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      1. Author :
        Yan, Eryun; Fu, Yilong; Wang, Xue; Ding, Yin; Qian, Hanqing; Wang, Chi-Hwa; Hu, Yong; Jiang, Xiqun
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2011
      5. Publication :
        Journal of Materials Chemistry
      6. Products :
      7. Volume :
        21
      8. Issue :
        N/A
      9. Page Numbers :
        3147
      10. Research Area :
        N/A
      11. Keywords :
        N/A
      12. Abstract :
        Here we report the synthesis of hybrid hollow chitosan-silica nanospheres (CS-Silica NPs) with chitosan-polyacrylic acid (CS-PAA) nanoparticles as the template and doxorubicin (DOX) delivery based on CS-Silica NPs. The morphology and the microstructure of CS-Silica NPs were characterized by field emission scanning electron microscopy (FESEM) and X-ray photoelectron spectroscopy (XPS). The confocal laser scanning microscopy (CLSM) and flow cytometry experiments showed that the cellular uptake of the DOX-loaded CS-Silica NPs was time dependent. In addition, cellular internalization and intracellular distribution of DOX-loaded CS-Silica NPs indicated that the DOX was mainly distributed in the cell nucleus while the carriers were primarily located in the cytoplasm. In vivo antitumor response indicated that the DOX loaded CS-Silica hybrid hollow nanospheres exhibited superior antitumor effect over the free drug in vivo, which might be ascribable to the enhanced cellular uptake efficiency and the effective delivery of drug to the cell nucleus.
      13. URL :
        http://dx.doi.org/10.1039/C0JM03234D
      14. Call Number :
        144619
      15. Serial :
        6323
      1. Author :
        Lan, K. L.; Lan, K. H.; Sheu, M. L.; Chen, M. Y.; Shih, Y. S.; Hsu, F. C.; Wang, H. M.; Liu, R. S.; Yen, S. H.
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2011
      5. Publication :
        International journal of radiation biology
      6. Products :
      7. Volume :
        87
      8. Issue :
        N/A
      9. Page Numbers :
        579
      10. Research Area :
        N/A
      11. Keywords :
        N/A
      12. Abstract :
        PURPOSE: Hypoxia-inducible factor-1alpha (HIF-1alpha) plays a pivotal role in the reaction of a tumour to hypoxia. In this study, we examined the inhibitory effect of a natural compound, honokiol, on HIF-1alpha activity and tumour growth in combination with radiation. METHODS: The inhibitory effect of honokiol on hypoxia-responsive element (HRE) controlled luciferase activity and HIF-1alpha accumulations stimulated by CoCl(2), or hypoxia was examined. Effect of honokiol on HIF-1alpha levels within hypoxic tumour microenvironment was investigated by immunohistochemical and in vivo bioluminescent studies. The in vivo radiosensitising activity of honokiol was evaluated with subcutaneous murine colon carcinoma, CT26, xenografts of BALB/c mice treated with honokiol, radiation, or both. RESULTS: Suppression of luciferase (luc) activity in HRE-luc stable cells by honokiol was in agreement with the results of decreased HIF-1alpha accumulation. In CT26-HRE-luc tumour-bearing mice, the inhibitory effect of intraperitoneally injected honokiol on HIF-1alpha-regulated luciferase activities induced by either CoCl(2) or radiation could be monitored non-invasively. Lastly, honokiol in combination with irradiation produced synergistic delay of CT26 tumour growth. CONCLUSIONS: Our data suggest that honokiol can exert its anticancer activity as a HIF-1alpha inhibitor by reducing HIF-1alpha protein level and suppressing the hypoxia-related signaling pathway. The animal experiment indicates that honokiol improves the therapeutic efficacy of radiation.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/21473672
      14. Call Number :
        139978
      15. Serial :
        6325
      1. Author :
        Deuse, T.; Seifert, M.; Phillips, N.; Fire, A.; Tyan, D.; Kay, M.; Tsao, P. S.; Hua, X.; Velden, J.; Eiermann, T.; Volk, H. D.; Reichenspurner, H.; Robbins, R. C.; Schrepfer, S.
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2011
      5. Publication :
        Circulation
      6. Products :
      7. Volume :
        124
      8. Issue :
        N/A
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        N/A
      12. Abstract :
        Background- Although human embryonic stem cells (hESC) have enormous potential for cell replacement therapy of heart failure, immune rejection of hESC derivatives inevitably would occur after transplantation. We therefore aimed to generate a hypoantigeneic hESC line with improved survival characteristics. Methods and Results- Using various in vivo, nonischemic, hindlimb xenotransplant models (immunocompetent and defined immunodefective mouse strains) as well as human in vitro T-cell and natural killer (NK)-cell assays, we revealed a central role for T cells in mediating hESC rejection. The NK-cell susceptibility of hESC in vivo was found to be low, and the NK response to hESC challenge in vitro was negligible. To reduce the antigenicity of hESC, we successfully generated human leukocyte antigen (HLA) I knockdown cells (hESC(siRNA+IB)) using both HLA I RNA interference (siRNA) and intrabody (IB) technology. HLA I expression was approximately 99% reduced after 7 days and remained low for weeks. Cellular immune recognition of these hESC(siRNA+IB) was strongly reduced in both xenogeneic and allogeneic settings. Immune rejection was profoundly mitigated after hESC(siRNA+IB) transplantation into immunocompetent mice, and even long-term graft survival was achieved in one third of the animals without any immunosuppression. The survival benefit of hESC(siRNA+IB) was further confirmed under ischemic conditions in a left anterior descending coronary artery ligation model. Conclusions- HLA I knockdown hESC(siRNA+IB) provoke T-cell ignorance and experience largely mitigated xenogeneic rejection. By generating hypoantigeneic hESC lines, the generation of acceptable hESC derivatives may become a practical concept and push cell replacement strategies forward.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/21911816
      14. Call Number :
        137392
      15. Serial :
        6336
      1. Author :
        McLean, K.; Gong, Y.; Choi, Y.; Deng, N.; Yang, K.; Bai, S.; Cabrera, L.; Keller, E.; McCauley, L.; Cho, K. R.; Buckanovich, R. J.
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2011
      5. Publication :
        The Journal of clinical investigation
      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 :
        Accumulating evidence suggests that mesenchymal stem cells (MSCs) are recruited to the tumor microenvironment; however, controversy exists regarding their role in solid tumors. In this study, we identified and confirmed the presence of carcinoma-associated MSCs (CA-MSCs) in the majority of human ovarian tumor samples that we analyzed. These CA-MSCs had a normal morphologic appearance, a normal karyotype, and were nontumorigenic. CA-MSCs were multipotent with capacity for differentiating into adipose, cartilage, and bone. When combined with tumor cells in vivo, CA-MSCs promoted tumor growth more effectively than did control MSCs. In vitro and in vivo studies suggested that CA-MSCs promoted tumor growth by increasing the number of cancer stem cells. Although CA-MSCs expressed traditional MSCs markers, they had an expression profile distinct from that of MSCs from healthy individuals, including increased expression of BMP2, BMP4, and BMP6. Importantly, BMP2 treatment in vitro mimicked the effects of CA-MSCs on cancer stem cells, while inhibiting BMP signaling in vitro and in vivo partly abrogated MSC-promoted tumor growth. Taken together, our data suggest that MSCs in the ovarian tumor microenvironment have an expression profile that promotes tumorigenesis and that BMP inhibition may be an effective therapeutic approach for ovarian cancer.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/21737876
      14. Call Number :
        141088
      15. Serial :
        6340
      1. Author :
        Li, X.; Ling, W.; Pennisi, A.; Wang, Y.; Khan, S.; Heidaran, M.; Pal, A.; Zhang, X.; He, S.; Zeitlin, A.; Abbot, S.; Faleck, H.; Hariri, R.; Shaughnessy, J. D.; Rhee, F. van; Nair, B.; Barlogie, B.; Epstein, J.; Yaccoby, S.
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2011
      5. Publication :
        Stem cells
      6. Products :
      7. Volume :
        29
      8. Issue :
        N/A
      9. Page Numbers :
        263
      10. Research Area :
        N/A
      11. Keywords :
        N/A
      12. Abstract :
        Human placenta has emerged as a valuable source of transplantable cells of mesenchymal and hematopoietic origin for multiple cytotherapeutic purposes, including enhanced engraftment of hematopoietic stem cells, modulation of inflammation, bone repair, and cancer. Placenta-derived adherent cells (PDACs) are mesenchymal-like stem cells isolated from postpartum human placenta. Multiple myeloma is closely associated with induction of bone disease and large lytic lesions, which are often not repaired and are usually the sites of relapses. We evaluated the antimyeloma therapeutic potential, in vivo survival, and trafficking of PDACs in the severe combined immunodeficiency (SCID)-rab model of medullary myeloma-associated bone loss. Intrabone injection of PDACs into nonmyelomatous and myelomatous implanted bone in SCID-rab mice promoted bone formation by stimulating endogenous osteoblastogenesis, and most PDACs disappeared from bone within 4 weeks. PDACs inhibitory effects on myeloma bone disease and tumor growth were dose-dependent and comparable with those of fetal human mesenchymal stem cells (MSCs). Intrabone, but not subcutaneous, engraftment of PDACs inhibited bone disease and tumor growth in SCID-rab mice. Intratumor injection of PDACs had no effect on subcutaneous growth of myeloma cells. A small number of intravenously injected PDACs trafficked into myelomatous bone. Myeloma cell growth rate in vitro was lower in coculture with PDACs than with MSCs from human fetal bone or myeloma patients. PDACs also promoted apoptosis in osteoclast precursors and inhibited their differentiation. This study suggests that altering the bone marrow microenvironment with PDAC cytotherapy attenuates growth of myeloma and that PDAC cytotherapy is a promising therapeutic approach for myeloma osteolysis. STEM CELLS 2011;29:263-273.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/21732484
      14. Call Number :
        140362
      15. Serial :
        6342
      1. Author :
        Chen, A. A.; Thomas, D. K.; Ong, L. L.; Schwartz, R. E.; Golub, T. R.; Bhatia, S. N.
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2011
      5. Publication :
        Proceedings of the National Academy of Sciences of the United States of America
      6. Products :
      7. Volume :
        108
      8. Issue :
        N/A
      9. Page Numbers :
        11842
      10. Research Area :
        N/A
      11. Keywords :
        N/A
      12. Abstract :
        “Humanized” mice offer a window into aspects of human physiology that are otherwise inaccessible. The best available methods for liver humanization rely on cell transplantation into immunodeficient mice with liver injury but these methods have not gained widespread use due to the duration and variability of hepatocyte repopulation. In light of the significant progress that has been achieved in clinical cell transplantation through tissue engineering, we sought to develop a humanized mouse model based on the facile and ectopic implantation of a tissue-engineered human liver. These human ectopic artificial livers (HEALs) stabilize the function of cryopreserved primary human hepatocytes through juxtacrine and paracrine signals in polymeric scaffolds. In contrast to current methods, HEALs can be efficiently established in immunocompetent mice with normal liver function. Mice transplanted with HEALs exhibit humanized liver functions persistent for weeks, including synthesis of human proteins, human drug metabolism, drug-drug interaction, and drug-induced liver injury. Here, mice with HEALs are used to predict the disproportionate metabolism and toxicity of “major” human metabolites using multiple routes of administration and monitoring. These advances may enable manufacturing of reproducible in vivo models for diverse drug development and research applications.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/21746904
      14. Call Number :
        136774
      15. Serial :
        6351
      1. Author :
        Chaumeil, M. M.; Ozawa, T.; Park, I.; Scott, K.; James, C. D.; Nelson, S. J.; Ronen, S. M.
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2011
      5. Publication :
        NeuroImage
      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 :
        Glioblastoma (GBM) is the most common and lethal primary malignant brain tumor in humans. Because the phosphatidylinositol-3-kinase (PI3K) signaling pathway is activated in more than 88% of GBM, new drugs which target this pathway, such as the mTOR inhibitor Everolimus, are currently in clinical trials. Early tumor response to molecularly targeted treatments remains challenging to assess non-invasively, because it is often associated with tumor stasis or slower tumor growth. Innovative neuroimaging methods are therefore critically needed to provide metabolic or functional information that is indicative of targeted therapeutic action at early time points during the course of treatment. In this study, we demonstrated for the first time that hyperpolarized (HP) (13)C magnetic resonance spectroscopic imaging (MRSI) can be used on a clinical MR system to monitor early metabolic response of orthotopic GBM tumors to Everolimus treatment through measurement of the HP lactate-to-pyruvate ratios. The study was performed on a highly invasive non-enhancing orthotopic GBM tumor model in rats (GS-2 tumors), which replicates many fundamental features of human GBM tumors. Seven days after initiation of treatment there was a significant drop in the HP lactate-to-pyruvate ratio from the tumor tissue in treated animals relative to day 0 (67%+/-27% decrease). In the control group, no significant changes in the HP lactate-to-pyruvate ratios were observed. Importantly, at the 7day time point, conventional MR imaging (MRI) was unable to detect a significant difference in tumor size between control and treated groups. Inhibition of tumor growth by conventional MRI was observed from day 15 of treatment. This implies that the decrease in the HP lactate-to-pyruvate ratio could be detected before any treatment-induced inhibition of tumor growth. Using immunohistochemical staining to further examine tumor response to treatment, we found that the decrease in the HP lactate-to-pyruvate ratio was associated with a drop in expression of lactate dehydrogenase, the enzyme that catalyzes pyruvate to lactate conversion. Also evident was decreased staining for carbonic anhydrase IX (CA-IX), an indicator of hypoxia-inducible factor 1alpha (HIF-1alpha) activity, which, in turn, regulates expression of lactate dehydrogenase. To our knowledge, this study is the first report of the use of HP (13)C MRSI at a clinical field strength to monitor GBM response to molecularly targeted treatments. It highlights the potential of HP lactate-to-pyruvate ratio as an early biomarker of response, thereby supporting further investigation of this non-invasive imaging approach for eventual clinical application.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/21807103
      14. Call Number :
        136762
      15. Serial :
        6354
      1. Author :
        Boutte, A. M.; Friedman, D. B.; Bogyo, M.; Min, Y.; Yang, L.; Lin, P. C.
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2011
      5. Publication :
        The FASEB journal : official publication of the Federation of American Societies for Experimental Biology
      6. Products :
      7. Volume :
        25
      8. Issue :
        N/A
      9. Page Numbers :
        2626
      10. Research Area :
        N/A
      11. Keywords :
        N/A
      12. Abstract :
        Myeloid-derived suppressor cells (MDSCs) are significantly increased in cancer patients and tumor bearing-animals. MDSCs infiltrate into tumors and promote tumor invasion and metastasis. To identify the mediator responsible for the prometastatic property of MDSCs, we used proteomics. We found neutrophilic granule protein (NGP) was decreased >2-fold in MDSCs from metastatic 4T1 tumor-bearing mice compared to nonmetastatic 67NR controls. NGP mRNA levels were decreased in bone marrow and in tumor-infiltrating MDSCs by 45 and 66%, respectively, in 4T1 tumor-bearing mice compared to 67NR controls. Interestingly, 4T1-conditioned medium reduced myeloid cell NGP expression by approximately 40%, suggesting that a secreted factor mediates gene reduction. Sequence analysis shows a putative cystatin domain in NGP, and biochemical analysis confirms NGP a novel cathepsin inhibitor. It inhibited cathepsin B activity by nearly 40% in vitro. NGP expression in 4T1 tumor cells suppressed cell invasion, delayed primary tumor growth, and greatly reduced lung metastasis in vivo. A 2.8-fold reduction of cathepsin activity was found in tumors expressing NGP compared to controls. NGP significantly reduced tumor angiogenesis to 12.6 from 19.6 and lymphangiogenesis to 4.6 from 9.1 vessels/field. Necrosis was detectable only in NGP-expressing tumors, and the number of apoptotic cells increased to 22.4 from 8.3 in controls. Taken together, this study identifies a negative regulator of tumor metastasis in MDSCs, NGP, which is down-regulated in metastatic conditions. The finding suggests that malignant tumors promote invasion/metastasis not only through up-regulation of proteases but also down-regulation of protease inhibitors.-Boutte, A. M., Friedman, D. B., Bogyo, M., Min, Y., Yang, L., Lin, P. C. Identification of a myeloid-derived suppressor cell cystatin-like protein that inhibits metastasis.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/21518852
      14. Call Number :
        136372
      15. Serial :
        6367
      1. Author :
        Wu, C. C.; Lin, E. H.; Lee, Y. C.; Tai, C. J.; Kuo, T. H.; Wang, H. E.; Luo, T. Y.; Fu, Y. K.; Chen, H. J.; Sun, M. D.; Wu, C. H.; Wu, C. W.; Leu, S. J.; Deng, W. P.
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2010
      5. Publication :
        Journal of biomedicine & biotechnology
      6. Products :
      7. Volume :
        2010
      8. Issue :
        N/A
      9. Page Numbers :
        167045
      10. Research Area :
        N/A
      11. Keywords :
        N/A
      12. Abstract :
        A 12-mer amino acid peptide SATTHYRLQAAN, denominated TK4, was isolated from a phage-display library with fibrosarcoma tumor-binding activity. In vivo biodistribution analysis of TK4-displaying phage showed a significant increased phage titer in implanted tumor up to 10-fold in comparison with normal tissues after systemic administration in mouse. Competition assay confirmed that the binding of TK4-phage to tumor cells depends on the TK4 peptide. Intravenous injection of (131)I-labeled synthetic TK4 peptide in mice showed a tumor retention of 3.3% and 2.7% ID/g at 1- and 4-hour postinjection, respectively. Tumor-to-muscle ratio was 1.1, 5.7, and 3.2 at 1-, 4-, and 24-hour, respectively, and tumors were imaged on a digital gamma-camera at 4-hour postinjection. The present data suggest that TK4 holds promise as a lead structure for tumor targeting, and it could be further applied in the development of diagnostic or therapeutic agent.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/21151669
      14. Call Number :
        144472
      15. Serial :
        6368
      1. Author :
        Cain, J. W.; Hauptschein, R. S.; Stewart, J. K.; Bagci, T.; Sahagian, G. G.; Jay, D. G.
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2011
      5. Publication :
        Molecular cancer research : MCR
      6. Products :
      7. Volume :
        9
      8. Issue :
        N/A
      9. Page Numbers :
        637
      10. Research Area :
        N/A
      11. Keywords :
        N/A
      12. Abstract :
        We developed surface proteome signatures (SPS) for identification of new biomarkers playing a role in cancer drug resistance. SPS compares surface antigen expression of different cell lines by immunocytochemistry of a phage display antibody library directed to surface antigens of HT1080 fibrosarcoma cells. We applied SPS to compare the surface proteomes of two epithelial derived cancer cell lines, MCF7 and NCI/ADR-RES, which is drug resistant because of overexpression of the P-glycoprotein (P-gp) drug efflux pump. Surface proteomic profiling identified CD44 as an additional biomarker that distinguishes between these two cell lines. CD44 immunohistochemistry can distinguish between tumors derived from these lines and predict tumor response to doxorubicin in vivo. We further show that CD44 plays a role in drug resistance, independently of P-gp, in NCI/ADR-RES cells and increases expression of the antiapoptotic protein Bcl-xL. Our findings illustrate the utility of SPS to distinguish between cancer cell lines and their derived tumors and identify novel biomarkers involved in drug resistance.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/21357442
      14. Call Number :
        136582
      15. Serial :
        6373
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