bluuebunny/crossref_metadata_2025_split huggingface dataset:
Altered deposition of basement‐membrane molecules in co‐cultures of colonic cancer cells and fibroblasts
Authors: Bouziges Françoise , Simo Pauline , Simon‐Assmann Patricia , Haffen Katy , Kedinger Michèle 
Published: July 2010

AbstractTwo human colon carcinoma cell lines, HT29 and Caco‐2 were co‐cultured with fetal rat or human skin fibroblasts. Their morphological features, ultra‐structural characteristics at the heterologous cell interface, and the deposition of basement‐membrane molecules [laminin, type‐IV collagen, heparan sulfate proteoglycan (HSPG)] at the epithelialstromal junction were analyzed. The 2 cell lines behaved differently. HT29 cells did not spread on the fibroblasts and grew as clusters, while Caco‐2 cells formed a monoiayer over the fibroblastic feeder layer. Only the latter carcinoma cells exhibited cytoplasmic processes towards the fibroblasts and, after 5 days in co‐cultures, a structured basement membrane (BM). The immunocytochemicai analysis of the BM constituents revealed the absence of the molecules studied at the sites of heterologous contacts in the case of HT29 cells. In contrast, in the co‐cultures comprising Caco‐2 cells, laminin and type‐IV collagen were progressively deposited in a polar fashion at the epithelial‐fibroblastic interface which, however, remained devoid of HSPG molecules. Together with earlier data indicating a dual origin of the BM molecules located at the epithelial‐fibroblastic interface in normal intestine, the present study shows that the cancer cells as well as the fibroblastic ones under the influence of carcinoma cells display an altered capacity to synthesize and/or secrete BM molecules. The extent of such abnormalities correlates with the differentiation of the cells. Finally, these modifications occur concomitantly with alterations in cell interactions which vary among cell lines.
Ultrastructural evidence of the mechanisms responsible for interleukin‐4‐activated rejection of a spontaneous murine adenocarcinoma
Authors: Modesti Andrea , D'Orazi Gabriella , Masuelli Laura , Modica Alessandro , Scarpa Susanna , Bosco Maria Carla , Forni Guido 
Published: July 2010

AbstractThe ultrastructural pattern of the anti‐tumor response elicited by interleukin‐4 (IL‐4) was investigated by using a spontaneous mammary adenocarcinoma (TS/A) unable to elicit protective immunity in syngeneic BALB/c mice as suggested by a variety of preimmunization‐challenge experiments. A subcutaneous lethal challenge of TS/A tumor cells was inhibited in a significant number of BALB/c mice receiving recombinant murine IL‐4 injected daily for 10 days around the tumor‐draining lymph node. Tumor rejection was mainly the result of direct membrane and cytoplasmic damage to tumor cells by eosinophils, neutrophils and macrophages that deeply penetrated the proliferating tumor mass. Lymphocytes and fibroblasts participated in the reaction by interacting with tumor cells, granulocytes and each other. The most frequent cell interactions in the peri‐ and intra‐tumoral areas and in the tumor‐draining lymph nodes are illustrated. The efficiency with which the IL‐4‐activated reaction leads to tumor inhibition and induction of a T‐lymphocyte‐dependent tumor‐specific immune memory appears to depend on interactions between distinct leukocytes.
The permissive role of oxygen‐derived free radicals in the development of colonic cancer in the rat. A new theory for carcinogenesis
Authors: Salim Aws S. 
Published: July 2010

AbstractThe colonic carcinogen I,Z‐dimethylhydmzine (DMH) was given to male rats at 10 weeks of age in the form of weekly S.C. injections for 28 weeks. The results obtained show that the incidence of colonic cancer is directly dependent on dietary fat intake and that carcinogens which produce colonic cancer in the presence of a high‐fat diet are rendered harmless when a low‐fat diet is consumed. These results suggest that dietary fat is permissive for colonic carcinogenesis. Administration of the radical scavengers allopurinol and dimethyl sulfoxide afforded dose‐dependent protection against this permissive role.
Trends in cancer mortality in the USSR, 1965–1990
Authors: La Vecchia Carlo , Levi Fabio , Lucchini Franca , Negri Eva , Boyle Peter 
Published: July 2010

AbstractTrends in age‐specific and age‐standardized mortality from 10 major cancer sites and total cancer mortality in the USSR were analyzed for the period 1965–1990, on the basis of the World Health Organization mortality database. Gastric cancer mortality declined substantially. Still, these rates were among the highest registered in the world, and in 1990 stomach cancer accounted for over 85, 000 deaths, being the second cause of cancer death (and the first one until 1980); further, there was some indication of a levelling of the declines in gastric‐cancer rates for both sexes over most recent calendar years. Likewise, uterine‐cancer mortality declined between 1965 and 1985, but there was no further decline over the last 5 years. Upward trends were registered for cancers of the intestine, of the breast and of the prostate. Mortality from these neoplasms, however, was still comparatively low by worldwide standards. Leukaemia rates were stable in both sexes. Substantial rises were observed for cancers of the oral cavity and pharynx, larynx and, chiefly, lung. Even more unfavourable was lung‐cancer mortality in young and middle‐aged males, since the truncated rate of 121/100, 000 in 1990 was higher than the values reached by countries like England and Wales or Finland even at the top of their epidemic in the 1960s, and trends in the USSR were still upwards. Thus, total cancer mortality was 176/100, 000 males in 1965, declined to 170 in 1970, but increased thereafter, particularly over the last decade, to reach 203/100, 000, i.e., one of the highest rates on a worldwide scale. Among females, the overall cancer mortality rate declined between 1965 and 1975, but rose thereafter to a value intermediate on a worldwide scale. These recent unfavourable trends of cancer mortality in the USSR indicate that, in the absence of adequate intervention, particularly on the tobacco‐related cancer epidemic, overall cancer mortality will continue to rise in the foreseeable future. © 1994 Wiley‐Liss, Inc.
p21‐ras‐peptide‐specific T‐cell responses in a patient with colorectal cancer. CD4+ and CD8+ T cells recognize a peptide corresponding to a common mutation (13Gly → Asp)
Authors: Fossum Beate , Gedde‐Dahl Tobias , Breivik Jarle , Eriksen Jon Amund , Spurkland Anne , Thorsby Erik , Gaudernack Gustav 
Published: July 2010

AbstractPeptides derived from mutated ras are immunogenic in mice and humans, and represent a group of specific tumor antigens that are potential targets for immunotherapy. T‐cell responses against mutant p21 ras can be initiated in vitro by repeated stimulation of peripheral‐blood mononuclear cells with mutant ras‐derived peptides. Patients with tumors commonly harbouring ras mutations may therefore show evidence of in vivo reactivity against such mutations. Peripheral‐blood mononuclear cells from 10 patients with colorectal adenocarcinoma were screened for reactivity against synthetic ras‐derived peptides corresponding to the most commonly found mutations in this type of cancer. In one patient, T‐cell reactivity against the 1–25, 13Gly → Asp peptide was detected. From this patient, both CD4+ and CD8+ T‐cell clones specific for the 1–25, 13Gly → Asp mutation could be raised. We were not, however, able to detect the corresponding mutation in the cancer. The 13Gly → Asp mutation in the ras oncogene is frequent and constitutes 9 to 27% of all K ras mutations found in biopsies from patients with colorectal carcinomas. Our study demonstrates a mutant ras‐specific T‐cell response of both the CD4+ and the CD8+ phenotype in a cancer patient. We speculate that in this patient a specific T‐cell response resulted in eradication of tumor cells harboring the 13Gly → Asp mutation. © 1994 Wiley‐Liss, Inc.
Inhibition of adsorption of human T‐cell‐leukemia virus type 1 by a plant lectin, wheat‐germ agglutinin
Authors: Yang Da‐wei , Haraguchi Yuji , Iwai Hideaki , Handa Atsushi , Shimizu Nobuaki , Hoshino Hiroo 
Published: July 2010

AbstractThirty‐six lectins that recognize various sugar chains were examined for inhibitory activities against infection with human T‐cell leukemia virus type I (HTLV‐I). Wheat‐germ agglutinin (WGA) was the most inhibitory among them: plating of the pseudotype of vesicular‐stomatitis virus (VSV) bearing envelope antigens of HTLV‐I was markedly inhibited by treatment of indicator cells with WGA just before adsorption, but not by treatment after virus adsorption. Treatment with WGA before adsorption, however, could not inhibit the plating of VSV, VSV pseudotypes of bovine leukemia virus, Moloney murine leukemia virus and human immunodeficiency virus type I. Syncytium formation induced by HTLV‐I was also inhibited by WGA upon co‐cultivation of U‐251 MG human glioma cells or MOLT‐4 human T‐cells with HTLV‐l‐producing C9I /PL cells. Formation of proviral DNA detected one day after infection was also inhibited when indicator cells had been treated with WGA before adsorption of HTLV‐I, but not after its adsorption. These findings indicated that WGA specifically inhibits plating of HTLV‐I when added to culture just before adsorption and suggested that a substance(s) containing sugar chains recognized by WGA might be involved in an adsorption step of HTLV‐I.
PEG‐based Polyplex Design for Gene and Nucleotide Delivery
Authors: Vachutinsky Yelena , Kataoka Kazunori 
Published: July 2010

AbstractGene delivery is a multiple‐step process which depends on the ability of a gene carrier to overcome several biological barriers and safely deliver a transgene to its target cells. Polymeric gene delivery systems, e. g., polyplexes, have emerged as a safe alternative to viral vectors. Poly(ethylene glycol) (PEG) conjugation is a common modification approach to provide polyplexes with prolonged circulation time and reduced toxicity, and to allow their accumulation in tumor tissue through the enhanced permeability and retention (EPR) effect. This review describes physicochemical properties related to the biological activity of PEG‐based polyplexes, and approaches undertaken to promote a rational design for their in vivo applications.
Adhesion and proliferation of human fibroblasts on sol‐gel coated titania
Authors: Meretoja V. V. , Rossi S. , Peltola T. , Pelliniemi L. J. , Närhi T. O. 
Published: July 2010

AbstractThe objective of this study was to evaluate growth and attachment of human gingival fibroblasts on nonresorbable sol‐gel‐derived nanoporous titania (TiO2) coated discs and noncoated commercially pure titania (cpTi) discs in vitro. The strength of attachment was evaluated using serial trypsinization. The number of cells detached from TiO2‐substrates was 30% ± 3%, whereas those detached from the cpTi was 58% ± 4% indicating a stronger cell attachment on the coated surfaces. In scanning electron microscopy (SEM) images fewer cells, with more rounded shape, were seen with cpTi than with TiO2 after the detachment assay. Fibroblasts grew more efficiently on TiO2 than on cpTi substrates, showing significantly higher cell activities at all times. In transmission electron microscopy (TEM), a continuous layer of two to three cells thick covered the coated and noncoated discs after 7 days of culture. The plasma membrane of cells in contact with the coating was in close opposition and the cytoplasm was ultrastructurally similar to the cells grown on noncoated discs with well‐preserved organelles. In conclusion, we demonstrated that the sol‐gel‐derived TiO2 coatings can facilitate cell growth and attachment of human gingival fibroblasts on titanium in vitro. This in vitro study is in line with our previous in vivo observations of improved soft tissue attachment of TiO2 coatings in comparison with cpTi. © 2010 Wiley Periodicals, Inc. J Biomed Mater Res Part A, 2010.
Parathyroid hormone gene family in a cartilaginous fish, the elephant shark (Callorhinchus milii)
Authors: Liu Yang , Ibrahim Alexander S , Tay Boon-Hui , Richardson Samantha J , Bell Justin , Walker Terence I , Brenner Sydney , Venkatesh Byrappa , Danks Janine A 
Published: July 2010

Abstract
The development of bone was a major step in the evolution of vertebrates. A bony skeleton provided structural support and a calcium reservoir essential for the movement from an aquatic to a terrestrial environment. Cartilaginous fishes are the oldest living group of jawed vertebrates. In this study we have identified three members of the parathyroid hormone (Pth) gene family in a cartilaginous fish, the elephant shark (Callorhinchus milii). The three genes include two Pth genes, designated as Pth1 and Pth2, and a Pthrp gene. Phylogenetic analysis suggested that elephant shark Pth2 is an ancient gene whose orthologue is lost in bony vertebrates. The Pth1 and Pth2 genes have the same structure as the Pth gene in bony vertebrates, whereas the structure of the Pthrp gene is more complex in tetrapods compared with elephant shark. The three elephant shark genes showed distinct patterns of expression, with Pth2 being expressed only in the brain and spleen. This contrasts with localization of the corresponding proteins, which showed considerable overlap in their distribution. There were conserved sites of localization for Pthrp between elephant shark and mammals, including tissues such as kidney, skin, skeletal and cardiac muscle, pancreas, and cartilage. The elephant shark Pth1(1–34) and Pthrp(1–34) peptides were able to stimulate cAMP accumulation in mammalian UMR106.01 cells. However, Pth2(1–34) peptide did not show such PTH-like biologic activity. The presence of Pth and Pthrp genes in the elephant shark indicates that these genes played fundamental roles before their recruitment to bone development in bony jawed vertebrates. © 2010 American Society for Bone and Mineral Research.
Predicting the accuracy of protein–ligand docking on homology models
Authors: Bordogna Annalisa , Pandini Alessandro , Bonati Laura 
Published: July 2010

AbstractLigand–protein docking is increasingly used in Drug Discovery. The initial limitations imposed by a reduced availability of target protein structures have been overcome by the use of theoretical models, especially those derived by homology modeling techniques. While this greatly extended the use of docking simulations, it also introduced the need for general and robust criteria to estimate the reliability of docking results given the model quality. To this end, a large‐scale experiment was performed on a diverse set including experimental structures and homology models for a group of representative ligand–protein complexes. A wide spectrum of model quality was sampled using templates at different evolutionary distances and different strategies for target–template alignment and modeling. The obtained models were scored by a selection of the most used model quality indices. The binding geometries were generated using AutoDock, one of the most common docking programs. An important result of this study is that indeed quantitative and robust correlations exist between the accuracy of docking results and the model quality, especially in the binding site. Moreover, state‐of‐the‐art indices for model quality assessment are already an effective tool for an a priori prediction of the accuracy of docking experiments in the context of groups of proteins with conserved structural characteristics. © 2010 Wiley Periodicals, Inc. J Comput Chem, 2010
Epigenetic pre‐patterning and dynamics during initial stages of mammalian preimplantation development
Authors: Rasmussen Theodore P. , Corry Gareth N. 
Published: July 2010

AbstractMammals, like all multicellular organisms, develop from a single cell—the totipotent zygote. During preimplantation development and subsequent development in utero, over 200 distinct cell types are established and integrated into the organ systems and tissues of the developing organism. Much of the field of mammalian developmental biology is devoted to investigation of mechanisms that govern the formation of complete organs and tissues. In contrast to later development, which consumes the vast majority of time associated with development in utero, preimplantation development and germ layer specification occur rapidly. Yet knowledge is limited regarding the regulatory mechanisms that specify the transient, but pluripotent, cellular lineages that form during the initial stages of mammalian development. Gametogenesis and preimplantation development are marked by dramatic and pervasive epigenetic changes rooted in chromatin dynamics. The fundamental mechanisms that specify subsequent cellular lineages of the conceptus are only now becoming understood, and tend to rely relatively heavily upon broad epigenetic mechanisms in addition to master transcription factors. This review considers epigenetic regulation in the very earliest stages of preimplantation development. In addition, recent advances which indicate that some epigenetic coding is imposed during gametogenesis and maintained during preimplantation development are considered. J. Cell. Physiol. 225: 333–336, 2010. © 2010 Wiley‐Liss, Inc.
TGFβ1 induces IL‐6 and inhibits IL‐8 release in human bronchial epithelial cells: The role of Smad2/3
Authors: Ge Qi , Moir Lyn M. , Black Judith L. , Oliver Brian G. , Burgess Janette K. 
Published: July 2010

AbstractHuman bronchial epithelial (HBE) cells contribute to asthmatic airway inflammation by secreting cytokines, chemokines, and growth factors, including interleukin (IL)‐6, IL‐8 and transforming growth factor (TGF) β1, all of which are elevated in asthmatic airways. This study examines the signaling pathways leading to TGFβ1 induced IL‐6 and IL‐8 in primary HBE cells from asthmatic and non‐asthmatic volunteers. HBE cells were stimulated with TGFβ1 in the presence or absence of signaling inhibitors. IL‐6 and IL‐8 protein and mRNA were measured by ELISA and real‐time PCR respectively, and cell signaling kinases by Western blot. TGFβ1 increased IL‐6, but inhibited IL‐8 production in both asthmatic and non‐asthmatic cells; however, TGF induced significantly more IL‐6 in asthmatic cells. Inhibition of JNK MAP kinase partially reduced TGFβ1 induced IL‐6 in both cell groups. TGFβ1 induced Smad2 phosphorylation, and blockade of Smad2/3 prevented both the TGFβ1 modulated IL‐6 increase and the decrease in IL‐8 production in asthmatic and non‐asthmatic cells. Inhibition of Smad2/3 also increased basal IL‐8 release in asthmatic cells but not in non‐asthmatic cells. Using CHIP assays we demonstrated that activated Smad2 bound to the IL‐6, but not the IL‐8 promoter region. We conclude that the Smad2/3 pathway is the predominant TGFβ1 signaling pathway in HBE cells, and this is altered in asthmatic bronchial epithelial cells. Understanding the mechanism of aberrant pro‐inflammatory cytokine production in asthmatic airways will allow the development of alternative ways to control airway inflammation. J. Cell. Physiol. 225: 846–854, 2010. © 2010 Wiley‐Liss, Inc.
Agents that bind annexin A2 suppress ocular neovascularization
Authors: Lima e Silva Raquel , Shen Jikui , Gong Yuan Yuan , Seidel Christopher P. , Hackett Sean F. , Kesavan Kamala , Jacoby Douglas B. , Campochiaro Peter A. 
Published: July 2010

AbstractTM601 is a synthetic polypeptide with sequence derived from the venom of the scorpion Leiurus quinquestriatus that has anti‐neoplastic activity. It has recently been demonstrated to bind annexin A2 on cultured tumor and vascular endothelial cells and to suppress blood vessel growth on chick chorioallantoic membrane. In this study, we investigated the effects of TM601 in models of ocular neovascularization (NV). When administered by intraocular injection, intravenous injections, or periocular injections, TM601 significantly suppressed the development of choroidal NV at rupture sites in Bruch's membrane. Treatment of established choroidal NV with TM601 caused apoptosis of endothelial cells and regression of the NV. TM601 suppressed ischemia‐induced and vascular endothelial growth factor‐induced retinal NV and reduced excess vascular permeability induced by vascular endothelial growth factor. Immunostaining with an antibody directed against TM601 showed that after intraocular or periocular injection, TM601 selectively bound to choroidal or retinal NV and co‐localized with annexin A2, which is undetectable in normal retinal and choroidal vessels, but is upregulated in endothelial cells participating in choroidal or retinal NV. Intraocular injection of plasminogen or tissue plasminogen activator, which like TM601 bind to annexin A2, also suppressed retinal NV. This study supports the hypothesis that annexin A2 is an important target for treatment of neovascular diseases and suggests that TM601, through its interaction with annexin A2, causes suppression and regression of ocular NV and reduces vascular leakage and thus may provide a new treatment for blinding diseases such as neovascular age‐related macular degeneration and diabetic retinopathy. J. Cell. Physiol. 225: 855–864, 2010. © 2010 Wiley‐Liss, Inc.
Association of core‐binding factor β with the malignant phenotype of prostate and ovarian cancer cells
Authors: Davis J. Nathan , Rogers Donna , Adams Lisa , Yong Thomas , Jung Jette S. , Cheng Bing , Fennell Katie , Borazanci Erkut , Moustafa Yara W. , Sun Amanda , Shi Runhua , Glass Jonathan , Mathis J. Michael , Williams B. Jill , Meyers Shari 
Published: July 2010

AbstractCore binding factor (CBF) is a transcription factor complex that plays roles in development, stem‐cell homeostasis, and human disease. CBF is a heterodimer composed of one of three DNA‐binding RUNX proteins plus the non‐DNA‐binding protein, CBFβ. Recent studies have showed that the RUNX factors exhibit complex expression patterns in prostate, breast, and ovarian cancers, and CBF has been implicated in the control of cancer‐related genes. However, the biologic roles of CBF in solid tumors have not been fully elucidated. To test whether CBF is required for the malignant phenotype of various epithelial cancers, we used lentiviral delivery of CBFβ‐specific shRNA to significantly decrease CBFβ expression in two prostate cancer cell lines (PPC1 and PC‐3) and the SKOV‐3 ovarian cancer cell line. We found that knockdown of CBFβ significantly inhibited anchorage independent growth of each cell line. Further, CBFβ knockdown in PPC1 cells suppressed xenograft tumor growth compared to controls. Mice injected with SKOV‐3 ovarian cancer cells knocked‐down for CBFβ exhibited a survival time similar to control mice. However, human cells recovered from the ascites fluid of these mice showed CBFβ expression levels similar to those from mice injected with control SKOV‐3 cells, suggesting that CBFβ knockdown is incompatible with tumor cell growth. Gene expression profiling of CBFβ knockdown cells revealed significant changes in expression in genes involved in various developmental and cell signaling pathways. These data collectively suggest that CBFβ is required for malignancy in some human cancers. J. Cell. Physiol. 225: 875–887, 2010. © 2010 Wiley‐Liss, Inc.