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      1. Author :
        Welti, J. C.; Powles, T.; Foo, S.; Gourlaouen, M.; Preece, N.; Foster, J.; Frentzas, S.; Bird, D.; Sharpe, K.; van Weverwijk, A.; Robertson, D.; Soffe, J.; Erler, J. T.; Pili, R.; Springer, C. J.; Mather, S. J.; Reynolds, A. R.
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2012
      5. Publication :
        Angiogenesis
      6. Products :
      7. Volume :
        15
      8. Issue :
        N/A
      9. Page Numbers :
        623-41
      10. Research Area :
        N/A
      11. Keywords :
        4T1-luc2, 4T1, Bioware, IVIS
      12. Abstract :
        Sunitinib is a potent and clinically approved tyrosine kinase inhibitor that can suppress tumour growth by inhibiting angiogenesis. However, conflicting data exist regarding the effects of this drug on the growth of metastases in preclinical models. Here we use 4T1 and RENCA tumour cells, which both form lung metastases in Balb/c mice, to re-address the effects of sunitinib on the progression of metastatic disease in mice. We show that treatment of mice with sunitinib prior to intravenous injection of tumour cells can promote the seeding and growth of 4T1 lung metastases, but not RENCA lung metastases, showing that this effect is cell line dependent. However, increased metastasis occurred only upon administration of a very high sunitinib dose, but not when lower, clinically relevant doses were used. Mechanistically, high dose sunitinib led to a pericyte depletion effect in the lung vasculature that correlated with increased seeding of metastasis. By administering sunitinib to mice after intravenous injection of tumour cells, we demonstrate that while sunitinib does not inhibit the growth of 4T1 lung tumour nodules, it does block the growth of RENCA lung tumour nodules. This contrasting response was correlated with increased myeloid cell recruitment and persistent vascularisation in 4T1 tumours, whereas RENCA tumours recruited less myeloid cells and were more profoundly devascularised upon sunitinib treatment. Finally, we show that progression of 4T1 tumours in sunitinib treated mice results in increased hypoxia and increased glucose metabolism in these tumours and that this is associated with a poor outcome. Taken together, these data suggest that the effects of sunitinib on tumour progression are dose-dependent and tumour model-dependent. These findings have relevance for understanding how anti-angiogenic agents may influence disease progression when used in the adjuvant or metastatic setting in cancer patients.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/22843200
      14. Call Number :
        PKI @ kd.modi @ 10
      15. Serial :
        10504
      1. Author :
        Smith, Eric L; Schuchman, Edward H
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2008
      5. Publication :
        Molecular therapy: the journal of the American Society of Gene Therapy
      6. Products :
      7. Volume :
        16
      8. Issue :
        9
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        Animals; Antineoplastic Agents; Autophagy; B16-F10-luc-G5 cells; Bioware; Cell Survival; Cells, Cultured; Ceramides; Cesium Radioisotopes; CHO Cells; Combined Modality Therapy; Cricetinae; Cricetulus; Endothelium, Vascular; Female; Gamma Rays; Gene Expression Regulation, Enzymologic; Gene Therapy; Humans; Melanoma, Experimental; Mice; Sphingomyelin Phosphodiesterase
      12. Abstract :
        Exposure of cells or animals to stress frequently induces acid sphingomyelinase (ASM)-mediated ceramide production that leads to cell death. Consistent with this, overexpression of ASM in subcutaneous B16-F10 mouse melanomas, in combination with irradiation, resulted in tumors that were up to 12-fold smaller than irradiated control melanomas. Similarly, when irradiated melanomas were pretreated with a single, peritumoral injection of recombinant ASM (rhASM), the tumors were up to threefold smaller. The in vivo effect of ASM was likely due to enhanced cell death of the tumor cells themselves, as well as the surrounding microvascular endothelial cells. In vitro, rhASM had little or no effect on the growth of tumor cells, even in combination with irradiation. However, when the culture media was acidified to mimic the acidic microenvironment of solid tumors, rhASM-mediated cell death was markedly enhanced when combined with irradiation. Microscopic analysis suggested that this was associated with an increase in autophagy. rhASM has been produced for the treatment of the lysosomal storage disorder, type B Niemann-Pick disease, and is currently being evaluated in a phase-1 clinical trial. Based on the data presented in this article, we propose that further investigation of this protein and gene as antineoplastic agents also is warranted.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/18628757
      14. Call Number :
        PKI @ catherine.lautenschlager @
      15. Serial :
        8999
      1. Author :
        Burkatovskaya, Marina; Castano, Ana P; Demidova-Rice, Tatiana N; Tegos, George P; Hamblin, Michael R
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2008
      5. Publication :
        Wound repair and regeneration: official publication of the Wound Healing Society [and] the European Tissue Repair Society
      6. Products :
      7. Volume :
        16
      8. Issue :
        3
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        Animals; Anti-Infective Agents; Bandages; Biocompatible Materials; Bioware; Chitosan; Cyclophosphamide; Male; Mice; Mice, Inbred BALB C; Staphylococcal Skin Infections; Staphylococcus aureus; Wound Healing; Wound Infection; Xen8.1
      12. Abstract :
        HemCon bandage is an engineered chitosan acetate preparation designed as a hemostatic dressing, and is under investigation as a topical antimicrobial dressing. We studied its effects on healing of excisional wounds that were or were not infected with Staphylococcus aureus, in normal mice or mice previously pretreated with cyclophosphamide (CY). CY significantly suppressed wound healing in both the early and later stages, while S. aureus alone significantly stimulated wound healing in the early stages by preventing the initial wound expansion. CY plus S. aureus showed an advantage in early stages by preventing expansion, but a significant slowing of wound healing in later stages. In order to study the conflicting clamping and stimulating effects of chitosan acetate bandage on normal wounds, we removed the bandage from wounds at times after application ranging from 1 hour to 9 days. Three days application gave the earliest wound closure, and all application times gave a faster healing slope after removal compared with control wounds. Chitosan acetate bandage reduced the number of inflammatory cells in the wound at days 2 and 4, and had an overall beneficial effect on wound healing especially during the early period where its antimicrobial effect is most important.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/18471261
      14. Call Number :
        PKI @ catherine.lautenschlager @
      15. Serial :
        9986
      1. Author :
        J-C Tseng; T Granot; V DiGiacomo; B Levin; D Meruelo
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2010
      5. Publication :
        Cancer Gene Therapy
      6. Products :
      7. Volume :
        17
      8. Issue :
        N/A
      9. Page Numbers :
        N/A
      10. Research Area :
        Cancer
      11. Keywords :
        Sindbis virus; viral vector; vascular leakiness; molecular imaging; chemotherapy; cancer
      12. Abstract :
        Genetic instability of cancer cells generates resistance after initial responses to chemotherapeutic agents. Several oncolytic viruses have been designed to exploit specific signatures of cancer cells, such as important surface markers or pivotal signaling pathways for selective replication. It is less likely for cancer cells to develop resistance given that mutations in these cancer signatures would negatively impact tumor growth and survival. However, as oncolytic viral vectors are large particles, they suffer from inefficient extravasation from tumor blood vessels. Their ability to reach cancer cells is an important consideration in achieving specific oncolytic targeting and potential vector replication. Our previous studies indicated that the Sindbis viral vectors target tumor cells by the laminin receptor. Here, we present evidence that modulating tumor vascular leakiness, using VEGF and/or metronomic chemotherapy regimens, significantly enhances tumor vascular permeability and directly enhances oncolytic Sindbis vector targeting in tumor models. Because host-derived vascular endothelium cells are genetically stable and less likely to develop resistance to chemotherapeutics, a combined metronomic chemotherapeutics and oncolytic vector regimen should provide a new approach for cancer therapy. This mechanism could explain the synergistic treatment outcomes observed in clinical trials of combined therapies.
      13. URL :
        http://www.nature.com/cgt/journal/v17/n4/full/cgt200970a.html
      14. Call Number :
        PKI @ sarah.piper @
      15. Serial :
        4485
      1. Author :
        Zhang, H-Y; Man, J-H; Liang, B; Zhou, T; Wang, C-H; Li, T; Li, H-Y; Li, W-H; Jin, B-F; Zhang, P-J; Zhao, J; Pan, X; He, K; Gong, W-L; Zhang, X-M; Li, A-L
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2010
      5. Publication :
        Cancer gene therapy
      6. Products :
      7. Volume :
        17
      8. Issue :
        5
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        Animals; Apoptosis; B16-F10-luc-G5 cells; Bioware; Blotting, Western; Cell Line, Tumor; Escherichia coli; Female; Flow Cytometry; Gene Therapy; Genetic Vectors; Humans; Immunohistochemistry; Mice; Mice, Inbred BALB C; Mice, Nude; NCI-H460-luc2; Neoplasms; Polymerase Chain Reaction; Survival Rate; TNF-Related Apoptosis-Inducing Ligand
      12. Abstract :
        The tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) is a potent inducer of tumor cell apoptosis, but concerns of considerable liver toxicity limit its uses in human cancer therapy. Here, we show that i.v. injected Escherichia coli DH5alpha (E. coli DH5alpha) specifically replicates in solid tumors and metastases in live animals. E. coli DH5alpha does not enter tumor cells and suits for being the vector for soluble TRAIL (sTRAIL), which induces apoptosis by activating cell-surface death receptors. With the high 'tumor-targeting' nature, we demonstrate that intratumoral (i.t.) and intravenous injection of sTRAIL-expressing E. coli DH5alpha results in the tumor-targeted release of biologically active molecules, which leads to a dramatic reduction in the tumor growth rate and the prolonged survival of tumor-bearing mice. TRAIL delivery by E. coli DH5alpha did not cause any detectable toxicity to any organs, suggesting that E. coli DH5alpha-delivered sTRAIL protein therapy may provide a feasible and effective form of treatment for solid tumors.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/20075981
      14. Call Number :
        PKI @ catherine.lautenschlager @
      15. Serial :
        8944
      1. Author :
        Hickson, J; Ackler, S; Klaubert, D; Bouska, J; Ellis, P; Foster, K; Oleksijew, A; Rodriguez, L; Schlessinger, S; Wang, B; Frost, D
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2010
      5. Publication :
        Cell death and differentiation
      6. Products :
      7. Volume :
        17
      8. Issue :
        6
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        Animals; Antineoplastic Agents; Apoptosis; Bioware; Caspase 3; Cell Line, Tumor; Female; Firefly Luciferin; Humans; Luminescent Agents; MDA-MB-231-D3H2LN cells; Mice; Mice, SCID; SKOV3-luc-D3 cells; Molecular Imaging; Neoplasms; Oligopeptides; Taxoids
      12. Abstract :
        Apoptosis is a highly regulated process of programmed cell death essential for normal physiology. Dysregulation of apoptosis contributes to the development and progression of various diseases, including cancer, neurodegenerative disorders, and chronic heart failure. Quantitative noninvasive imaging of apoptosis in preclinical models would allow for dynamic longitudinal screening of compounds and facilitates a more rapid determination of therapeutic efficacy. In this study, we report the in vivo characterization of Z-DEVD-aminoluciferin, a modified firefly luciferase substrate that in apoptotic cells is cleaved by caspase-3 to liberate aminoluciferin, which can be consumed by luciferase to generate a luminescent signal. In two oncology models, namely SKOV3-luc and MDA-MB-231-luc-LN, at 24, 48, and 72 h after treatment with docetaxel, animals were injected with Z-DEVD-aminoluciferin and bioluminescent images were acquired. Significantly more light was detected at 24 (P<0.05), 48 (P<0.01), and 72 h (P<0.01) in the docetaxel-treated group compared with the vehicle-treated group, with caspase-3 activation at these time points confirmed using immunohistochemistry. Importantly, whereas significant differences between groups were detected as early as 24 h after treatment by molecular imaging, caliper measurements were unable to detect a difference for 4-5 additional days. Taken together, these data show that in vivo imaging of apoptosis using Z-DEVD-aminoluciferin could provide a sensitive and rapid method for early detection of drug efficacy, which could potentially be used by numerous therapeutic programs.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/20057500
      14. Call Number :
        PKI @ catherine.lautenschlager @
      15. Serial :
        8950
      1. Author :
        Razavi, Reza; Harrison, Lawrence E
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2010
      5. Publication :
        Annals of surgical oncology
      6. Products :
      7. Volume :
        17
      8. Issue :
        1
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        Animals; Bioware; Carcinoma; Cell Proliferation; Colonic Neoplasms; DNA Damage; Drug Therapy, Combination; Female; HT-29-luc-D6 cells; Humans; Hydrogen peroxide; Hyperthermia, Induced; Injections, Intraperitoneal; Mice; Mice, Nude; Oxidants; Oxidative Stress; Survival Rate; tert-Butylhydroperoxide; Treatment Outcome; Tumor Cells, Cultured
      12. Abstract :
        BACKGROUND The purpose of this study was to extend our in vitro observations that induced oxidative stress under hyperthermic conditions decreases tumor cell growth into a preclinical murine model of hyperthermic perfusion. METHODS A nude mouse model of colon cancer carcinomatosis with HT-29-Luc-D6 colon cancer cells was established, and tumor growth was measured by serial bioluminescent imaging. RESULTS By means of a survival model of hyperthermic perfusion, we demonstrated that perfusion with normothermic saline decreased tumor growth compared with no perfusion controls, and tumor growth was further decreased with hyperthermic perfusion alone. The induction of oxidative stress with hydrogen peroxide in the perfusate at concentrations as high as 600 microM was well tolerated in this model of hyperthermic perfusion. Importantly, induced oxidative stress using hydrogen peroxide under hyperthermic conditions significantly decreased in vivo tumor cell growth compared with all other controls. CONCLUSIONS On the basis of our observations, thermal sensitization through modulation of cellular oxidative stress may represent a novel approach to increase the efficacy of hyperthermia as an anticancer modality.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/19711132
      14. Call Number :
        PKI @ catherine.lautenschlager @
      15. Serial :
        9008
      1. Author :
        Tseng, J. C.; Granot, T.; DiGiacomo, V.; Levin, B.; Meruelo, D.
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2010
      5. Publication :
        Cancer Gene Ther
      6. Products :
      7. Volume :
        17
      8. Issue :
        N/A
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        AngioSense, IVIS, Alphavirus Infections/pathology/*therapy/virology; Animals; Antineoplastic Agents, Phytogenic/therapeutic use; Blotting, Western; Cell Membrane Permeability; Combined Modality Therapy; Cricetinae; Drug Delivery Systems; Female; *Genetic Vectors; Humans; Mice; Mice, SCID; Neovascularization, Pathologic/*prevention & control; Neuroblastoma/blood supply/therapy/virology; *Oncolytic Virotherapy; Ovarian Neoplasms/*blood supply/*therapy/virology; Paclitaxel/therapeutic use; Sindbis Virus/*physiology; Vascular Endothelial Growth Factor A/metabolism; Xenograft Model Antitumor Assays
      12. Abstract :
        Genetic instability of cancer cells generates resistance after initial responses to chemotherapeutic agents. Several oncolytic viruses have been designed to exploit specific signatures of cancer cells, such as important surface markers or pivotal signaling pathways for selective replication. It is less likely for cancer cells to develop resistance given that mutations in these cancer signatures would negatively impact tumor growth and survival. However, as oncolytic viral vectors are large particles, they suffer from inefficient extravasation from tumor blood vessels. Their ability to reach cancer cells is an important consideration in achieving specific oncolytic targeting and potential vector replication. Our previous studies indicated that the Sindbis viral vectors target tumor cells by the laminin receptor. Here, we present evidence that modulating tumor vascular leakiness, using VEGF and/or metronomic chemotherapy regimens, significantly enhances tumor vascular permeability and directly enhances oncolytic Sindbis vector targeting in tumor models. Because host-derived vascular endothelium cells are genetically stable and less likely to develop resistance to chemotherapeutics, a combined metronomic chemotherapeutics and oncolytic vector regimen should provide a new approach for cancer therapy. This mechanism could explain the synergistic treatment outcomes observed in clinical trials of combined therapies.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/19798121
      14. Call Number :
        PKI @ kd.modi @ 2
      15. Serial :
        10442
      1. Author :
        Panizzi, P.; Nahrendorf, M.; Figueiredo, J. L.; Panizzi, J.; Marinelli, B.; Iwamoto, Y.; Keliher, E.; Maddur, A. A.; Waterman, P.; Kroh, H. K.; Leuschner, F.; Aikawa, E.; Swirski, F. K.; Pittet, M. J.; Hackeng, T. M.; Fuentes-Prior, P.; Schneewind, O.; Bock, P. E.; Weissleder, R.
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2011
      5. Publication :
        Nat Med
      6. Products :
      7. Volume :
        17
      8. Issue :
        N/A
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        IVIS, Xen29, Xen 29, Staphylococcus aureus Xen29, Animals; Coagulase/metabolism; Endocarditis, Bacterial/*diagnosis; Mice; Microscopy, Fluorescence; Positron-Emission Tomography; Protein Engineering; Prothrombin/*diagnostic use/*metabolism; Quorum Sensing/physiology; Staphylococcus aureus/*metabolism/pathogenicity
      12. Abstract :
        Coagulase-positive Staphylococcus aureus (S. aureus) is the major causal pathogen of acute endocarditis, a rapidly progressing, destructive infection of the heart valves. Bacterial colonization occurs at sites of endothelial damage, where, together with fibrin and platelets, the bacteria initiate the formation of abnormal growths known as vegetations. Here we report that an engineered analog of prothrombin could be used to detect S. aureus in endocarditic vegetations via noninvasive fluorescence or positron emission tomography (PET) imaging. These prothrombin derivatives bound staphylocoagulase and intercalated into growing bacterial vegetations. We also present evidence for bacterial quorum sensing in the regulation of staphylocoagulase expression by S. aureus. Staphylocoagulase expression was limited to the growing edge of mature vegetations, where it was exposed to the host and co-localized with the imaging probe. When endocarditis was induced with an S. aureus strain with genetic deletion of coagulases, survival of mice improved, highlighting the role of staphylocoagulase as a virulence factor.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/21857652
      14. Call Number :
        PKI @ kd.modi @ 16
      15. Serial :
        10454
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