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      1. Author :
        Chantry, A. D.; Heath, D.; Mulivor, A. W.; Pearsall, S.; Baud'huin, M.; Coulton, L.; Evans, H.; Abdul, N.; Werner, E. D.; Bouxsein, M. L.; Key, M. L.; Seehra, J.; Arnett, T. R.; Vanderkerken, K.; Croucher, P.
      2. Title :
        Inhibiting activin-A signaling stimulates bone formation and prevents cancer-induced bone destruction in vivo
      3. Type :
        Journal Article
      4. Year :
        2010
      5. Publication :
        J Bone Miner Res
      6. Products :

        Bioware cell linesIVIS Imaging Systems

      7. Volume :
        25
      8. Issue :
        N/A
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        MDA-MB-231-D3H2Ln, IVIS, Bioluminescence, Activins/*metabolism; Animals; Bone Neoplasms/*complications/pathology/physiopathology/secondary; Bone Resorption/*etiology/pathology/physiopathology/*prevention & control; Calcification, Physiologic/drug effects; Cell Line, Tumor; HEK293 Cells; Humans; Mice; Multiple Myeloma/complications/pathology/physiopathology; Neoplasm Transplantation; Organ Size/drug effects; Osteoblasts/drug effects/pathology; *Osteogenesis/drug effects; Osteolysis/blood/complications/physiopathology/prevention & control; Paraproteins/metabolism; Recombinant Fusion Proteins/pharmacology; *Signal Transduction/drug effects; Survival Analysis; Tumor Burden/drug effects
      12. Abstract :
        Cancers that grow in bone, such as myeloma and breast cancer metastases, cause devastating osteolytic bone destruction. These cancers hijack bone remodeling by stimulating osteoclastic bone resorption and suppressing bone formation. Currently, treatment is targeted primarily at blocking bone resorption, but this approach has achieved only limited success. Stimulating osteoblastic bone formation to promote repair is a novel alternative approach. We show that a soluble activin receptor type IIA fusion protein (ActRIIA.muFc) stimulates osteoblastogenesis (p < .01), promotes bone formation (p < .01) and increases bone mass in vivo (p < .001). We show that the development of osteolytic bone lesions in mice bearing murine myeloma cells is caused by both increased resorption (p < .05) and suppression of bone formation (p < .01). ActRIIA.muFc treatment stimulates osteoblastogenesis (p < .01), prevents myeloma-induced suppression of bone formation (p < .05), blocks the development of osteolytic bone lesions (p < .05), and increases survival (p < .05). We also show, in a murine model of breast cancer bone metastasis, that ActRIIA.muFc again prevents bone destruction (p < .001) and inhibits bone metastases (p < .05). These findings show that stimulating osteoblastic bone formation with ActRIIA.muFc blocks the formation of osteolytic bone lesions and bone metastases in models of myeloma and breast cancer and paves the way for new approaches to treating this debilitating aspect of cancer.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/20533325
      14. Call Number :
        PKI @ kd.modi @ 4
      15. Serial :
        10413
      1. Author :
        Defresne, F.; Bouzin, C.; Grandjean, M.; Dieu, M.; Raes, M.; Hatzopoulos, A. K.; Kupatt, C.; Feron, O.
      2. Title :
        Preconditioned endothelial progenitor cells reduce formation of melanoma metastases through SPARC-driven cell-cell interactions and endocytosis
      3. Type :
        Journal Article
      4. Year :
        2011
      5. Publication :
        Cancer Res
      6. Products :

        Bioware cell linesIVIS Imaging Systems

      7. Volume :
        N/A
      8. Issue :
        N/A
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        MDA-MB-231-D3H2Ln, IVIS, Bioluminescence
      12. Abstract :
        Tumor progression is associated with the release of signaling substances from the primary tumor into the bloodstream. Tumor-derived cytokines are known to promote the mobilization and the recruitment of cells from the bone marrow, including endothelial progenitor cells (EPC). Here, we examined whether such paracrine influence could also influence the capacity of EPC to interfere with circulating metastatic cells. We therefore consecutively injected EPC pre-stimulated by tumor conditioned medium (CM-EPC) and luciferase-expressing B16 melanoma cells to mice. A net decrease in metastases spreading (vs non-stimulated EPC) led us to carry out a 2D-DIGE proteomic study to identify possible mediators of EPC-driven protection. Among 33 proteins exhibiting significant changes in expression, SPARC presented the highest induction after EPC exposure to CM. We then showed that contrary to control EPC, SPARC-silenced EPC were not able to reduce the extent of metastases when injected with B16 melanoma cells. Using adhesion tests and the hanging drop assay, we further documented that cell-cell interactions between CM-EPC and melanoma cells were promoted in a SPARC-dependent manner. This interaction led to the engulfment of melanoma cells by CM-EPC, a process prevented by SPARC silencing and mimicked by recombinant SPARC. Finally, we showed that contrary to melanoma cells, the pro-metastatic human breast cancer cell line MDA-MB231-D3H2 reduced SPARC expression in human EPC and stimulated metastases spreading. Our findings unravel the influence of tumor cells on EPC phenotypes through a SPARC-driven accentuation of macrophagic capacity associated with limitations to metastatic spread.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/21616936
      14. Call Number :
        PKI @ kd.modi @ 1
      15. Serial :
        10415
      1. Author :
        Lim, E.; Modi, K.; Christensen, A.; Meganck, J.; Oldfield, S.; Zhang, N.
      2. Title :
        Monitoring tumor metastases and osteolytic lesions with bioluminescence and micro CT imaging
      3. Type :
        Journal Article
      4. Year :
        2011
      5. Publication :
        J Vis Exp
      6. Products :

        Bioware cell lines

      7. Volume :
        N/A
      8. Issue :
        N/A
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        MDA-MB-231-D3H2Ln, IVIS, Bioluminescence, Animals; Bone Neoplasms/*secondary; Breast Neoplasms/*pathology; Cell Line, Tumor; Female; Humans; Luminescent Measurements/*methods; Mice; Mice, Nude; Neoplasm Metastasis; Neoplasm Transplantation; Tomography, X-Ray Computed/*methods; Transplantation, Heterologous
      12. Abstract :
        Following intracardiac delivery of MDA-MB-231-luc-D3H2LN cells to Nu/Nu mice, systemic metastases developed in the injected animals. Bioluminescence imaging using IVIS Spectrum was employed to monitor the distribution and development of the tumor cells following the delivery procedure including DLIT reconstruction to measure the tumor signal and its location. Development of metastatic lesions to the bone tissues triggers osteolytic activity and lesions to tibia and femur were evaluated longitudinally using micro CT. Imaging was performed using a Quantum FX micro CT system with fast imaging and low X-ray dose. The low radiation dose allows multiple imaging sessions to be performed with a cumulative X-ray dosage far below LD50. A mouse imaging shuttle device was used to sequentially image the mice with both IVIS Spectrum and Quantum FX achieving accurate animal positioning in both the bioluminescence and CT images. The optical and CT data sets were co-registered in 3-dimentions using the Living Image 4.1 software. This multi-mode approach allows close monitoring of tumor growth and development simultaneously with osteolytic activity.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/21525842
      14. Call Number :
        PKI @ kd.modi @ 5
      15. Serial :
        10416
      1. Author :
        Xu, D.; Takeshita, F.; Hino, Y.; Fukunaga, S.; Kudo, Y.; Tamaki, A.; Matsunaga, J.; Takahashi, R. U.; Takata, T.; Shimamoto, A.; Ochiya, T.; Tahara, H.
      2. Title :
        miR-22 represses cancer progression by inducing cellular senescence
      3. Type :
        Journal Article
      4. Year :
        2011
      5. Publication :
        J Cell Biol
      6. Products :

        Bioware cell lines

      7. Volume :
        193
      8. Issue :
        N/A
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        MDA-MB-231-D3H2Ln, IVIS, Bioluminescence
      12. Abstract :
        Cellular senescence acts as a barrier to cancer progression, and microRNAs (miRNAs) are thought to be potential senescence regulators. However, whether senescence-associated miRNAs (SA-miRNAs) contribute to tumor suppression remains unknown. Here, we report that miR-22, a novel SA-miRNA, has an impact on tumorigenesis. miR-22 is up-regulated in human senescent fibroblasts and epithelial cells but down-regulated in various cancer cell lines. miR-22 overexpression induces growth suppression and acquisition of a senescent phenotype in human normal and cancer cells. miR-22 knockdown in presenescent fibroblasts decreased cell size, and cells became more compact. miR-22-induced senescence also decreases cell motility and inhibits cell invasion in vitro. Synthetic miR-22 delivery suppresses tumor growth and metastasis in vivo by inducing cellular senescence in a mouse model of breast carcinoma. We confirmed that CDK6, SIRT1, and Sp1, genes involved in the senescence program, are direct targets of miR-22. Our study provides the first evidence that miR-22 restores the cellular senescence program in cancer cells and acts as a tumor suppressor.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/21502362
      14. Call Number :
        PKI @ kd.modi @ 3
      15. Serial :
        10417
      1. Author :
        Zeng, Q.; Yang, Z.; Gao, Y. J.; Yuan, H.; Cui, K.; Shi, Y.; Wang, H.; Huang, X.; Wong, S. T.; Wang, Y.; Kesari, S.; Ji, R. R.; Xu, X.
      2. Title :
        Treating triple-negative breast cancer by a combination of rapamycin and cyclophosphamide: an in vivo bioluminescence imaging study
      3. Type :
        Journal Article
      4. Year :
        2010
      5. Publication :
        Eur J Cancer
      6. Products :

        Bioware cell lines

      7. Volume :
        46
      8. Issue :
        N/A
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        MDA-MB-231-D3H2Ln, IVIS, Bioluminescence, Animals; Antineoplastic Combined Chemotherapy Protocols/*therapeutic use; Cell Hypoxia/physiology; Cell Line, Tumor; Cyclophosphamide/*therapeutic use; Female; Immunohistochemistry; Lung Neoplasms/prevention & control/secondary; Mammary Neoplasms, Experimental/*drug therapy/genetics/pathology; Mice; Mice, Nude; Sirolimus/*therapeutic use; Tumor Burden; Xenograft Model Antitumor Assays
      12. Abstract :
        Rapamycin, a mammalian target of rapamycin (mTOR) inhibitor, has been shown to inhibit the growth of oestrogen positive breast cancer. However, triple-negative (TN) breast cancer is resistant to rapamycin treatment in vitro. We set to test a combination treatment of rapamycin with DNA-damage agent, cyclophosphamide, in a TN breast cancer model. By binding to and disrupting cellular DNA, cyclophosphamide kills cells via interfering with their normal functions. We assessed the responses of nude mice bearing tumour xenografts of TN MDA-MB-231 cells to the combination of rapamycin and cyclophosphamide in both orthotopic mammary and lung-metastasis models. We tracked tumour growth and metastasis by bioluminescent imaging and examined the expression of Ki67, CD34 and HIF-1alpha in tumour tissues by immunohistochemistry and apoptosis index with TUNEL assay, and found that MDA-MB-231 cells are sensitive to rapamycin therapy in orthotopic mammary, but not in lung with metastasis. Rapamycin when combined with cyclophosphamide is found to have a more significant effect in reducing tumour volume and metastasis with a much improved survival rate. Our data also show that the sensitivity of TN tumours to rapamycin is associated with the microenvironment of the tumour cells. The data indicate that in a relatively hypoxic environment HIF-1alpha may play a role in mediating the anti-cancer effect of rapamycin and cyclophosphamide may prevent the feedback activation of Akt by rapamycin. Overall our results show that rapamycin plus cyclophosphamide can achieve an improved efficacy in suppressing tumour growth and metastasis, suggesting that the combination therapy can be a promising treatment option for TN cancer.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/20156674
      14. Call Number :
        PKI @ kd.modi @ 2
      15. Serial :
        10414
      1. Author :
        Cernak, I.
      2. Title :
        The importance of systemic response in the pathobiology of blast-induced neurotrauma
      3. Type :
        Journal Article
      4. Year :
        2010
      5. Publication :
        Front Neurol
      6. Products :

        XenoLightIVIS Imaging Systems

      7. Volume :
        1
      8. Issue :
        N/A
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        IVIS, RediJect Inflammation Probe, chemiluminescence, XenoLight
      12. Abstract :
        Due to complex injurious environment where multiple blast effects interact with the body parallel, blast-induced neurotrauma is a unique clinical entity induced by systemic, local, and cerebral responses. Activation of autonomous nervous system; sudden pressure increase in vital organs such as lungs and liver; and activation of neuroendocrine-immune system are among the most important mechanisms that contribute significantly to molecular changes and cascading injury mechanisms in the brain. It has been hypothesized that vagally mediated cerebral effects play a vital role in the early response to blast: this assumption has been supported by experiments where bilateral vagotomy mitigated bradycardia, hypotension, and apnea, and also prevented excessive metabolic alterations in the brain of animals exposed to blast. Clinical experience suggests specific blast-body-nervous system interactions such as (1) direct interaction with the head either through direct passage of the blast wave through the skull or by causing acceleration and/or rotation of the head; and (2) via hydraulic interaction, when the blast overpressure compresses the abdomen and chest, and transfers its kinetic energy to the body's fluid phase, initiating oscillating waves that traverse the body and reach the brain. Accumulating evidence suggests that inflammation plays important role in the pathogenesis of long-term neurological deficits due to blast. These include memory decline, motor function and balance impairments, and behavioral alterations, among others. Experiments using rigid body- or head protection in animals subjected to blast showed that head protection failed to prevent inflammation in the brain or reduce neurological deficits, whereas body protection was successful in alleviating the blast-induced functional and morphological impairments in the brain.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/21206523
      14. Call Number :
        PKI @ kd.modi @ 1
      15. Serial :
        10420
      1. Author :
        Cheung, R.; Shen, F.; Phillips, J. H.; McGeachy, M. J.; Cua, D. J.; Heyworth, P. G.; Pierce, R. H.
      2. Title :
        Activation of MDL-1 (CLEC5A) on immature myeloid cells triggers lethal shock in mice
      3. Type :
        Journal Article
      4. Year :
        2011
      5. Publication :
        J Clin Invest
      6. Products :

        XenoLightIVIS Imaging Systems

      7. Volume :
        121
      8. Issue :
        N/A
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        IVIS, RediJect Inflammation Probe, chemiluminescence, XenoLight, Adaptor Proteins, Signal Transducing/metabolism; Animals; Cell Differentiation; Concanavalin A/toxicity; Dengue Hemorrhagic Fever/etiology; Disease Models, Animal; Disease Progression; Female; Humans; Immunity, Innate; Intracellular Signaling Peptides and Proteins/metabolism; Lectins, C-Type/deficiency/genetics/*immunology; Liver/metabolism/pathology; Mice; Mice, Inbred C57BL; Mice, Knockout; Models, Immunological; Myeloid Cells/*immunology/pathology; Nitric Oxide/biosynthesis; Nitric Oxide Synthase Type II/metabolism; Nitric Oxide Synthase Type III/metabolism; Phosphatidylinositol 3-Kinases/metabolism; Protein-Tyrosine Kinases/metabolism; Proto-Oncogene Proteins c-akt/metabolism; Receptors, Cell Surface/deficiency/genetics/*immunology; Receptors, Immunologic/metabolism; Shock/*etiology/*immunology/metabolism/pathology; Signal Transduction; Systemic Inflammatory Response; Syndrome/etiology/immunology/metabolism/pathology; Tumor Necrosis Factor-alpha/biosynthesis
      12. Abstract :
        Systemic inflammatory response syndrome (SIRS) is a potentially lethal condition, as it can progress to shock, multi-organ failure, and death. It can be triggered by infection, tissue damage, or hemorrhage. The role of tissue injury in the progression from SIRS to shock is incompletely understood. Here, we show that treatment of mice with concanavalin A (ConA) to induce liver injury triggered a G-CSF-dependent hepatic infiltration of CD11b+Gr-1+Ly6G+Ly6C+ immature myeloid cells that expressed the orphan receptor myeloid DAP12-associated lectin-1 (MDL-1; also known as CLEC5A). Activation of MDL-1 using dengue virus or an agonist MDL-1-specific antibody in the ConA-treated mice resulted in shock. The MDL-1+ cells were pathogenic, and in vivo depletion of MDL-1+ cells provided protection. Triggering MDL-1 on these cells induced production of NO and TNF-alpha, which were found to be elevated in the serum of treated mice and required for MDL-1-induced shock. Surprisingly, MDL-1-induced NO and TNF-alpha production required eNOS but not iNOS. Activation of DAP12, DAP10, Syk, PI3K, and Akt was critical for MDL-1-induced shock. In addition, Akt physically interacted with and activated eNOS. Therefore, triggering of MDL-1 on immature myeloid cells and production of NO and TNF-alpha may play a critical role in the pathogenesis of shock. Targeting the MDL-1/Syk/PI3K/Akt/eNOS pathway represents a potential new therapeutic strategy to prevent the progression of SIRS to shock.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/22005300
      14. Call Number :
        PKI @ kd.modi @ 2
      15. Serial :
        10421
      1. Author :
        Lee, H. L.; Chen, C. C.; Baasov, T.; Ron, Y.; Dougherty, J. P.
      2. Title :
        Post-transcriptionally regulated expression system in human xenogeneic transplantation models
      3. Type :
        Journal Article
      4. Year :
        2011
      5. Publication :
        Mol Ther
      6. Products :

        XenoLight

      7. Volume :
        19
      8. Issue :
        N/A
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        RediJect Coelenterazine h, XenoLight
      12. Abstract :
        Cells have developed a mechanism to discriminate between premature termination codons (PTCs) and normal stop codons during translation, sparking vigorous research to develop drugs promoting readthrough at PTCs to treat genetic disorders caused by PTCs. It was posed that this concept could also be applied to regulated gene therapy protocols by incorporating a PTC into a therapeutic gene, so active protein would only be made after administration of a readthrough agent. The strengths of the system are highlighted here by results demonstrating: (i) background expression levels were reduced to 0.01% to 0.0005% of wild type in unselected mass populations of cells depending upon the specific stop codon utilized and its position within the gene; (ii) expression levels responded well to multiple “On” and “Off” regulation cycles in vivo in human xenograft systems; (iii) the level of induction approached three logs using aminoglycoside activators including NB54, a newly synthesized aminoglycoside with significantly reduced toxicity; and (iv) expression levels could be appreciably altered when employing different promoters in a variety of cell types. These results strongly support the contention that this system should have important clinical applications when tight control of gene expression is required.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/21587212
      14. Call Number :
        PKI @ kd.modi @ 1
      15. Serial :
        10422
      1. Author :
        Vandamme, M.; Robert, E.; Lerondel, S.; Sarron, V.; Ries, D.; Dozias, S.; Sobilo, J.; Gosset, D.; Kieda, C.; Legrain, B.; Pouvesle, J. M.; Pape, A. L.
      2. Title :
        ROS implication in a new antitumor strategy based on non-thermal plasma
      3. Type :
        Journal Article
      4. Year :
        2011
      5. Publication :
        Int J Cancer
      6. Products :

        Bioware cell linesIVIS Imaging Systems

      7. Volume :
        N/A
      8. Issue :
        N/A
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        U87-MG-luc2, U-87-MG-luc2, U87MG-luc2, Bioluminescence, Glioma, IVIS
      12. Abstract :
        Non-thermal plasma (NTP) is generated by ionizing neutral gas molecules/atoms leading to a highly reactive gas at ambient temperature containing excited molecules, reactive species and generating transient electric fields. Given its potential to interact with tissue or cells without a significant temperature increase, NTP appears as a promising approach for the treatment of various diseases including cancer. The aim of our study was to evaluate the interest of NTP both in vitro and in vivo. To this end, we evaluated the antitumor activity of NTP in vitro on two human cancer cell lines (glioblastoma U87MG and colorectal carcinoma HCT-116). Our data showed that NTP generated a large amount of reactive oxygen species (ROS), leading to the formation of DNA damages. This resulted in a multiphase cell cycle arrest and a subsequent apoptosis induction. In addition, in vivo experiments on U87MG bearing mice showed that NTP induced a reduction of bioluminescence and tumor volume as compared to nontreated mice. An induction of apoptosis was also observed together with an accumulation of cells in S phase of the cell cycle suggesting an arrest of tumor proliferation. In conclusion, we demonstrated here that the potential of NTP to generate ROS renders this strategy particularly promising in the context of tumor treatment.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/21702038
      14. Call Number :
        PKI @ kd.modi @ 1
      15. Serial :
        10424
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