bluuebunny/crossref_metadata_2025_split huggingface dataset:
Clinical impact of molecular and cytogenetic findings in synovial sarcoma
Authors: Panagopoulos Ioannis , Mertens Fredrik , Isaksson Margareth , Limon Janusz , Gustafson Pelle , Skytting Björn , Åkerman Måns , Sciot Raf , Dal Cin Paola , Samson Ignace , Iliszko Mariola , Ryoe Janusz , Dêbiec‐Rychter Maria , Szadowska Anna , Brosjö Otte , Larsson Olle , Rydholm Anders , Mandahl Nils 
Published: September 2002

AbstractSynovial sarcoma is an aggressive soft‐tissue tumor that accounts for up to 10% of soft‐tissue sarcomas. Cytogenetically, synovial sarcoma is characterized by the t(X;18)(p11;q11), found in more than 95% of the tumors. This translocation results in rearrangements of the SYT gene in 18q11 and one of the SSX1, SSX2, or SSX4 genes in Xp11, creating a SYT/SSX1, SYT/SSX2, or SYT/SSX4 chimeric gene. It has been shown that patients with SYT/SSX1 fusion genes have a shorter metastasis‐free survival than do patients with SYT/SSX2. Previous studies have also suggested that clonal evolution may be associated with disease progression. In the present study, RT‐PCR analysis showed that all 64 examined synovial sarcomas from 54 patients had SYT‐SSX chimeric genes. SYT/SSX1 was found in 40 tumors from 33 patients, SYT/SSX2 in 23 tumors from 20 patients, and SYT/SSX4 in one case. Two patients had variant SYT/SSX2 transcripts, with 57 bp and 141 bp inserts, respectively, between the known SYT and SSX2 sequences. Patients with tumors with SYT/SSX1 fusions had a higher risk of developing metastases compared to those with SYT/SSX2 fusions (P = 0.01). The reciprocal transcripts SSX1/SYT and SSX2/SYT were detected using nested PCR in 11 of the 40 samples with SYT/SSX1 and 5 of the 23 samples with SYT/SSX2, respectively. Among 20 blood samples, SYT/SSX1 and SYT/SSX2 were detected in one sample each. The t(X;18), or variants thereof, was found cytogenetically in all patients but three. Among 32 primary tumors, the t(X;18) or a variant translocation was the sole anomaly in 10. In contrast, of the seven metastatic lesions that were investigated prior to radiotherapy, only one had a t(X;18) as the sole anomaly; all other tumors displayed complex karyotypes. Cytogenetic complexity in primary tumors was, however, not associated with the development of metastases. Tumors with SYT/SSX2 less often (4/12 vs. 7/15) showed complex karyotypes than did tumors with SYT/SSX1, but the difference was not significant. Combining cytogenetic complexity and transcript data, we found that the subgroup of patients with tumors showing simple karyotypes and SYT/SSX2 fusion had the best clinical outcome (2/8 patients developed metastases), and those with tumors showing complex karyotypes together with SYT/SSX1 fusion the worst (6/7 patients developed metastases). This corresponded to 5‐year metastasis‐free survival rates of 0.58 and 0.0, respectively (P = 0.02). © 2001 Wiley‐Liss, Inc.
A plains ceramic clay source characterization by comparative geochemical and petrographic analyses: Results from the Calhan Paint Mines, Colorado, U.S.A.
Authors: Phillips Scott C. , Morgenstein Maury 
Published: September 2002

AbstractThe Calhan Paint Mines District, 5EP3258, Colorado, presents exposures of an exceptional clay source. When the area also produced prehistoric Ceramic stage sites, it provided the opportunity for both pottery and potential clay source analysis by optical petrography, X‐ray diffraction, and neutron activation. Although the main purpose of this study is the characterization of the ceramics and outcrop clays, results from a limited number of samples suggest that the colorful clays, the figurative “paints,” of the Calhan Paint Mines were purposely used in prehistoric times as clay source materials for ceramic production. The Calhan Paint Mines are quite possibly the only prehistoric Plains Ceramic stage clay source currently confirmed within the state of Colorado. © 2002 Wiley Periodicals, Inc.
Studies on low‐coordinated nitrogen, phosphorus, sulfur, and selenium compounds
Authors: Inamoto Naoki 
Published: September 2002

AbstractThe major studies of my laboratory on heteroatom chemistry are briefly outlined and include the following topics: (1) novel radical reactions to kinetic stabilization of organosulfur and selenium compounds, (2) novel reactions of organophosphorus compounds, (3) reaction of the S atom to stabilization of o‐thioquinonemethides, (4) N‐nitrosoimines stabilized by heterocycles to hypervalent sulfur compounds, and (5) phosphinidenes (R‐P) to kinetic stabilization of low‐coordinated organophosphorus compounds. © 2001 John Wiley & Sons, Inc. Heteroatom Chem 12:183–194, 2001
Radico‐catalysis: possible involvement of a cobalt(II) complex in the free radical reactions of sulfur functions
Authors: Tada Masaru 
Published: September 2002

AbstractA cobalt(II) complex is paramagnetic and can be coordinated with sulfur functions; the coordination complex delocalizes an unpaired electron from cobalt(II) to the sulfur functions such as thioester and vinyl sulfide. Thus, the generation of partial unpaired electron density on the sulfur functions induces or modifies the reactions of the organo free radical containing the sulfur function. © 2001 John Wiley & Sons, Inc. Heteroatom Chem 12:204–208, 2001
Formation of antimony–sulfur double‐bond compounds and their trapping with nitrile oxides
Authors: Tokitoh Norihiro , Arai Yoshimitsu , Sasamori Takahiro , Takeda Nobuhiro , Okazaki Renji 
Published: September 2002

AbstractThe reaction of a highly crowded dihydrostibine [2,4,6‐tris[bis(trimethylsilyl)methyl]phenyl‐SbH2 (TbtSbH2) (1)] with elemental sulfur in the presence of nitrile oxides resulted in the formation of [2 + 3] cycloaddition reaction products of a thioxostibine [TbtSb=S (6)] and a dithioxostiborane [TbtSb(S)=S (7)], which are among a novel class of antimony–sulfur double‐bond compounds. The structures of the [2 + 3] cycloadducts of dithioxostiborane 7 with nitrile oxides were determined by X‐ray structural analysis. Desulfurization of highly crowded antimony‐containing cyclic polysulfides [TbtSbSx (4: x = 5; 5: x = 7)] with phosphine reagents also resulted in the formation of 6 and 7. © 2001 John Wiley & Sons, Inc. Heteroatom Chem 12:244–249, 2001
Ifosamide, epirubicin and granulocyte colony‐stimulating factor: a regimen for successful mobilization of peripheral blood progenitor cells in patients with multiple myeloma
Authors: Arland M. , Leuner S. , Lange S. , Bartsch R. , Kahl C. , Florschütz A. , Franke A. , Höffkes H.‐G. 
Published: September 2002

AbstractIn general, the mobilization of peripheral blood progenitor cells (PBPC) in multiple myeloma (MM) patients is poor and is achieved in most cases by combined cyclophosphamide and G‐CSF. This study was performed to examine the efficacy of combined ifosfamide/epirubicine and G‐CSF for PBPC mobilization and purging. Sixteen patients suffering from multiple myeloma in stage II/A and III/A according to Durie and Salmon underwent chemotherapy consisting of a total of three cycles of ifosfamide (3 g/m2 on days 1 and 2 and epirubicine 80 mg/m2 on day 1) and G‐CSF (10 or 20 µg/kg body weight (BW) daily until harvesting). PBPC harvesting was performed after the first and third cycle of chemotherapy. The median number of PBPC after the first cycle of chemotherapy was 7.79×106 CD34+ cells/kg BW (ranging from 0.94–26.36×106) and 6.38×106 CD34+ cells/kg BW (ranging from 0.79–29.31×106) after the third cycle of chemotherapy. Clinical re‐evaluation after three cycles of chemotherapy showed 13 (81 per cent) patients in partial remission (PR), two (12 per cent) in complete remission (CR) and one (6.25 per cent) in stable disease (SD). No major side‐effects were observed, six patients developed hematological toxicity stage IV WHO for a median of 3.9 days but no serious infection episodes occurred. Combined ifosfamide/epirubicin and standard G‐CSF is able to mobilize sufficient PBPC without serious side‐effects for patients with MM and for purging procedures resulting in a high proportion of complete remissions after tandem high‐dose melphalan chemotherapy. Copyright © 2001 John Wiley & Sons, Ltd.
Organizational socialization as instrument and symbol: An extended institutional theory perspective
Authors: Fogarty Timothy J. , Dirsmith Mark W. 
Published: September 2002

AbstractOrganizational socialization can be viewed from the perspective of institutional theory, and institutional theory plays a key role in helping organizations achieve their missions. This article applies a framework to suggest that socialization can be interpreted as a symbolic response to societal expectations. Research propositions are presented that can be used to guide future research on the role of socialization.
Self‐report of memory and affective dysfunction in association with medication use in a sample of individuals with chronic sleep disturbance
Authors: McAndrews Mary Pat , Kayumov Leonid , Phillipson Ron , Shapiro Colin M. 
Published: September 2002

AbstractBenzodiazepines produce memory disturbance after acute administration. It is not clear whether chronic use of benzodiazepines is hazardous to memory processes. Epidemiological data indicate that a large proportion (10–30 per cent) of individuals with sleep dysfunction take hypnotic aids for a year or longer. The purpose of the present study was to evaluate self‐reported memory dysfunction in a sample of individuals who considered their sleep disturbance sufficiently severe to seek investigation in sleep clinics. It was hypothesized that individuals taking benzodiazepines for sleep would report greater perceived everyday memory failures than individuals taking other sleep aids or no medication. Questionnaires were given to 368 individuals referred into the study by investigators in six sleep disorders clinics. All respondents completed a lengthy (700‐item) questionnaire, which included scales assessing memory difficulties, affective status and sleep disturbance. Respondents also reported any medication use for sleep problems and duration of use of the current drug. Information on medication use was reported by 289 participants. Fifty‐six per cent of respondents reported using some form of psychoactive medication (antidepressants, benzodiazepines, Zopiclone). Twenty‐two per cent reported using no medication. Analysis of covariance showed that these medications had no detectable effect on subjective memory difficulties during chronic use, F(4,226)=1·34, p=0·25. Copyright © 2000 John Wiley & Sons, Ltd.
Enhancement of cisplatin‐induced apoptosis by infection with adeno‐associated virus type 2
Authors: Duverger Valerie , Sartorius Ute , Klein‐Bauernschmitt Petra , Krammer Peter H. , Schlehofer Jörg R. 
Published: September 2002

AbstractThe non‐pathogenic human adeno‐associated virus, AAV, has been shown to sensitize human cancer cells and experimental tumors towards the action of chemotherapeutic agents such as cisplatin. Since chemotherapeutic drugs mainly involve the induction of apoptosis, we investigated whether 1 possible mechanism of AAV‐mediated sensitization of human tumor cells may result from an enhancement of cisplatin‐induced apoptosis. In HeLa and A549 cells, infection with AAV type 2 (AAV‐2) increased cisplatin‐induced DNA fragmentation but had no cytotoxic effect by itself. This enhanced apoptosis appeared to be mediated at least in part by a component of the viral capsid since empty or UV‐inactivated AAV‐2 particles were also able to boost cisplatin‐induced DNA fragmentation. Interestingly, these effects were not observed after infection with AAV type 5 (AAV‐5) or the autonomous parvovirus, H‐1. AAV‐2‐mediated enhancement of apoptosis was not associated with a modification of the expression of CD95 ligand, CD95 receptor or other death receptors, as shown by RT‐PCR and RNase protection assay. In contrast, using the mitochondrial fluorescent dye, JC‐1 in flow cytometry, AAV‐2 infection was found to further reduce the mitochondrial transmembrane potential after treatment with cisplatin in a caspase‐independent manner, suggesting that increase of apoptosis by AAV‐2 occurred at the mitochondrial level. In contrast, in cells of the small cell lung cancer line, P693, an enhancement of cisplatin‐induced DNA fragmentation was not observed after infection with AAV‐2. In these cells, sensitization to cisplatin‐toxicity was associated with cell cycle arrest in G2/M. The data indicate that in the absence of viral gene expression, AAV‐2‐mediated sensitization to cisplatin involves multiple cellular pathways promoting cell death signals in a cell type‐dependent manner. The results further support that AAV‐2 particles may be appropriate adjuvants for improving cancer chemotherapy and may also have consequences regarding AAV‐2‐based vectors for gene therapy. © 2001 Wiley‐Liss, Inc.
Dominant‐negative inhibition of breast cancer resistance protein as drug efflux pump through the inhibition of S‐S dependent homodimerization
Authors: Kage Kumie , Tsukahara Satomi , Sugiyama Tomomi , Asada Sakiyo , Ishikawa Etsuko , Tsuruo Takashi , Sugimoto Yoshikazu 
Published: September 2002

AbstractBreast cancer resistance protein (BCRP) is a half‐molecule ABC transporter highly expressed in mitoxantrone‐resistant cells. In our study we established PA317 transfectants expressing Myc‐tagged BCRP (MycBCRP) or HA‐tagged BCRP (HABCRP). The exogenous BCRP protein migrated as a 70‐kDa protein in SDS‐PAGE under reducing condition, but migrated as a 140‐kDa complex in the absence of reducing agents. The 140‐kDa BCRP complex was heat‐stable but dissociated into 70‐kDa BCRP with the addition of 2‐mercaptoethanol. The 140‐kDa BCRP complex was immunoprecipitated with anti‐Myc antibody from the lysates of PA317 cells double‐transfected with MycBCRP and HABCRP. The 140‐kDa complex reacted with anti‐HA and anti‐BCRP antibodies and after the addition of reducing agents, a 70‐kDa protein reacting with anti‐Myc, anti‐HA and anti‐BCRP antibodies was detected. These results clearly indicate that BCRP forms a homodimer bridged by disulfide bonds. To assess the possible dominant‐negative inhibition of BCRP drug efflux pump, various mutant BCRP cDNAs were isolated by PCR mutagenesis. First, mutant BCRP cDNAs were introduced to parental PA317 cells and tested for their function as drug‐resistance genes. Next, inactive BCRP cDNA clones were introduced to MycBCRP‐transfected cells and tested for the ability to lower drug resistance. Among the 8 inactive mutant cDNA clones tested, HABCRP cDNA clone 15 with an amino acid change from Leu to Pro at residue 554 in the fifth transmembrane domain of BCRP partially reversed the drug resistance of MycBCRP‐transfected cells. These results suggest that homodimer formation is essential for BCRP drug resistance, implicating this dominant‐negative inhibition as a new strategy to circumvent drug resistance. © 2001 Wiley‐Liss, Inc.
RPR‐115135, a farnesyltransferase inhibitor, increases 5‐FU‐ cytotoxicity in ten human colon cancer cell lines: Role of p53
Authors: Russo Patrizia , Malacarne Davide , Falugi Carla , Trombino Sonya , O'Connor Patrick M. 
Published: September 2002

AbstractA new non peptidic farnesyltransferase inhibitor, RPR‐115135, in combination with 5‐FU was studied in 10 human colon cancer cell lines (HCT‐116, RKO, DLD‐1, Colo‐320, LoVo, SW‐620, HT‐29, HCT‐15, Colo‐205 and KM‐12) carrying several mutations but well characterized for p53 and Ras status. We found that there was a slight tendency (not statistically significant) for the p53 inactivated cells to be less sensitive to 5‐FU after 6 days continuous treatment. Simultaneous administration of RPR‐115135 and 5‐FU, at subtoxic concentrations, resulted in a synergistic enhancement of 5‐FU cytotoxicity in the p53 wildtype cells (HCT‐116, RKO, DLD‐1, Colo‐320, LoVo). In the p53 mutated cells (SW‐620, HT‐29, HCT‐15, Colo‐205, KM‐12) the effect was very complicated. In HCT‐15 the combination resulted in antagonism, in KM‐12 in antagonism or in synergy (at different concentrations) and in SW‐620, HT‐29 and Colo‐205 cells in synergy but only when 5‐FU was administered at high concentrations. Growth inhibition could be accounted for on the basis of a specific cell cycle arrest phenotype (G2‐M arrest), as assayed by flow cytometry, only in the p53 functioning cell lines. The combination RPR‐115135 + 5‐FU increases apoptotic events only in these cell lines. In the mutated cell lines no major alterations on cell cycle arrest phenotype and no induction of apoptosis was observed. Although RPR‐115135 can potentiate the effect of 5‐FU in cells in which p53 function is disrupted, these data suggest strongly that RPR‐115135 significantly enhances the efficacy of 5‐FU only when p53 is functioning. © 2002 Wiley‐Liss, Inc.
Food groups and laryngeal cancer risk: A case‐control study from Italy and Switzerland
Authors: Bosetti Cristina , La Vecchia Carlo , Talamini Renato , Negri Eva , Levi Fabio , Dal Maso Luigino , Franceschi Silvia 
Published: September 2002

AbstractBesides tobacco and alcohol, diet has been thought to be associated with laryngeal cancer risk. We thus analyzed the role of various food groups, as well as specific seasoning fats, in a case‐control study conducted in Northern Italy and the Swiss Canton of Vaud from 1992 to 2000. Our study included 527 incident, histologically confirmed cases and 1,297 frequency‐matched controls, selected among patients admitted to the same hospitals as cases for acute, nonneoplastic conditions, unrelated to smoking, alcohol consumption and long‐term modifications of diet. The subjects' usual diet was investigated through a validated food frequency questionnaire, including 78 foods and beverages. Odds ratios (OR) and 95% confidence intervals (CI) were estimated using unconditional multiple logistic regression models. After adjustment for major confounding factors, a significant trend of increasing risk was observed for eggs (OR = 1.7 for the highest compared to the lowest quintile), red meat (OR = 3.1), processed meat (OR = 1.7), fish (OR = 1.6) and sugars (OR = 1.6). Significant inverse associations were observed for pulses (OR = 0.7), raw vegetables (OR = 0.2), cooked vegetables (OR = 0.3), citrus fruit (OR = 0.6) and other fruit (OR = 0.5). In regard to seasoning fats, a significant reduction of cancer risk was observed for olive oil (OR = 0.4) and specific seed oils (OR = 0.6), while mixed seed oils were directly associated with laryngeal cancer risk (OR = 2.2). Our study suggests that increasing vegetables and fruit, decreasing meat consumption and perhaps substituting olive oil or specific seed oils for other types of seasoning lipids might help reduce laryngeal cancer risk. © 2002 Wiley‐Liss, Inc.
Human breast adenocarcinoma cell lines promote angiogenesis by providing cells with uPA‐PAI‐1 and by enhancing their expression
Authors: Bajou Khalid , Lewalle Jean‐Marc , Martinez Christian Rodriguez , Soria Claudine , Lu He , Noël Agnès , Foidart Jean‐Michel 
Published: September 2002

AbstractDuring angiogenesis, endothelial cells use uPA and PAI‐1 to migrate and degrade the basement membrane surrounding capillary blood vessels. Invasive tumor cells produce a large amount of uPA that could bind uPAR present at the endothelial cell surface to facilitate their invasion. To verify this hypothesis, endothelial cells were incubated with conditioned medium (CM) from two breast cancer cell lines (MCF7 and MDA MB 231 cells). Within a short incubation period (30 min) with both CM, an increase of uPA, PAI‐1 and uPA‐PAI‐1 complex was detected in endothelial cell layer as assessed by casein zymography, ELISA and uPA immunostaining. The extent of this enhancement was related to the levels of uPA secreted by tumor cells (high in MDA MB 231 cells and low in MCF7 cells). After 2 hr of incubation, the CM from both tumor cells upregulated uPA and PAI‐1 mRNA levels in endothelial cells in a time‐dependent manner. The uPA increase in the cell layer could not be attributable to an increase of uPAR level. Only the CM from highly invasive MDA MB 231 cells increased the angiogenic morphotype of endothelial cells assessed in a collagen gel. A single addition of amino‐terminal fragment of uPA (ATF) was able to abolish the angiogenic effect induced by MDA MB 231 cell CM. Our data demonstrate that the interactions occurring between breast tumor cells and endothelial cells can modulate tumor angiogenesis at least by two mechanisms: an increase of uPA and PAI‐1 cell surface‐binding and of their expression by endothelial cells. © 2002 Wiley‐Liss, Inc.
Protein phosphatase‐2A regulates endothelial cell motility and both the phosphorylation and the stability of focal adhesion complexes
Authors: Young M. Rita I. , Kolesiak Kristin , Meisinger Jeremy 
Published: September 2002

AbstractSolid cancers must stimulate expansion of the vascular network for continued growth. The process of angiogenesis involves endothelial cell migration so as to reorganize into vessel structures. The extent of cellular motility is regulated in part by the balance between serine/threonine kinases and protein phosphatases. In the present study, we show a decline in the activity of the serine/threonine phosphatase PP‐2A in endothelial cells whose motility is stimulated by exposure to medium conditioned by either murine LLC cells or human HNSCC cells. Inhibition of endothelial cell PP‐2A pharmacologically by treatment with okadaic acid also stimulated endothelial cell motility. Identification of mechanisms by which PP‐2A inhibition might stimulate endothelial cell motility focused on proteins of the focal adhesions. Inhibition of PP‐2A caused hyperphosphorylation of the paxillin serine residues and dephosphorylation of its tyrosine residues, dissolution of FAK/Src/paxillin complexes and decreased phosphorylation of the inhibitory Y529 residue of Src, suggesting increased Src activity. Inhibition of Src activity prevented the stimulation of PP‐2A‐inhibited cell motility. Our results suggest an interrelationship between tumor inhibition of PP‐2A, dissolution of focal adhesion complexes and stimulated motility of endothelial cells. © 2002 Wiley‐Liss, Inc.
SH2D1A expression in Burkitt lymphoma cells is restricted to EBV positive group I lines and is downregulated in parallel with immunoblastic transformation
Authors: Nagy Noémi , Maeda Akihiko , Bandobashi Kentaro , Kis Loránd L. , Nishikawa Jun , Trivedi Pankaj , Faggioni Alberto , Klein George , Klein Eva 
Published: September 2002

AbstractThe SH2 domain containing SH2D1A protein has been characterized in relation to the X‐linked lymphoproliferative disease (XLP), a primary immunodeficiency that leads to serious clinical conditions after Epstein‐Barr virus (EBV) infection. The SH2D1A gene is mutated in the majority of XLP patients. We previously detected SH2D1A in activated T and NK cells, but not in B lymphocytes. We have found SH2D1A protein in Burkitt lymphoma (BL) lines, but only in those that carried EBV and had a Group I (germinal center) phenotype. All the EBV‐carrying Group III (immunoblastic) and the EBV‐negative BL lines tested were SH2D1A‐negative. Motivated by these differences, we studied the impact of EBV and the cellular phenotype on SH2D1A expression. We approached the former question with BL sublines after both the loss of the virus and subsequent reinfection. We also tested original EBV‐negative BL lines carrying transfected EBV genes, such as EBNA1, EBNA2, EBNA6, EBER1, 2 and LMP1, respectively. In our experiments, no direct relationship could be seen between EBV and SH2D1A expression. We modified the phenotype of the Group I BL cells by LMP1 transfection or CD40 ligation. The phenotypic changes, indicated by expression of immunoblastic markers, e.g., SLAM, were accompanied by downregulation of SH2D1A. It seems, therefore, that the presence of EBV and the phenotype of the cell together regulate SH2D1A expression in the BL cells. It is possible that SH2D1A is expressed in a narrow window of B cell development represented by germinal center cells. © 2002 Wiley‐Liss, Inc.