decade, there has been a dramatic increase in intravenous drug use in young adults in Estonia with an increased incidence of both hepatitis B and C as a consequence. Since genetic data are limited regarding hepatitis C virus (HCV) strains in Estonia, the aim of the study was to characterize HCV strains in different risk groups to determine their relatedness to strains from other geographical regions. Three hundred fifty‐three anti‐HCV positive sera collected during 1994–2004 from hospitalized patients, blood donors and health care workers were used as source of HCV RNA. Two hundred nine (59%) of the sera were positive for HCV RNA by PCR directed to the 5′‐UTR region. For 174 strains the HCV subtype was determined by analyses of the NS5B and/or the 5′UTR‐core regions. 1b (71%) was the most common subtype followed by 3a (24%), 2c (2%), 1a (1%), and 2a (1%). The 1b and 3a strains were similar to strains from other regions of the former USSR. Within genotype 1b there were several HCV lineages. However, for 3a there seemed to be two separate introductions into Estonia. There was a relative shift from subtype 1b to 3a in 1999–2000 with a further replacement of 3a with 1b in intravenous drug users in 2001 and onwards (P < 0.05). However, both subtypes were found to co‐circulate in the community independent of risk factors. One patient was infected with the 2k/1b recombinant presumed to originate from St. Petersburg being the first isolate of this recombinant recovered outside Russia. J. Med. Virol. 79:374–382, 2007. © 2007 Wiley‐Liss, Inc.
Effects of post‐hepatectomized rat sera on cultured cells
Authors: Gentile John M. , Ali Elizabeth , Grace James T. 
Published: February 2007

AbstractThese experiments suggest that serum obtained subsequent to partial hepatectomy of rats is capable of stimulating the growth of and enhancing the final population and cell viability achieved in antibiotic‐free suspension cultures of L929 cells. Preliminary enzymatic inhibition of post‐hepatectomy serum suggests that one of the humoral factors involved may be RNA.
A computer approach to cancer patient follow‐up
Authors: Graham Thomas D. , Ausman Robert K. 
Published: February 2007

AbstractA computer based system to follow until death all discharged patients with a malignant diagnosis has been implemented at Roswell Park Memorial Institute. The automated system has relieved the follow‐up clerks of tedious clerical procedures and the human decision‐making that was prevalent in its manual predecessor. The system automatically prepares letters based on the patient's condition and, when the patient expires, a physician letter is generated to obtain details of the death (autopsy, mechanism of death, etc.). All correspondence is stored on magnetic tape for patient as well as system evaluation. Less than one percent of the cases registered has been lost to follow‐up. The system has shown that the family physician contact is most desirable. The system is economically feasible.
Lack of effect of diphenylhydantoin ingestion on vesical transitional epithelium in the rat
Authors: McDonald D. F. 
Published: February 2007

AbstractSeizure‐prone patients may be chronically treated with diphenylhydantoin, a mitogenic agent excreted in the urine. Chronic ingestion of diphenylhydantoin by 64 rats failed to demonstrate vesical epithelial tumor formation under conditions which demonstrate the tumorigenicity of other vesical carcinogens. Vesical neoplasms occurring in patients chronically ingesting diphenylhydantoin are probably co‐incidental.