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      1. Author :
        Kosaka, N.; Iguchi, H.; Yoshioka, Y.; Hagiwara, K.; Takeshita, F.; Ochiya, T.
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2012
      5. Publication :
        J Biol Chem
      6. Products :
      7. Volume :
        287
      8. Issue :
        N/A
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        PC-3M-luc-C6, PC-3M-luc, IVIS, Bioware, Prostate cancer, Bioluminescence
      12. Abstract :
        Normal epithelial cells regulate the secretion of autocrine and paracrine factors that prevent aberrant growth of neighboring cells, leading to healthy development and normal metabolism. One reason for tumor initiation is considered to be a failure of this homeostatic cell competitive system. Here we identify tumor-suppressive microRNAs (miRNAs) secreted by normal cells as anti-proliferative signal entities. Culture supernatant of normal epithelial prostate PNT-2 cells attenuated proliferation of PC-3M-luc cells, prostate cancer cells. Global analysis of miRNA expression signature revealed that a variety of tumor-suppressive miRNAs are released from PNT-2 cells. Of these miRNAs, secretory miR-143 could induce growth inhibition exclusively in cancer cells in vitro and in vivo. These results suggest that secretory tumor-suppressive miRNAs can act as a death signal in a cell competitive process. This study provides a novel insight into a tumor initiation mechanism.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/22123823
      14. Call Number :
        PKI @ kd.modi @ 2
      15. Serial :
        10537
      1. Author :
        McCann CM, Waterman P, Figueiredo JL, Aikawa E, Weissleder R and Chen JW
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2009
      5. Publication :
        Neuroimage
      6. Products :
      7. Volume :
        45
      8. Issue :
        2
      9. Page Numbers :
        N/A
      10. Research Area :
        Neuroscience
      11. Keywords :
        FMT; in vivo imaging; ProSense
      12. Abstract :
        Fluorescent molecular tomographic (FMT) imaging can noninvasively monitor molecular function in living animals using specific fluorescent probes. However, macroscopic imaging methods such as FMT generally exhibit low anatomical details. To overcome this, we report a quantitative technique to image both structure and function by combining FMT and magnetic resonance (MR) imaging. We show that FMT-MR imaging can produce three-dimensional, multimodal images of living mouse brains allowing for serial monitoring of tumor morphology and protease activity. Combined FMT-MR tumor imaging provides a unique in vivo diagnostic parameter, protease activity concentration (PAC), which reflects histological changes in tumors and is significantly altered by systemic chemotherapy. Alterations in this diagnostic parameter are detectable early after chemotherapy and correlate with subsequent tumor growth, predicting tumor response to chemotherapy. Our results reveal that combined FMT-MR imaging of fluorescent molecular probes could be valuable for brain tumor drug development and other neurological and somatic imaging applications.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/19154791
      14. Call Number :
        PKI @ sarah.piper @
      15. Serial :
        4544
      1. Author :
        Hensley, H. H.; Roder, N. A.; O'Brien, S. W.; Bickel, L. E.; Xiao, F.; Litwin, S.; Connolly, D. C.
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2012
      5. Publication :
        Neoplasia
      6. Products :
      7. Volume :
        14
      8. Issue :
        N/A
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        ProSense, IntegriSense, MMPSense, Annexin-Vivo, Annexin vivo, IVIS, Animals; Antineoplastic Agents/administration & dosage/pharmacology; Carcinoma/*diagnosis/*metabolism/pathology; Cathepsins/metabolism; Cell Line, Tumor; Disease Progression; Female; Fluorescent Dyes/chemistry/metabolism; Integrin alphaVbeta3/metabolism; Integrins/genetics/*metabolism; Magnetic Resonance Imaging; Matrix Metalloproteinases/metabolism; Mice; Mice, Transgenic; *Molecular Imaging; Ovarian Neoplasms/*diagnosis/drug therapy/*metabolism; Peptide Hydrolases/*metabolism; Protein Binding; Tumor Burden/drug effects
      12. Abstract :
        Most patients with epithelial ovarian cancer (EOC) experience drug-resistant disease recurrence. Identification of new treatments is a high priority, and preclinical studies in mouse models of EOC may expedite this goal. We previously developed methods for magnetic resonance imaging (MRI) for tumor detection and quantification in a transgenic mouse model of EOC. The goal of this study was to determine whether three-dimensional (3D) fluorescence molecular tomography (FMT) and fluorescent molecular imaging probes could be effectively used for in vivo detection of ovarian tumors and response to therapy. Ovarian tumor-bearing TgMISIIR-TAg mice injected with fluorescent probes were subjected to MRI and FMT. Tumor-specific probe retention was identified in vivo by alignment of the 3D data sets, confirmed by ex vivo fluorescent imaging and correlated with histopathologic findings. Mice were treated with standard chemotherapy, and changes in fluorescent probe binding were detected by MRI and FMT. Ovarian tumors were detected using probes specific for cathepsin proteases, matrix metalloproteinases (MMPs), and integrin alpha(v)beta(3). Cathepsin and integrin alpha(v)beta(3) probe activation and retention correlated strongly with tumor volume. MMP probe activation was readily detected in tumors but correlated less strongly with tumor volume. Tumor regression associated with response to therapy was detected and quantified by serial MRI and FMT. These results demonstrate the feasibility and sensitivity of FMT for detection and quantification of tumor-associated biologic targets in ovarian tumors and support the translational utility of molecular imaging to assess functional response to therapy in mouse models of EOC.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/22787427
      14. Call Number :
        PKI @ kd.modi @ 1
      15. Serial :
        10425
      1. Author :
        Bucki, Robert; Leszczynska, Katarzyna; Byfield, Fitzroy J; Fein, David E; Won, Esther; Cruz, Katrina; Namiot, Andrzej; Kulakowska, Alina; Namiot, Zbigniew; Savage, Paul B; Diamond, Scott L; Janmey, Paul A
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2010
      5. Publication :
        Antimicrobial agents and chemotherapy
      6. Products :
      7. Volume :
        54
      8. Issue :
        6
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        Animals; Anti-Bacterial Agents; Anti-Inflammatory Agents; Bacterial Infections; Biofilms; Cathelicidins; Cattle; Cells, Cultured; Dexamethasone; Drug Design; Humans; Interleukins; Macrophages; Microbial Sensitivity Tests; Neutrophils; Phagocytosis; Pseudomonas aeruginosa; Receptors, Glucocorticoid; Spermine; Staphylococcus aureus; Xen5
      12. Abstract :
        The rising number of antibiotic-resistant bacterial strains represents an emerging health problem that has motivated efforts to develop new antibacterial agents. Endogenous cationic antibacterial peptides (CAPs) that are produced in tissues exposed to the external environment are one model for the design of novel antibacterial compounds. Here, we report evidence that disubstituted dexamethasone-spermine (D2S), a cationic corticosteroid derivative initially identified as a by-product of synthesis of dexamethasone-spermine (DS) for the purpose of improving cellular gene delivery, functions as an antibacterial peptide-mimicking molecule. This moiety exhibits bacterial killing activity against clinical isolates of Staphylococcus aureus, Pseudomonas aeruginosa present in cystic fibrosis (CF) sputa, and Pseudomonas aeruginosa biofilm. Although compromised in the presence of plasma, D2S antibacterial activity resists the proteolytic activity of pepsin and is maintained in ascites, cerebrospinal fluid, saliva, and bronchoalveolar lavage (BAL) fluid. D2S also enhances S. aureus susceptibility to antibiotics, such as amoxicillin (AMC), tetracycline (T), and amikacin (AN). Inhibition of interleukin-6 (IL-6) and IL-8 release from lipopolysaccharide (LPS)- or lipoteichoic acid (LTA)-treated neutrophils in the presence of D2S suggests that this molecule might also prevent systemic inflammation caused by bacterial wall products. D2S-mediated translocation of green fluorescent protein (GFP)-labeled glucocorticoid receptor (GR) in bovine aorta endothelial cells (BAECs) suggests that some of its anti-inflammatory activities involve engagement of glucocorticoid receptors. The combined antibacterial and anti-inflammatory activities of D2S suggest its potential as an alternative to natural CAPs in the prevention and treatment of some bacterial infections.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/20308375
      14. Call Number :
        PKI @ catherine.lautenschlager @
      15. Serial :
        9996
      1. Author :
        Wang, M.; Gartel, A. L.
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2012
      5. Publication :
        Cancer Biol Ther
      6. Products :
      7. Volume :
        13
      8. Issue :
        N/A
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        MDA-MB-231-luc-D3H2Ln, D3H2Ln, IVIS, Breast cancer, Bioware, Adenocarcinoma/*drug therapy/pathology; Animals; Antineoplastic Combined Chemotherapy; Protocols/pharmacokinetics/pharmacology/*therapeutic use; Apoptosis; Boronic Acids/administration & dosage; Breast Neoplasms/*drug therapy/pathology; Cell Line, Tumor; Drug Synergism; Female; Humans; Male; Mice; Mice, Nude; Nanocapsules/administration & dosage; Proteasome Endopeptidase Complex/metabolism; Pyrazines/administration & dosage; Random Allocation; Thiostrepton/administration & dosage; Tissue Distribution; Tumor Burden/drug effects; Xenograft Model Antitumor Assays
      12. Abstract :
        Bortezomib is well-known for inducing cell death in cancer cells, specifically through the mechanism of proteasome inhibition. Thiostrepton, a thiazole antibiotic, has also been described for its proteasome inhibitory action, although differing slightly to bortezomib in the proteasomal site to which it is active. Previously we had shown the synergic effect of bortezomib and thiostrepton in breast cancer cells in vitro, where sub-apoptotic concentrations of both proteasome inhibitors resulted in synergic increase in cell death when combined as a treatment. Here, we administered such a combination to MDA-MB-231 xenograft tumors in vivo, and found that the effect of complementary proteasome inhibitors reduced tumor growth rates more efficiently than compared with when administered alone. Increased induction of apoptotic activity in tumors was found be associated with the growth inhibitory activity of combination treatment. Further examination additionally revealed that combination-treated tumors exhibited reduced proteasome activity, compared with non-treated and single drug-treated tumors. These data suggest that this drug combination may be useful as a therapy for solid tumors.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/22353937
      14. Call Number :
        PKI @ kd.modi @ 3
      15. Serial :
        10510
      1. Author :
        Steve H. Thorne; Yoram Barak; Wenchuan Liang; Michael H. Bachmann; Jianghong Rao; Christopher H. Contag; A. Matin
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2009
      5. Publication :
        Molecular Cancer Therapeutics
      6. Products :
      7. Volume :
        8
      8. Issue :
        2
      9. Page Numbers :
        N/A
      10. Research Area :
        Cancer
      11. Keywords :
        Cancer; in vivo imaging; drug discovery; chemotherapy
      12. Abstract :
        We report the discovery of a new prodrug, 6-chloro-9-nitro-5-oxo-5H-benzo(a)phenoxazine (CNOB). This prodrug is efficiently activated by ChrR6, the highly active prodrug activating bacterial enzyme we have previously developed. The CNOB/ChrR6 therapy was effective in killing several cancer cell lines in vitro. It also efficiently treated tumors in mice with up to 40% complete remission. 9-Amino-6-chloro-5H-benzo(a)phenoxazine-5-one (MCHB) was the only product of CNOB reduction by ChrR6. MCHB binds DNA; at nonlethal concentration, it causes cell accumulation in the S phase, and at lethal dose, it induces cell surface Annexin V and caspase-3 and caspase-9 activities. Further, MCHB colocalizes with mitochondria and disrupts their electrochemical potential. Thus, killing by CNOB involves MCHB, which likely induces apoptosis through the mitochondrial pathway. An attractive feature of the CNOB/ChrR6 regimen is that its toxic product, MCHB, is fluorescent. This feature proved helpful in in vitro studies because simple fluorescence measurements provided information on the kinetics of CNOB activation within the cells, MCHB killing mechanism, its generally efficient bystander effect in cells and cell spheroids, and its biodistribution. The emission wavelength of MCHB also permitted its visualization in live animals, allowing noninvasive qualitative imaging of MCHB in mice and the tumor microenvironment. This feature may simplify exploration of barriers to the penetration of MCHB in tumors and their amelioration.
      13. URL :
        http://mct.aacrjournals.org/content/8/2/333.abstract
      14. Call Number :
        PKI @ sarah.piper @
      15. Serial :
        4500
      1. Author :
        Shiota, M.; Zardan, A.; Takeuchi, A.; Kumano, M.; Beraldi, E.; Naito, S.; Zoubeidi, A.; Gleave, M. E.
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2012
      5. Publication :
        Cancer Res
      6. Products :
      7. Volume :
        72
      8. Issue :
        N/A
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        PC-3M-luc-C6, PC-3M-luc, IVIS, Bioware, Prostate cancer, Bioluminescence, Animals; Base Sequence; Blotting, Western; Chromatin Immunoprecipitation; Clusterin/genetics/*physiology; DNA Primers; Epithelial-Mesenchymal Transition/*physiology; Humans; Male; Mice; *Neoplasm Metastasis; Nuclear Proteins/*physiology; Promoter Regions, Genetic; Prostatic Neoplasms/*pathology; Reverse Transcriptase Polymerase Chain Reaction; Transforming Growth Factor beta/*physiology; Twist Transcription Factor/*physiology
      12. Abstract :
        TGF-beta promotes epithelial-mesenchymal transition (EMT) and induces clusterin (CLU) expression, linking these genes to cancer metastasis. CLU is a pleiotropic molecular chaperone that confers survival and proliferative advantage to cancer cells. However, the molecular mechanisms by which TGF-beta regulates CLU expression and CLU affects metastasis remain unknown. In this study, we report that the transcription factor Twist1 mediates TGF-beta-induced CLU expression. By binding to E-boxes in the distal promoter region of CLU gene, Twist1 regulated basal and TGF-beta-induced CLU transcription. In addition, CLU reduction reduced TGF-beta induction of the mesenchymal markers, N-cadherin and fibronectin, thereby inhibiting the migratory and invasive properties induced by TGF-beta. Targeted inhibition of CLU also suppressed metastasis in an in vivo model. Taken together, our findings indicate that CLU is an important mediator of TGF-beta-induced EMT, and suggest that CLU suppression may represent a promising therapeutic option for suppressing prostate cancer metastatic progression.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/22896337
      14. Call Number :
        PKI @ kd.modi @ 7
      15. Serial :
        10540
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