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      1. Author :
        Wang, K.; Ruan, J.; Qian, Q.; Song, H.; Bao, C.; Zhang, X.; Kong, Y.; Zhang, C.; Hu, G.; Ni, J.; Cui, D.
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2011
      5. Publication :
        Journal of nanobiotechnology
      6. Products :
      7. Volume :
        9
      8. Issue :
        N/A
      9. Page Numbers :
        23
      10. Research Area :
        N/A
      11. Keywords :
        N/A
      12. Abstract :
        ABSTRACT: BACKGROUND: Gastric cancer is 2th most common cancer in China, and is still the second most common cause of cancer-related death in the world. How to recognize early gastric cancer cells is still a great challenge for early diagnosis and therapy of patients with gastric cancer. This study is aimed to develop one kind of multifunctional nanoprobes for in vivo targeted magnetofluorescent imaging of gastric cancer. METHODS: BRCAA1 monoclonal antibody was prepared, was used as first antibody to stain 50 pairs of specimens of gastric cancer and control normal gastric mucous tissues, and conjugated with fluorescent magnetic nanoparticles with 50 nm in diameter, the resultant BRCAA1-conjugated fluorescent magnetic nanoprobes were characterized by transmission electron microscopy and photoluminescence spectrometry, as-prepared nanoprobes were incubated with gastric cancer MGC803 cells, and were injected into mice model loaded with gastric cancer of 5 mm in diameter via tail vein, and then were imaged by fluorescence optical imaging and magnetic resonance imaging, their biodistribution was investigated. The tissue slices were observed by fluorescent microscopy, and the important organs such as heart, lung, kidney, brain and liver were analyzed by hematoxylin and eosin (HE) stain method. RESULTS: BRCAA1 monoclonal antibody was successfully prepared, BRCAA1 protein exhibited over-expression in 64% gastric cancer tissues, no expression in control normal gastric mucous tissues, there exists statistical difference between two groups (P < 0.01). The BRCAA1-conjugated fluorescent magnetic nanoprobes exhibit very low-toxicity, lower magnetic intensity and lower fluorescent intensity with peak-blue-shift than pure FMNPs, could be endocytosed by gastric cancer MGC803 cells, could target in vivo gastric cancer tissues loaded by mice, and could be used to image gastric cancer tissues by fluorescent imaging and magnetic resonance imaging, and mainly distributed in local gastric cancer tissues within 12 h post-injection. HE stain analysis showed that no obvious damages were observed in important organs. CONCLUSIONS: The high-performance BRCAA1 monoclonal antibody-conjugated fluorescent magnetic nanoparticles can target in vivo gastric cancer cells, can be used for simultaneous magnetofluorescent imaging, and may have great potential in applications such as dual-model imaging and local thermal therapy of early gastric cancer in near future.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/21612621
      14. Call Number :
        144088
      15. Serial :
        5613
      1. Author :
        Filonov, G. S.; Piatkevich, K. D.; Ting, L. M.; Zhang, J.; Kim, K.; Verkhusha, V. V.
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2011
      5. Publication :
        Nature biotechnology
      6. Products :
      7. Volume :
        N/A
      8. Issue :
        N/A
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        N/A
      12. Abstract :
        Imaging biological processes in mammalian tissues will be facilitated by fluorescent probes with excitation and emission bands within the near-infrared optical window of high transparency. Here we report a phytochrome-based near-infrared fluorescent protein (iRFP) with excitation and emission maxima at 690 nm and 713 nm, respectively. iRFP does not require an exogenous supply of the chromophore biliverdin and has higher effective brightness, intracellular stability and photostability than earlier phytochrome-derived fluorescent probes. Compared with far-red GFP-like proteins, iRFP has a substantially higher signal-to-background ratio in a mouse model due to its infrared-shifted spectra.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/21765402
      14. Call Number :
        137776
      15. Serial :
        5619
      1. Author :
        Zhao, D.; Alizadeh, D.; Zhang, L.; Liu, W.; Farrukh, O.; Manuel, E.; Diamond, D. J.; Badie, B.
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2011
      5. Publication :
        Clinical cancer research : an official journal of the American Association for Cancer Research
      6. Products :
      7. Volume :
        17
      8. Issue :
        N/A
      9. Page Numbers :
        771
      10. Research Area :
        N/A
      11. Keywords :
        N/A
      12. Abstract :
        PURPOSE: Stimulation of toll-like receptor-9 (TLR9) by CpG oligodeoxynucleotides (CpG) has been shown to counteract the immunosuppressive microenvironment and to inhibit tumor growth in glioma models. Because TLR9 is located intracellularly, we hypothesized that methods that enhance its internalization may also potentiate its immunostimulatory response. The goal of this study was to evaluate carbon nanotubes (CNT) as a CpG delivery vehicle in brain tumor models. EXPERIMENTAL DESIGN: Functionalized single-walled CNTs were conjugated with CpG (CNT-CpG) and evaluated in vitro and in mice bearing intracranial GL261 gliomas. Flow cytometry was used to assess CNT-CpG uptake and antiglioma immune response. Tumor growth was measured by bioluminescent imaging, histology, and animal survival. RESULTS: CNT-CpG was nontoxic and enhanced CpG uptake both in vitro and intracranial gliomas. CNT-mediated CpG delivery also potentiated proinflammatory cytokine production by primary monocytes. Interestingly, a single intracranial injection of low-dose CNT-CpG (but not free CpG or blank CNT) eradicated intracranial GL261 gliomas in half of tumor-bearing mice. Moreover, surviving animals exhibited durable tumor-free remission (>3 months), and were protected from intracranial tumor rechallenge, demonstrating induction of long-term antitumor immunity. CONCLUSIONS: These findings suggest that CNTs can potentiate CpG immunopotency by enhancing its delivery into tumor-associated inflammatory cells.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/21088258
      14. Call Number :
        145096
      15. Serial :
        5635
      1. Author :
        Dasmahapatra, G.; Lembersky, D.; Son, M. P.; Attkisson, E.; Dent, P.; Fisher, R. I.; Friedberg, J. W.; Grant, S.
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2011
      5. Publication :
        Molecular cancer therapeutics
      6. Products :
      7. Volume :
        N/A
      8. Issue :
        N/A
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        N/A
      12. Abstract :
        Interactions between the proteasome inhibitor carfilzomib and the HDAC inhibitors vorinostat and SNDX-275 were examined in mantle cell lymphoma (MCL) cells in vitro and in vivo. Co-administration of very low, marginally toxic carfilzomib concentrations (e.g., 3-4 nM) with minimally lethal concentrations of vorinostat or SNDX-275 resulted in sharp increases in mitochondrial injury and apoptosis in multiple MCL cell lines and primary MCL cells. Potentiation of cell death was associated with activation of JNK1/2, increased DNA damage, reflected by induction of lambdaH2A.X, and inactivation of ERK1/2 and AKT1/2. Co-administration of carfilzomib and HDACIs resulted in a marked increase in ROS generation, and arrest of cells in G2M. Significantly, the free radical scavenger TBAP blocked carfilzomib/HDACI-mediated ROS generation, lambdaH2A.X formation, JNK1/2 activation, and lethality. Genetic (shRNA) knock down of JNK1/2 significantly attenuated carfilzomib/HDACI-induced apoptosis in MCL cells, but did not prevent ROS generation or DNA damage. Carfilzomib/HDACI regimens were also active against bortezomib-resistant MCL cells. Finally, co-administration of carfilzomib and vorinostat resulted in a pronounced reduction in tumor growth compared to single agent treatment in a MCL xenograft model associated with enhanced apoptosis, lambdaH2A.X formation, and JNK activation. Collectively, these findings suggest that carfilzomib/HDACI regimens warrant attention in MCL.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/21750224
      14. Call Number :
        137263
      15. Serial :
        5638
      1. Author :
        Emmett, M. S.; Lanati, S.; Dunn, D. B.; Stone, O. A.; Bates, D. O.
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2011
      5. Publication :
        Microcirculation
      6. Products :
      7. Volume :
        18
      8. Issue :
        N/A
      9. Page Numbers :
        172
      10. Research Area :
        N/A
      11. Keywords :
        N/A
      12. Abstract :
        OBJECTIVE: To determine whether chemotactic-metastasis, the preferential growth of melanomas towards areas of high lymphatic density, is CCL21/CCR7 dependent in vivo. Lymphatic endothelial cells (LECs) produce the chemokine CCL21. Metastatic melanoma cells express CCR7, its receptor, and exhibit chemotactic-metastasis, whereby metastatic cells recognise and grow towards areas of higher lymphatic density. METHODS: We used two in vivo models of directional growth towards depots of LECs of melanoma cells over-expressing CCR7. Injected LEC were tracked by intravital fluorescence microscopy, and melanoma growth by bioluminescence. RESULTS: Over-expression of the chemokine receptor CCR7 enables non-metastatic tumor cells to recognise and grow towards LECs (3.9 fold compared with control), but not blood endothelial cells (0.9 fold), in vitro and in vivo in the absence of increased lymphatic clearance. Chemotactic metastasis was inhibited by a CCL21 neutralising antibody (4-17% of control). Furthermore, CCR7 expression in mouse B16 melanomas resulted in in-transit metastasis (50-100% of mice) that was less often seen with control tumors (0-50%) in vivo. CONCLUSION: These results suggest that recognition of LEC by tumors expressing receptors for lymphatic specific ligands contributes towards the identification and invasion of lymphatics by melanoma cells and provides further evidence for a chemotactic metastasis model of tumor spread.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/21166932
      14. Call Number :
        137692
      15. Serial :
        5648
      1. Author :
        Lee, T. K.; Castilho, A.; Cheung, V. C.; Tang, K. H.; Ma, S.; Ng, I. O.
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2011
      5. Publication :
        Cell stem cell
      6. Products :
      7. Volume :
        9
      8. Issue :
        N/A
      9. Page Numbers :
        50
      10. Research Area :
        N/A
      11. Keywords :
        N/A
      12. Abstract :
        Tumor-initiating cells (T-ICs) are a subpopulation of chemoresistant tumor cells that have been shown to cause tumor recurrence upon chemotherapy. Identification of T-ICs and their related pathways are therefore priorities for the development of new therapeutic paradigms. We established chemoresistant hepatocellular carcinoma (HCC) xenograft tumors in immunocompromised mice in which an enriched T-IC population was capable of tumor initiation and self-renewal. With this model, we found CD24 to be upregulated in residual chemoresistant tumors when compared with bulk tumor upon cisplatin treatment. CD24(+) HCC cells were found to be critical for the maintenance, self-renewal, differentiation, and metastasis of tumors and to significantly impact patients' clinical outcome. With a lentiviral-based knockdown approach, CD24 was found to be a functional liver T-IC marker that drives T-IC genesis through STAT3-mediated NANOG regulation. Our findings point to a CD24 cascade in liver T-ICs that may provide an attractive therapeutic target for HCC patients.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/21726833
      14. Call Number :
        140170
      15. Serial :
        5652
      1. Author :
        Ahmadi, M.; King, J. W.; Xue, S. A.; Voisine, C.; Holler, A.; Wright, G. P.; Waxman, J.; Morris, E.; Stauss, H. J.
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2011
      5. Publication :
        Blood
      6. Products :
      7. Volume :
        N/A
      8. Issue :
        N/A
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        N/A
      12. Abstract :
        The function of T cell receptor (TCR) gene modified T cells is dependent on efficient surface expression of the introduced TCR alpha/beta heterodimer. We tested whether endogenous CD3 chains are rate-limiting for TCR expression and antigen-specific T cell function. We show that co-transfer of CD3 and TCR genes into primary murine T cells enhanced TCR expression and antigen-specific T cell function in vitro. Peptide titration experiments showed that T cells expressing introduced CD3 and TCR genes recognised lower concentration of antigen than T cells expressing TCR only. In vivo imaging revealed that TCR+CD3 gene modified T cells infiltrated tumors faster and in larger numbers, which resulted in more rapid tumor elimination compared to T cells modified by TCR only. Following tumor clearance, TCR+CD3 engineered T cells persisted in larger numbers than TCR-only T cells and mounted a more effective memory response when re-challenged with antigen. The data demonstrate that provision of additional CD3 molecules is an effective strategy to enhance the avidity, anti-tumor activity and functional memory formation of TCR gene modified T cells in vivo.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/21750319
      14. Call Number :
        135769
      15. Serial :
        5654
      1. Author :
        Claser, C.; Malleret, B.; Gun, S. Y.; Wong, A. Y.; Chang, Z. W.; Teo, P.; See, P. C.; Howland, S. W.; Ginhoux, F.; Renia, L.
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2011
      5. Publication :
        PloS one
      6. Products :
      7. Volume :
        6
      8. Issue :
        N/A
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        N/A
      12. Abstract :
        BACKGROUND: Infection with Plasmodium berghei ANKA (PbA) in susceptible mice induces a syndrome called experimental cerebral malaria (ECM) with severe pathologies occurring in various mouse organs. Immune mediators such as T cells or cytokines have been implicated in the pathogenesis of ECM. Red blood cells infected with PbA parasites have been shown to accumulate in the brain and other tissues during infection. This accumulation is thought to be involved in PbA-induced pathologies, which mechanisms are poorly understood. METHODS AND FINDINGS: Using transgenic PbA parasites expressing the luciferase protein, we have assessed by real-time in vivo imaging the dynamic and temporal contribution of different immune factors in infected red blood cell (IRBC) accumulation and distribution in different organs during PbA infection. Using deficient mice or depleting antibodies, we observed that CD8(+) T cells and IFN-gamma drive the rapid increase in total parasite biomass and accumulation of IRBC in the brain and in different organs 6-12 days post-infection, at a time when mice develop ECM. Other cells types like CD4(+) T cells, monocytes or neutrophils or cytokines such as IL-12 and TNF-alpha did not influence the early increase of total parasite biomass and IRBC accumulation in different organs. CONCLUSIONS: CD8(+) T cells and IFN-gamma are the major immune mediators controlling the time-dependent accumulation of P. berghei-infected red blood cells in tissues.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/21494565
      14. Call Number :
        136987
      15. Serial :
        5662
      1. Author :
        Bruyn, M. de; Wei, Y.; Wiersma, V. R.; Samplonius, D. F.; Klip, H. G.; Zee, A. G. van der; Yang, B.; Helfrich, W.; Bremer, E.
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2011
      5. Publication :
        Clinical cancer research : an official journal of the American Association for Cancer Research
      6. Products :
      7. Volume :
        N/A
      8. Issue :
        N/A
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        N/A
      12. Abstract :
        PURPOSE: Adoptive T-cell therapy generally fails to induce meaningful anti-cancer responses in patients with solid tumors. Here, we present a novel strategy designed to selectively enhance the tumoricidal activity of T-cells by targeted delivery of TRAIL to the T-cell surface.EXPERIMENTAL DESIGN: We constructed two recombinant fusion proteins: anti-CD3:TRAIL and K12:TRAIL. Tumoricidal activity of T-cells in the presence of these fusion proteins was assessed in solid tumor cell lines, primary patient-derived malignant cells and in a murine xenograft model.RESULTS: When added to T-cells, K12:TRAIL and anti-CD3:TRAIL selectively bind to the T-cell surface antigens CD3 and CD7, respectively, leading to cell surface accretion of TRAIL. Subsequently, anti-CD3:TRAIL and K12:TRAIL increased the tumoricidal activity of T-cells towards cancer cell lines and primary patient-derived malignant cells greater than 500-fold. Furthermore, T-cell surface delivery of TRAIL strongly inhibited tumor growth and increased survival time of xenografted mice greater than 6-fold. CONCLUSIONS: Targeted delivery of TRAIL to cell surface antigens of T-cells potently enhances the tumoricidal activity of T-cells. This approach may be generally applicable to enhance the efficacy of adoptive T-cell therapy.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/21753155
      14. Call Number :
        137299
      15. Serial :
        5670
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