bluuebunny/crossref_metadata_2025_split huggingface dataset:
Regulation of intercellular adhesion molecule‐1 expression by retinoic acid: Analysis of the 5′ regulatory region of the gene
Authors: Aoudjit Fawzi , Bosse Marc , Stratowa Christian , Voraberger Günter , Audette Marie 
Published: February 2007

AbstractHuman intercellular adhesion molecule‐1 (ICAM‐1), a specific ligand for the lymphocyte‐function‐associated antigen‐1, plays an important role in immune responses. ICAM‐I expression is regulated by various proinflammatory cytokines, by PMA, and by retinoic acid. In this study, we have investigated the mechanisms of transcriptional control involved in the stimulation of ICAM‐I gene expression by retinoic acid in SK‐N‐SH cells. Northern‐blot analysis demonstrated that ICAM‐I mRNA is maximally induced at 24 hr, suggesting that it is not an early‐response gene with respect to retinoic‐acid responsiveness, whereas the retinoic acid receptorβ mRNA level was maximal 12 hr following retinoic acid treatment. To analyze the 5′‐regulatory region of the ICAM‐I gene, an EcoRI/Sall fragment spanning the first 1.3 kb upstream of the translational start site was used to direct the expression of a linked luciferase reporter gene in transient transaction assays in SK‐N‐SH cells. A 24‐hr treatment of transfected cells with 10μ retinoic acid resulted in a 10‐ to 13‐fold increase in luciferase activity compared with untreated cells. Deletion mutant analysis revealed that a region located between ‐393 and ‐ 176 bp from the translational start site is critical for retinoic acid stimulation of luciferase activity. This region harbors a consensus sequence for a retinoic‐acid‐responsive element (RARE) homologous to the element found upstream of the alcohol dehydrogenase‐3 gene. Co‐transfection of expression vectors encoding the retinoic acid receptor‐α, ‐β, or ‐γ, with reporter plasmids harboring the putative RARE, confirmed that the ICAM‐I gene is regulated by retinoic acid in a retinoic acid receptor‐dependent fashion.
The PRAD‐1/cyclin D1 oncogene product accumulates aberrantly in a subset of colorectal carcinomas
Authors: Bartkova Jirina , Lukas Jiri , Strauss Michael , Bartek Jiri 
Published: February 2007

AbstractThe PRAD‐l/cyclin Dl proto‐oncogene is localized on chromosome 11 q 13 and it is overexpressed in several tumour types as a consequence of gene amplification or chromosomal rearrangements. In this study, the abundance and patterns of cyclin Dl protein expression in normal/non‐involved colon (n = 44), primary (n = 48) and metastatic (n = 9) colorectal carcinomas, and in a series of 4 colon cancer cell lines were investigated by immunochemical methods using the DCS‐6 monoclonal antibody specific for cyclin Dl. While examination of all normal colorectal tissue samples and 56% of the primary tumours revealed only weak to undetectable immunostaining signals, 23% of the primary carcinomas showed moderate and 21% showed strong aberrant accumulation of this cell‐cycle regulatory oncoprotein. The immunohistochemical patterns in the secondary lesions were concordant with the matched primary tumours in all cases. The staining was nuclear both in the clinical specimens and in the colon cancer cell lines, in which the antibody‐mediated knock‐out experiments demonstrated a positive regulatory role of the cyclin Dl protein whose function was required for progression through the G1 phase of the cell cycle. These results indicate that the PRAD‐l/cyclin Dl protooncogene may be deregulated in a significant subset of colorectal tumours, and warrant further analyses of such aberrations of the cyclin Dl/retinoblastoma protein pathway to elucidate its potential involvement in the multistep pathogenesis of human colorectal cancer.
Sulfonated aluminium phthalocyanines as sensitizers for photochemotherapy. Effects of small light doses on localization, dye fluorescence and photosensitivity in V79 cells
Authors: Moan Johan , Berg Kristian , Anholt Helle , Madslien Kari 
Published: February 2007

AbstractV79 cells incubated with di‐ or tetrasulfonated aluminium phthalocyanines (AIPcS2 or AIPcS4) showed a granular fluorescence pattern. Co‐staining with the lysosomotropic dye acridine orange (AO) indicated that the granules that were stained by these photoactive phthalocyanines were identical to lysosomes. Small light exposures made the lysosomes permeable to the dyes without inactivating the cells. Also, the lysosomal enzymes β‐AGA and cathepsin (L + B) were inactivated by small light exposures when AIPcS4 was present. Such small and almost nontoxic light exposures caused a redistribution of the dyes in the cells that was accompanied by a more than 10‐fold increase in the fluorescence quantum yields of the dyes. Surprisingly, this redistribution and increase in fluorescence did not result in any significant increase in the photosensitivity of the cells.
Fermented dairy products, dietary calcium and colon cancer: A case‐control study in the netherlands
Authors: Kampman Ellen , Van't Veer Pieter , Hiddink Gert Jan , Van Aken‐Schneijder Petra , Kok Frans J. , Hermus Rudolph J. J. 
Published: February 2007

AbstractTo examine whether the consumption of fermented dairy products or the dietary intake of calcium decreases colon cancer risk, a case‐control study was conducted in The Netherlands. Dietary patterns were assessed in detail (for cases before diagnosis or symptoms occurred) using a structured dietary history questionnaire. After adjustment for potential confounding variables, consumption of fermented dairy products, hard cheese and unfermented dairy products was not significantly associated with risk of colon cancer: an odds ratio (OR) of I. I was found for individuals consuming more than one serving of fermented dairy products per day as compared to those consuming less than 10% of one serving a day. Adjustment for dietary calcium attenuated the associations. Total dietary calcium was positively but non‐significantly associated with colon cancer risk after adjustment for age, gender, urbanization level and total energy intake. Additional adjustment for a positive family history of colorectal cancer, cholecystectomy and energy‐adjusted intake of total fat, dietary fibre, vitamin C and alcohol increased the association. No differences were observed between calcium from fermented and from unfermented dairy sources. The observed associations for fermented dairy products and dietary calcium differed between men and women: positive significant associations were observed in men, while in women non‐significant inverse associations were found. Our results do not support the hypothesis that an increased intake of commercially available, commonly used fermented dairy products or dietary calcium decreases the risk of colon cancer.
Production and response of human prostate cancer cell lines to granulocyte macrophage‐colony stimulating factor
Authors: Lang Shona H. , Miller William R. , Duncan William , Habib Fouad K. 
Published: February 2007

AbstractProstate cancer selectively metastasises to skeletal sites, where it normally produces osteoblastic lesions. This study investigated whether haematopoietic growth factors known to be present in the bone environment could be involved in the survival and proliferation of prostate skeletal metastases. To evaluate this hypothesis we investigated the effects of recombinant granulocyte/macrophage colony‐stimulating factor (rGMGSF), recombinant granulocyte colony‐stimulating factor (rGCSF), recombinant erythropoietin (rEPO) and recombinant interleukin‐3 (rIL‐3) on the growth of 3 human prostate cancer cell lines. Two hormone‐insensitive cell lines, PC‐3 and DUI45, were significantly stimulated by rGM‐CSF and rEPO in serumfree medium but their growth was unaffected by incubation with rIL‐3 or rG‐CSF. A hormone‐sensitive cell line, LNCaP, was stimulated only by rGM‐CSF.To investigate further the involvement of GM‐CSF in prostate cancer, the presence of GM‐CSF protein in the 3 prostate cancer cell lines was examined by immunohistochemistry, and analysis of cell line conditioned media was carried out by ELISA and Western blotting. These techniques demonstrated that GM‐CSF‐like material was produced by both DUI45 and PC‐3 cells but not by LNCaP. The results from ELISA found that media conditioned by DUI45 and PC‐3 cells contained 1.7 and 2.5 pg GM‐CSF/μg protein, respectively, whereas no GM‐CSF was detectable in the LNCaP conditioned media. Our results were also confirmed by Western blot analysis demonstrating one single band for DUI45 and PC‐3 conditioned media which co‐migrated along with the standard rGM‐CSF band. No bands were associated with the LNCaP conditioned media. The presence of GM‐CSF gene transcripts in DUI45 and PC‐3 cells was established by reverse transcription and polymerase chain reaction of total RNA.
H‐2Kb AND H‐2Db gene transfections in B16 melanoma differently affect non‐immunological properties relevant to the metastatic process. Involvement of integrin molecules
Authors: De Giovanni Carla , Nicoletti Giordano , Sensi Marialuisa , Santoni Angela , Palmieri Gabriella , Landuzzi Lorena , Nanni Patrizia , Lollini Pier‐Luigi 
Published: February 2007

AbstractModification of non‐immunological cell adhesion properties plays a major role in the decrease in metastatic ability observed after transfection of the H‐2Kb gene in H‐2‐negative BI6‐derived melanoma clone cells. To investigate the role played by different class‐l major histocompatibility complex (MHC) genes on non‐immunological properties relevant for metastasis, transfection with the H‐2Db gene alone or in conjunction with the H‐2Kb gene was performed. H‐2Db gene transfection did not modify either metastatic potential or non‐immunological cell adhesion properties. Double KbDb transfectants showed a decreased metastatic ability when compared to control clones and to Db transfectants; a decrease in homotypic adhesive ability was also observed, even though not in all clones studied: therefore expression of the Db gene is also relevant. The mechanisms of homotypic cell adhesion were studied and found to be dependent upon temperature and divalent cations. Adhesion was partially inhibited by an antiserum directed against the β1 integrin subunit, whereas anti‐αllbβ3 was ineffective. Cell pre‐treatment with anti‐β1 serum reduced metastatic ability. A decreased expression of α4 and α6 integrin subunits was observed in Kb clones, whereas no difference in the levels of some homophilic cell adhesion molecules, such as N‐CAM and αllbβ3, was found. Adhesion required the activity of tyrosine kinases, as suggested by the decreased adhesive properties and impaired metastatic ability of cells pre‐treated with the tyrosine‐kinaseinhibitor genistein. These results are compatible with involvement of integrin molecules of the β1 family in the adhesive ability of these cells. Our data show that: (a) immunological and non‐immunological effects of MHC transfection are correlated and depend on the class‐l gene used, suggesting that MHC gene therapy can be highly successful only if appropriate MHC genes are transfected; (b) non‐immunological cell‐adhesion properties modified after MHC transfection could be related to an impairment of integrin‐mediated adhesive interactions.
Resistance to verapamil sensitization of multidrug‐resistant cells grown as multicellular spheroids
Authors: Sakata Koh‐Ichi , Kwok Tim T. , Gordon G. Ross , Waleh Nahid S. , Sutherland Robert M. 
Published: February 2007

AbstractThe ability of verapamil to overcome resistance to adriamycin in a multidrug‐resistant derivative of the V79 cell line (LZ), grown as multicellular spheroids or as monolayers, was examined. Verapamil was much less effective in overcoming resistance to adriamycin in spheroids than in monolayers. Verapamil increased the adriamycin content of cells grown as monolayers, but had no significant effect on the drug content of spheroids. This occurred in spite of the same mdr‐I mRNA and protein levels in monolayers and spheroids. When the surviving fraction of cells was normalized to the cellular adriamycin content, cells both in monolayers and spheroids treated with verapamil were still more sensitive to adriamycin than their counterparts not treated with verapamil. The observed resistance of spheroids to adriamycin and verapamil sensitization may be caused by a drug‐resistance mechanism that is functional only in spheroids, in addition to the activity of P‐glycoprotein. Multicellular tissue architecture and cell‐cell contact may play significant roles in this type of multidrug‐resistance mechanism.
Neuroblastoma cell apoptosis induced by the synthetic retinoid N‐(4‐hydroxyphenyl)retinamide
Authors: Di Vinci Angela , Geido Elio , Infusini Edmondo , Giaretti Walter 
Published: February 2007

AbstractN‐(4‐hydroxyphenyl)retinamide (HPR) is a synthetic retinoid with anti‐cancer properties and lower toxicity than all‐trans retinoic acid (RA). Neuroblastoma cells treated with HPR and observed by fluorescence microscopy showed clear signs of apoptosis, such as chromatin condensation and margination, nuclear fragmentation and the presence of “apoptotic bodies”. Moreover, measurements on a cell‐by‐cell basis by the flowcytometric DNA‐content in situ‐terminal‐deoxinucleotidyltransferase(TDT) assay showed that apoptosis induced by HPR was dose‐ and time‐dependent and that the fraction of apoptotic cells increased from approximately 15% at 1.25 μM at 2 days after treatment up to approximately 90% at 5 μM and 8 days of continuous treatment. Additionally, we found that cells were induced into apoptosis independently from the cell‐cycle phase. In contrast, equimolar or higher doses of RA, from 5 μM to 80 μM, were able to inhibit growth by differentiation, but failed to induce apoptosis. We conclude that the functional effects of HPR and RA in LA‐N‐5 neuroblastoma cells are mediated by apoptosis and differentiation respectively, suggesting a potential clinical use of HPR in the management of neuroblastoma patients. © 1994 Wiley‐Liss, Inc.
The fibronectin isoform containing the ed‐b oncofetal domain: A marker of angiogenesis
Authors: Castellani Patrizia , Viale Giuseppe , Dorcaratto Alessandra , Nicolo Guido , Kaczmarek Janusz , Querze Germano , Zardi Luciano 
Published: February 2007

AbstractDifferent fibronectin (FN) isoforms are generated by the alternative splicing of 3 regions (ED‐A, ED‐B and IIICS) of the primary transcript. The FN isoform containing the ED‐B sequence, a complete type‐III‐homology repeat, while having extremely restricted distribution in normal adult tissues, reveals high expression in fetal and tumor tissues. Using the monoclonal antibody (MAb) BC‐1, specific for the FN isoform containing the ED‐B sequence (B+·FN), we demonstrate here, using immunohistochemical techniques, that while this FN isoform is undetectable in mature vessels, it is highly expressed during angiogenesis both in neoplastic and in normal tissues, as in the case of the functional layer of endometrium during the proliferative phase. B+·FN is thus a marker for the formation of new vessels, and the BC‐I MAb may be a useful reagent for evaluating the level of the angiogenetic process in different neoplasms.
Protracted treatment with phorbol ester modulates j‐7 human hepatoma‐cell‐induced aggregation and coagulation of human platelet‐rich plasma
Authors: Ko Feng N. , Yu Sheu M. , Teng Che M. 
Published: February 2007

AbstractIn heparinized human platelet‐rich plasma (PRP), J‐7 human hepatoma cells initially induced platelet aggregation; then a clot formed. ADP‐scavenger systems, apyrase and creatine phosphate/creatine phosphokinase did not inhibit this tumor‐cell‐induced platelet aggregation (TCIPA), whereas hirudin and concanavalin A completely blocked it. J‐7 cells also shortened the recalcification time of normal and of Factor‐VIII‐ and ‐IX‐deficient human plasma, although it was inactive in shortening the recalcification time of Factor‐VII‐deficient plasma. After treatment with phorbol 12,13‐dibutyrate (PDBu) for 5 to 90 min, the aggregation and coagulation abilities of J‐7 cells were unaffected. Prolonged treatment of J‐7 cells with PDBu but not with α‐PDBu for 24 and 72 hr resulted in gradual loss of aggregation and coagulation. Staurosporine antagonized the effect of PDBu and restored aggregation and coagulation in J‐7 cells. Protracted treatment with PDBu (24 or 72 hr) did not affect adherence of J‐7 cells to the extracellular‐matrix proteins (i.e., fibrinogen, fibronectin, laminin, vitronectin and collagen types I and IV) or to the surface of plastic culture dishes. The treatment also did not affect J‐7 cell detachment from plastic culture dishes. These in vitro results demonstrate that protracted phorbol ester treatment diminishes TCIPA and blood coagulation of tumor cells.
Role of mature leukemic cells in the amplification of leukemic stem cells in a murine model
Authors: Dührsen Ulrich , Knieling Gabriele , Hossfeld Dieter Kurt 
Published: February 2007

AbstractThe recently described PGM‐2 leukemia displays a hierarchical structure with bipotential stem cells, B‐lymphocyte and macrophage progenitor cells, and post‐mitotic end cells. Because the different cell types can easily be identified in vitro by clonal culture assays and simple staining procedures, this leukemia is a useful model for the study of the interactions between different cell compartments in a leukemic clone. Our analysis of the impact of mature leukemic macrophages on the proliferation of stem cells was facilitated by the establishment of long‐term cultures producing new stem cells over prolonged periods of time. A prerequisite was the development of an adherent layer of fibroblasts and leukemic macrophages. Enumeration of adherent cells revealed a good correlation between the number of macrophages and the number of stem cells generated, and expansion of the macrophage population by treatment with interieukin 3 (IL‐3) resulted in a significant improvement of the culture conditions. Leukemic macrophages were also able to induce the formation of stem‐cell colonies in agar culture, suggesting a role for humoral mediators. Antibody neutralization experiments and bioassays identified IL‐7 and IL‐6 as factors cooperating in the stimulation of stem‐cell self‐renewal. Feed‐back stimulation of leukemic stem cells by mature leukemic cells may also be relevant to human leukemias and have implications for differentiation therapy.
Nucleotide sequence analysis of a full‐length human T‐cell leukemia virus type I from adult T‐cell leukemia cells: A prematurely terminated PX open reading frame II
Authors: S.Chou Kuan , Okayama Akihiko , Tachibana Nobuyoshi , Lee Tun‐Hou , Essex Max 
Published: February 2007

AbstractHuman T‐cell leukemia virus type 1 (HTLV‐I) is etiologically associated with adult T‐cell leukemia/lymphoma (ATL). The prototypic HTLV‐I, ATK, is the only full‐length provirus cloned from uncultured leukemic cells and completely sequenced prior to this study. We have determined the complete nucleotide sequence of another full‐length HTLV‐I provirus cloned directly from leukemic cells. A premature termination codon was found in the second open reading frame (orf II) of the pX region. Our finding indicates that open reading frame II of the HTLV‐I pX region is not required for outgrowth of ATL leukemic clones in vivo.
Modulation of intraepithelial expansion of human T24 bladder‐carcinoma cells in murine urothelium by growth factors and extracellular‐matrix components
Authors: Rebel Johanna M. J. , Thijssen Cornelia D. E. M. , Vermey Marcel , Zwarthoff Ellen C. , Van Der Kwast Theodorus H. 
Published: February 2007

AbstractThe high recurrence rate of bladder cancer is probably due to an efficient repopulation of the bladder by residual transformed cells after resection of the tumour. However, the regenerating capacity of the normal urothelial cells is very high. To study the balance between regenerating normal urothelium and outgrowth of transformed urothelial cells, we recently developed an in vitro co‐cultivation model. With this model system we studied the effects of growth factors and extracellular‐matrix components on the intra‐epithelial expansion of human T24 bladder‐carcinoma cells in primary mouse‐bladder explants. Exposure of the cultures to acidic fibroblast growth factor (aFGF) and laminin led to a dramatic increase in the number of invasive T24 cells into the primary urothelium. Epidermal growth factor (EGF) and collagen types I and IV counteracted the infiltration of individual T24 cells. EGF, aFGF, laminin and collagen types I and IV did not directly affect the migration and proliferation of T24 cells. Apparently, the efficacy of invasion of transformed urothelial cells into primary urothelium is not only dependent on the intrinsic characteristics of the transformed cells, but can be influenced to a considerable extent by exogenous components exerting their influence on the normal urothelium. The clinical relevance of this observation needs to be studied further.
Targeted inhibition of tumor‐cell growth by recombinant heregulin‐toxin fusion proteins
Authors: Jeschke Margit , Wels Winfried , Dengler Wolfgang , Imber Roland , Stöcklin Elisabeth , Groner Bernd 
Published: February 2007

AbstractFusion of functional domains of proteins by in vitro recombination of gene fragments can be used to generate novel anti‐tumor agents. The combination of tumor‐cell‐recognition functions and toxic functions results in cytotoxic molecules with a high specificity for tumor cells. Human adenocarcinomas are frequently characterized by over‐expression of members of the epidermal‐growth‐factor (EGF) receptor family (ErbB‐1, 2, 3 and 4), when compared with normal cells. These tumors are particularly suited to treatment with recombinant toxins. The human heregulins (HRG) and their rat counterparts (neu differentiation factor, NDF) have been identified as ligands for these receptors. Two chimeric heregulin‐toxin fusions consisting of the EGF‐like receptor recognition domain of the heregulin isoforms HRGα and HRGβ1, and the domains II, lb and III of the Pseudomonas exotoxin A (ETA) were constructed. HRGβ1‐ETA is highly cytotoxic for the mammary carcinoma cell lines SK‐BR‐3 and MDA‐MB‐453. HRGα‐ETA was less active than HRGβ1‐ETA. The killing activity of the recombinant toxins correlated with the expression levels of ErbB‐3 and/or ErbB‐4 in the cell lines studied. High expression of ErbB‐2 is not sufficient to confer sensitivity towards the HRG‐ETA. Treatment of mice with 0.4 mg/kg/day of HRGβ1‐ETA caused growth retardation of transplanted human breast tumor cells. Higher levels of HRGβ1‐ETA administration resulted in acute hemorrhagic necrosis of the liver.