bluuebunny/crossref_metadata_2025_split huggingface dataset:
Role of hepatocyte growth factor activator (HGF activator) in invasive growth of human glioblastoma cells in vivo
Authors: Uchinokura Shunro , Miyata Shiro , Fukushima Tsuyoshi , Itoh Hiroshi , Nakano Shinichi , Wakisaka Shinichiro , Kataoka Hiroaki 
Published: August 2005

AbstractHepatocyte growth factor/scatter factor (HGF/SF) is a multifunctional growth factor that is involved in invasive growth of tumor cells via its receptor MET, a protein product of c‐met proto‐oncogene. HGF activator (HGFA) is a serine proteinase responsible for the activation of proform of HGF/SF (proHGF/SF). In our study, we examined the effects of engineered expression of HGFA on 2 human glioblastoma cell lines (YKG‐1 and U251). Both cells expressed MET, while only YKG‐1 expressed endogenous proHGF/SF. Enhanced MET phosphorylation and increased migratory activity were induced by the expression of HGFA in YKG‐1 cells in vitro in the presence of thrombin, which is a known activator of proHGFA. In contrast, MET phosphorylation was consistently observed in U251 that lacked endogenous HGF/SF, suggesting ligand‐independent activation of MET in this cell line. Consequently, the expression of HGFA in U251 did not enhance the MET phosphorylation and following cellular response even with the thrombin treatment. However, addition of exogenous proHGF/SF resulted in enhanced migratory activity of HGFA‐expressing U251 cells in the presence of thrombin in vitro. The engineered HGFA expression resulted in significantly enhanced tumor growth with increased vascular density in vivo when YKG‐1 cells were implanted in nude mouse brain. This effect was not observed in U251 lacking endogenous proHGF/SF. These results indicate the possible existence of multiple mechanisms of MET activation in glioblastomas and that the activation system of proHGF/SF is important in progression of glioblastomas that express endogenous proHGF/SF and require ligand‐dependent MET activation. © 2005 Wiley‐Liss, Inc.
Ursodeoxycholic acid inhibits interleukin beta 1 and deoxycholic acid‐induced activation of NF‐κB and AP‐1 in human colon cancer cells
Authors: Shah Syed A. , Volkov Yuri , Arfin Qamrul , Abdel‐Latif Mohamed M. , Kelleher Dermot 
Published: August 2005

AbstractDeoxycholic acid (DCA) has been implicated in colorectal carcinogenesis in humans with effects on proliferation and apoptosis, mediated at least in part by activation of transcription factors nuclear factor kappa B (NF‐κB), activator protein 1 (AP‐1) and protein kinase C (PKC) enzymes. Ursodeoxycholic acid (UDCA) is reported to reduce the frequency of colonic carcinogenesis in ulcerative colitis patients. Hence, we postulated that it might differ from DCA in its regulation of these transcription factors. The aim of the study was to determine effects of DCA and UDCA on NF‐κB and AP‐1 activation and explore its relationship to PKC. Human colonic tumour cell lines HCT116 were treated with DCA, UDCA, alone or pretreated with UDCA followed by DCA or IL‐1β. In other experiments, cells were pretreated with PKC inhibitors and then stimulated with DCA and IL‐1β or PMA. Gel shift assays were performed on nuclear extracts of the cells for NF‐κB and AP‐1 analysis. Western blot analyses and immunofluorescence were performed for Rel A (p65) and IκB‐α levels on the treated cells. DCA increased NF‐κB and AP‐1 DNA binding. UDCA did not increase DNA binding of NF‐κB and AP‐1 and UDCA pretreatment inhibited DCA‐induced NF‐κB and AP‐1 DNA binding. PKC inhibitors blocked DCA‐induced NF‐κB and AP‐1 activation. These results were validated by Western blot analysis for RelA and IκB‐α. In conclusion, UDCA did not induce NF‐κB and AP‐1 DNA binding but also blocked DCA‐induced NF‐κB and AP‐1 activation. These findings suggest a possible mechanistic role for UDCA in blocking pathways thought to be involved in colon carcinogenesis. © 2005 Wiley‐Liss, Inc.
Conjugated linoleic acid inhibits peritoneal metastasis in human gastrointestinal cancer cells
Authors: Kuniyasu Hiroki , Yoshida Kazuhiro , Sasaki Takamitsu , Sasahira Tomonori , Fujii Kiyomu , Ohmori Hitoshi 
Published: August 2005

AbstractThe effect of conjugated linoleic acid (CLA) on peritoneal metastasis was examined by in vitro treatment of cancer cells and mouse peritoneal metastasis models. First, cell growth of MKN28 human gastric cancer cells and Colo320 human colon cancer cells was suppressed by CLA in a dose‐dependent manner with an increment in apoptosis. CLA significantly inhibited invasion into type IV collagen‐coated membrane of MKN28 and Colo320 cells (p < 0.05). CLA‐induced growth inhibition was recovered by the exposure to antisense S‐oligodeoxynucleotide for peroxisome proliferator‐activated receptor (PPAR)‐γ in both cell lines. BALB/c nu‐nu mice were inoculated with MKN28 and Colo320 cells into their peritoneal cavity, and administrated with CLA intraperitoneally (weekly, 4 times). CLA treatment did not affect food intake or weight gain of mice. CLA treatment significantly decreased metastatic foci of both cells in the peritoneal cavity (p < 0.005). Survival rate in mice inoculated with MKN28 or Colo320 cells was significantly recovered by CLA treatment (p = 0.0025 and 0.0052, respectively). Protein production in MKN28 and Colo320 cells treated with CLA showed a decrease in epidermal growth factor receptor and transforming growth factor‐α and an increase in Bax. These findings suggest that CLA inhibits metastasis of human gastric and colon cancer cells. © 2005 Wiley‐Liss, Inc.
Retracted: Curcumin (diferuloylmethane) inhibits constitutive active NF‐κB, leading to suppression of cell growth of human T‐cell leukemia virus type I‐infected T‐cell lines and primary adult T‐cell leukemia cells
Authors: Tomita Mariko , Kawakami Hirochika , Uchihara Jun‐nosuke , Okudaira Taeko , Masuda Masato , Takasu Nobuyuki , Matsuda Takehiro , Ohta Takao , Tanaka Yuetsu , Ohshiro Kazuiku , Mori Naoki 
Published: August 2005

AbstractRetraction: The following article has been retracted through agreement between the first author and several coauthors, the journal Editor‐in‐Chief, Peter Lichter, and John Wiley & Sons, Ltd.: Tomita M, Kawakami H, Uchihara JN, Okudaira T, Masuda M, Takasu N, Matsuda T, Ohta T, Tanaka Y, Ohshiro K, Mori N. (2006). Curcumin (diferuloylmethane) inhibits constitutive activeNF‐kappaB, leading to suppression of cell growth of human T‐cell leukemia virus type I‐infected T‐cell lines and primary adult T‐cell leukemia cells. Int J Cancer; 118 (February (3)): 765‐772, published online on 16 AUG 2005 in Wiley Online Library (www.onlinelibrary.wiley.com). After an investigation the retraction has been agreed due to inappropriate duplication of images and overlap with other published work
Distribution of Epstein‐Barr viral load in serum of individuals from nasopharyngeal carcinoma high‐risk families in Taiwan
Authors: Yang Xiaohong (Rose) , Goldstein Alisa M. , Chen Chien‐Jen , Rabkin Charles S. , Chen Jen‐Yang , Cheng Yu‐Juen , Hsu Wan‐Lun , Sun Brenda , Diehl Scott R. , Liu Mei‐Ying , Walters Michael , Shao Wen , Ortiz‐Conde Betty A. , Whitby Denise , Elmore Sandra H. , Gulley Margaret L. , Hildesheim Allan 
Published: August 2005

AbstractThe utility of EBV load as a tumor marker in nasopharyngeal carcinoma (NPC) patients suggests that it might also serve as a screening test for individuals who are at high risk for developing NPC. We previously demonstrated that unaffected individuals from high‐risk families had elevated anti‐EBV antibody levels compared to community controls. In this study, we measured EBV load using 2 different real‐time PCR assays (targeting BamH1W and polymerase gene sequences, respectively) carried out in 2 independent research labs in serum samples from 19 untreated NPC cases, 11 healthy community controls and 100 unaffected individuals from families in which 2 or more individuals were affected with NPC. EBV genomes were detectable in 68% of NPC cases by the EBV BamH1W assay and in 74% by the EBV polymerase assay (κ = 0.64). Patients with stage III or IV disease had significantly higher EBV load compared to those with stage I or II disease (p = 0.008). EBV DNA was detected in a single community control sample by the EBV BamH1W assay and in none of the samples by the EBV polymerase assay. Only one of 100 unaffected family members tested positive by both assays. An additional 14 were positive by only one of the 2 EBV load assays used and usually in only one of the duplicate wells tested, all with very low viral loads (3–50 copies/ml). In addition, EBV load did not correlate with EBV serology results (anti‐VCA, anti‐DNase, anti‐EBNA‐1) among these unaffected family members. In conclusion, our study suggests limited clinical utility of the EBV load test, in its current configuration, to screen individuals from high‐risk families. Should a more sensitive or specific molecular assay be developed that is capable of detecting and distinguishing tumor‐derived EBV genomes or gene products from true negatives, it could be evaluated as a possible screening tool for asymptomatic and early‐stage NPC. © 2005 Wiley‐Liss, Inc.
U‐2940, a human B‐cell line derived from a diffuse large cell lymphoma sequential to Hodgkin lymphoma
Authors: Sambade Clara , Berglund Mattias , Lagercrantz Svetlana , Sällström Jan , Reis Rui M. , Enblad Gunilla , Glimelius Bengt , Sundström Christer 
Published: August 2005

AbstractSeveral patterns of association between Hodgkin and non‐Hodgkin lymphomas are recognized, some of which support a common cellular origin or shared transformation events for both malignancies. We describe the U‐2940 cell line derived from a diffuse large B‐cell lymphoma with some features consistent with mediastinal large B‐cell lymphoma, clinically apparent 1 month after the initial course of chemotherapy for Hodgkin's disease, fulfilling the criteria for composite malignancies. U‐2940 cells display a mature B phenotype with hypermutated IgH rearrangement typical of germinal/postgerminal center origin. The cell line is negative for Epstein‐Barr virus and no evidence of t(14;18) was found. U‐2940 cells display multiple chromosomal rearrangements similar to recurrent aberrations described in both Hodgkin and non‐Hodgkin lymphomas, also partially shared by U‐2932 derived from a B‐cell lymphoma sequential to Hodgkin's disease. The original large B‐cell lymphoma and the U‐2940 cell line bear microsatellite instability, an abnormality associated with particular subtypes of non‐Hodgkin lymphomas and found in tissues involved by Hodgkin lymphoma. Therefore, U‐2940 cells bear several features known to occur in Hodgkin and in non‐Hodgkin lymphomas, leading to the assumption that this cell line may constitute a useful tool to address elective pathways of lymphomagenesis and eventually the Hodgkin and non‐Hodgkin lymphoma association. © 2005 Wiley‐Liss, Inc.
Macrophage migration and gene expression in response to tumor hypoxia
Authors: Murdoch Craig , Lewis Claire E. 
Published: August 2005

AbstractMonocytes are recruited into tumors from the circulation along defined chemotactic gradients and they then differentiate into tumor‐associated macrophages (TAMs). Recent evidence has shown that large numbers of TAMs are attracted to and retained in avascular and necrotic areas, where they are exposed to tumor hypoxia. At these sites, TAMs appear to undergo marked phenotypic changes with activation of hypoxia‐inducible transcription factors, dramatically upregulating the expression of a large number of genes encoding mitogenic, proangiogenic and prometastatic cytokines and enzymes. As a consequence, high TAMs density has been correlated with increased tumor growth and angiogenesis in various tumor types. Since hypoxia is a hallmark feature of malignant tumors and hypoxic tumor cells are relatively resistant to radio‐ and chemotherapy, these areas have become a target for novel forms of anticancer therapy. These include hypoxia‐targeted gene therapy in which macrophages are armed with therapeutic genes that are activated by hypoxia‐responsive promoter elements. This restricts transgene expression to hypoxic areas, where the gene product is then released and acts on neighboring hypoxic tumor cells or proliferating blood vessels. In this way, the responses of macrophages to tumor hypoxia can be exploited to deliver potent antitumor agents to these poorly vascularized, and thus largely inaccessible, areas of tumors. © 2005 Wiley‐Liss, Inc.
Spectrum of cancers among HIV‐infected persons in Africa: The Uganda AIDS‐Cancer Registry Match Study
Authors: Mbulaiteye Sam M. , Katabira Elly T. , Wabinga Henry , Parkin Donald M. , Virgo Phillip , Ochai Robert , Workneh Meklit , Coutinho Alex , Engels Eric A. 
Published: August 2005

AbstractAlthough more than 25 million people in sub‐Saharan Africa have human immunodeficiency virus (HIV) infection, little is known regarding their cancer risk. We investigated cancer risk among persons with HIV/AIDS in Uganda using record‐linkage. We linked records of 12,607 HIV‐infected persons attending The AIDS Support Organization (TASO) in Kyadondo County from October 1988 through December 2002 to the Kampala Cancer Registry. We calculated standardized incidence ratios (SIRs) to identify increased cancer risks in the early (4–27 months after TASO registration), late (28–60 months), or combined (4–60 months) incidence periods. We identified 378 cancers (181 prevalent, 197 incident) among TASO participants. Of incident cancers, 137 (70%) were AIDS‐defining cancers. Risk was increased in the early‐incident period, compared to the general population, for the AIDS‐defining cancers: Kaposi sarcoma (SIR 6.4, 95%CI 4.8–8.4), non‐Hodgkin lymphoma (6.7, 1.8–17), and cervical carcinoma (2.4, 1.1–4.4). These three cancers were also increased in the combined periods. Risks of five non‐AIDS‐defining cancers were increased in the combined periods: Hodgkin lymphoma (5.7, 1.2–17) and cancers of the conjunctiva (SIR 4.0; 1.5–8.7), kidney (16, 1.8–58), thyroid (5.7, 1.1–16), and uterus (5.5, 1.5–14). Cancers of the breast, nasopharynx, and lung were increased either in the early or late incident periods only. Among 407 children, seven cancers were observed, of which five were Kaposi sarcoma. The application of a record‐linkage design in Africa broadens the repertoire of epidemiological tools for studying HIV‐infected populations. We confirm the increased risks of AIDS‐defining cancers and report increased risks of a few non‐AIDS‐defining cancers. © 2005 Wiley‐Liss, Inc.
Vitamin antioxidants, lipid peroxidation and the systemic inflammatory response in patients with prostate cancer
Authors: Almushatat Ahmed S.K. , Talwar Dinesh , McArdle Peter A. , Williamson Cathy , Sattar Naveed , O'Reilly Denis St. J , Underwood Mark A. , McMillan Donald C. 
Published: August 2005

AbstractThe relationship between lipid soluble antioxidant vitamins, lipid peroxidation, disease stage and the systemic inflammatory response were examined in healthy subjects (n = 14), patients with benign prostate hyperplasia BPH (n = 20), localized (n = 40) and metastatic (n = 38) prostate cancer. Prostate cancer patients had higher concentrations of malondialdehyde (p < 0.05) and lower circulating concentrations of lutein (p < 0.05), lycopene (p < 0.001) and β‐carotene (p < 0.05). Patients with metastatic prostate cancer, when compared with patients having localized disease, had a higher Gleason score (p < 0.01) and had more hormonal treatment, but lower concentrations of PSA (p < 0.05), α‐tocopherol (p ≤ 0.05), retinol (p < 0.01), lutein (p < 0.05) and lycopene (p < 0.01). In the prostate cancer patients, PSA was correlated with the concentrations of the lipid peroxidation product, malondialdehyde (rs = 0.353, p = 0.002). C‐reactive protein was not correlated with the vitamin antioxidants nor malondialdehyde. In contrast, there was a negative correlation between malondialdehyde concentrations and both lutein (rs = −0.263, p = 0.020) and lycopene (rs = −0.269, p = 0.017). These results indicate that lower concentrations of carotenoids, in particular, lycopene reflect disease progression rather than the systemic inflammatory response in patients with prostate cancer. © 2005 Wiley‐Liss, Inc.
In vivo effects of RGD‐coated titanium implants inserted in two bone‐gap models
Authors: Elmengaard Brian , Bechtold Joan E. , Søballe Kjeld 
Published: August 2005

AbstractRGD (Arg‐Gly‐Asp) coating has been suggested to enhance implant fixation by facilitating the adhesion of osteogenic cells to implant surfaces. Orthopedic implants are unavoidably surrounded partly by gaps, and these regions represent a challenging environment for osseointegration. We examined the effects of cyclic RGD‐coated implants on tissue integration and implant fixation in two cancellous bone‐gap models. In canines, we inserted loaded RGD‐coated implants with 0.75‐mm gap (n = 8) and unloaded RGD‐coated implants with 1.5‐mm gap (n = 8) into the distal femur and proximal tibia, respectively. Control gap implants without RGD were inserted contralaterally. The titanium alloy (Ti‐6Al‐4V) implants were plasma sprayed and cylindrical. The observation period was 4 weeks and the fixation was evaluated by push‐out test and histomorphometry. Mechanical implant fixation was improved for RGD‐coated implants. Unloaded RGD‐coated implants showed a significant increase in bone whereas both loaded and unloaded implants showed a significant reduction in fibrous tissue anchorage. The results are encouraging, because RGD had an overall positive effect on the fixation of titanium implants in regions where gaps exist with the surrounding bone. RGD peptide coatings can potentially be used to enhance tissue integration in these challenging environments. © 2005 Wiley Periodicals, Inc. J Biomed Mater Res, 2005
Assimilating cell sheets and hybrid scaffolds for dermal tissue engineering
Authors: Ng Kee Woei , Tham Wanrong , Lim Thiam Chye , Werner Hutmacher Dietmar 
Published: August 2005

AbstractCell sheets can be used to produce neo‐tissue with mature extracellular matrix. However, extensive contraction of cell sheets remains a problem. We devised a technique to overcome this problem and applied it to tissue engineer a dermal construct. Human dermal fibroblasts were cultured with poly(lactic‐co‐glycolic acid)‐collagen meshes and collagen‐hyaluronic acid foams. Resulting cell sheets were folded over the scaffolds to form dermal constructs. Human keratinocytes were cultured on these dermal constructs to assess their ability to support bilayered skin regeneration. Dermal constructs produced with collagen‐hyaluronic acid foams showed minimal contraction, while those with poly(lactic‐co‐glycolic acid)‐collagen meshes curled up. Cell proliferation and metabolic activity profiles were characterized with PicoGreen® and AlamarBlue™ assays, respectively. Fluorescent labeling showed high cell viability and F‐actin expression within the constructs. Collagen deposition was detected by immunocytochemistry and electron microscopy. Transforming Growth Factor‐α and β1, Keratinocyte Growth Factor and Vascular Endothelial Growth Factor were produced at various stages of culture, measured by RT‐PCR and ELISA. These results indicated that assimilating cell sheets with mechanically stable scaffolds could produce viable dermal‐like constructs that do not contract. Repeated enzymatic treatment cycles for cell expansion is unnecessary, while the issue of poor cell seeding efficiency in scaffolds is eliminated. © 2005 Wiley Periodicals, Inc. J Biomed Mater Res, 2005
Interaction of human osteoblasts with bioinert and bioactive ceramic substrates
Authors: Rokusek Debra , Davitt Christine , Bandyopadhyay Amit , Bose Susmita , Hosick Howard L. 
Published: August 2005

AbstractThe objective of this study was to compare adhesion, replication, and differentiation of human osteoblasts (OPC1 cell line) on two different ceramic substrates: a bioinert alumina (A12O3), and a bioactive hydroxyapatite (HAp). Scanning electron microscopy (SEM) and confocal scanning microscopy were used to assess production and distribution of specific osteoblast proteins. Cells grew readily on HAp and alumina. On alumina and HAp, OPC1 cells produced distinctive cell‐to‐cell and cell‐to‐scaffold filopodia and microextensions. OPC1 cells proliferated faster on HAp than on alumina substrates. Adhesion was further assessed by observing production of the protein vinculin. On alumina, vinculin was detected throughout the cytoplasm, with some peripheral punctate regions. On HAp, OPC1 cells developed few punctate peripheral regions of vinculin; rather, the protein was strongly localized within the cytoplasm. Finally, we measured accumulation of the marker osteopontin (OPN). OPN was first detectable on day 5 and increased through day 11 of culture on alumina. OPC1 cells on HAp produced substantial amounts of OPN beginning at day 5, with apparent secretion from the cells by culture day 11. These results suggest that the function of osteoblasts is strongly affected by the properties of ceramic surfaces, and rapid attachment of osteoblasts may result in earlier differentiation on HAp than on alumina. © 2005 Wiley Periodicals, Inc. J Biomed Mater Res, 2005
Fibrillar assembly and stability of collagen coating on titanium for improved osteoblast responses
Authors: Kim Hae‐Won , Li Long‐Hao , Lee Eun‐Jung , Lee Su‐Hee , Kim Hyoun‐Ee 
Published: August 2005

AbstractCollagen, as a major constituent of human connective tissues, has been regarded as one of the most important biomaterials. As a coating moiety on Ti hard‐tissue implants, the collagen has recently attracted a great deal of attention. This article reports the effects of fibrillar assembly and crosslinking of collagen on its chemical stability and the subsequent osteoblastic responses. The fibrillar self‐assembly of collagen was carried out by incubating acid‐dissolved collagen in an ionic‐buffered medium at 37°C. The degree of assembly was varied with the incubation time and monitored by the turbidity change. The differently assembled collagen was coated on the Ti and crosslinked with a carbodiimide derivative. The partially assembled collagen contained fibrils with varying diameters as well as nonfibrillar aggregates. On the other hand, the fully assembled collagen showed the complete formation of fibrils with uniform diameters of ∼100–200 nm with periodic stain patterns within the fibrils, which are typical of native collagen fibers. Through this fibrillar assembly, the collagen coating had significantly improved chemical stability in both the saline and collagenase media. The subsequent crosslinking step also improved the stability of the collagen coating, particularly in the unassembled collagen. The fibrillar assembly and the crosslinking of collagen significantly influenced the osteoblastic cell responses. Without the assembly, the collagen layer on Ti adversely affected the cell attachment and proliferation. However, those cellular responses were improved significantly when the collagen was assembled to fibrils and the assembly degree was increased. After crosslinking the collagen coating, these cellular responses were significantly enhanced in the case of the unassembled collagen but were not altered much in the assembled collagen. Based on these observations, it is suggested that the fibrillar assembly and the crosslinking of collagen require careful considerations in the collagen administration as a coating moiety. © 2005 Wiley Periodicals, Inc. J Biomed Mater Res, 2005