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      1. Author :
        Kristof Schutters and Chris Reutelingsperger
      2. Title :
        Phosphatidylserine targeting for diagnosis and treatment of human diseases
      3. Type :
        Journal Article
      4. Year :
        2010
      5. Publication :
        Apoptosis
      6. Products :

        FMT Imaging SystemsAnnexin-Vivo

      7. Volume :
        15
      8. Issue :
        9
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        Apoptosis; Phosphatidylserine; Annexin A5; Molecular Imaging; Targeted Drug Delivery; in vivo imaging; FMT; fluorescence molecular tomography; Annexin-Vivo
      12. Abstract :
        Cells are able to execute apoptosis by activating series of specific biochemical reactions. One of the most prominent characteristics of cell death is the externalization of phosphatidylserine (PS), which in healthy cells resides predominantly in the inner leaflet of the plasma membrane. These features have made PS-externalization a well-explored phenomenon to image cell death for diagnostic purposes. In addition, it was demonstrated that under certain conditions viable cells express PS at their surface such as endothelial cells of tumor blood vessels, stressed tumor cells and hypoxic cardiomyocytes. Hence, PS has become a potential target for therapeutic strategies aiming at Targeted Drug Delivery. In this review we highlight the biomarker PS and various PS-binding compounds that have been employed to target PS for diagnostic purposes. We emphasize the 35 kD human protein annexin A5, that has been developed as a Molecular Imaging agent to measure cell death in vitro, and non-invasively in vivo in animal models and in patients with cardiovascular diseases and cancer. Recently focus has shifted from diagnostic towards therapeutic applications employing annexin A5 in strategies to deliver drugs to cells that express PS at their surface.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2929432/?tool=pubmed
      14. Call Number :
        PKI @ sarah.piper @
      15. Serial :
        4562
      1. Author :
        Hu, Guohong; Chong, Robert A; Yang, Qifeng; Wei, Yong; Blanco, Mario A; Li, Feng; Reiss, Michael; Au, Jessie L-S; Haffty, Bruce G; Kang, Yibin
      2. Title :
        MTDH activation by 8q22 genomic gain promotes chemoresistance and metastasis of poor-prognosis breast cancer
      3. Type :
        Journal Article
      4. Year :
        2009
      5. Publication :
        Cancer cell
      6. Products :

        Bioware cell lines

      7. Volume :
        15
      8. Issue :
        1
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        Aldehyde Dehydrogenase; Animals; Bioware; Breast Neoplasms; Cell Adhesion Molecules; Cell Line, Tumor; Chromosomes, Human, Pair 8; Drug Resistance, Neoplasm; Gene Expression Profiling; Genome, Human; Humans; MDA-MB-231-D3H2LN cells; Mice; Mice, Nude; Neoplasm Metastasis; Neoplasm Recurrence, Local; Prognosis; Proto-Oncogene Proteins; Proto-Oncogene Proteins c-met; Receptors, Growth Factor; Survival Rate; Xenograft Model Antitumor Assays
      12. Abstract :
        Targeted therapy for metastatic diseases relies on the identification of functionally important metastasis genes from a large number of random genetic alterations. Here we use a computational algorithm to map minimal recurrent genomic alterations associated with poor-prognosis breast cancer. 8q22 genomic gain was identified by this approach and validated in an extensive collection of breast tumor samples. Regional gain of 8q22 elevates expression of the metastasis gene metadherin (MTDH), which is overexpressed in more than 40% of breast cancers and is associated with poor clinical outcomes. Functional characterization of MTDH revealed its dual role in promoting metastatic seeding and enhancing chemoresistance. These findings establish MTDH as an important therapeutic target for simultaneously enhancing chemotherapy efficacy and reducing metastasis risk.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/19111877
      14. Call Number :
        PKI @ catherine.lautenschlager @
      15. Serial :
        8957
      1. Author :
        Palma, Joann P; Wang, Yi-Chun; Rodriguez, Luis E; Montgomery, Debra; Ellis, Paul A; Bukofzer, Gail; Niquette, Amanda; Liu, Xuesong; Shi, Yan; Lasko, Loren; Zhu, Gui-Dong; Penning, Thomas D; Giranda, Vincent L; Rosenberg, Saul H; Frost, David J; Donawho, Cherrie K
      2. Title :
        ABT-888 confers broad in vivo activity in combination with temozolomide in diverse tumors
      3. Type :
        Journal Article
      4. Year :
        2009
      5. Publication :
        Clinical cancer research: an official journal of the American Association for Cancer Research
      6. Products :

        Bioware cell lines

      7. Volume :
        15
      8. Issue :
        23
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        Animals; Antineoplastic Agents, Alkylating; Antineoplastic Combined Chemotherapy Protocols; Benzimidazoles; Bioware; Dacarbazine; DNA Damage; DNA Modification Methylases; DNA Repair; DNA Repair Enzymes; Drug Resistance, Neoplasm; Drug Screening Assays, Antitumor; Humans; MDA-MB-231-D3H2LN cells; Mice; Mice, SCID; Neoplasm Metastasis; Neoplasm Transplantation; Tumor Suppressor Proteins
      12. Abstract :
        PURPOSE ABT-888, currently in phase 2 trials, is a potent oral poly(ADP-ribose) polymerase inhibitor that enhances the activity of multiple DNA-damaging agents, including temozolomide (TMZ). We investigated ABT-888+TMZ combination therapy in multiple xenograft models representing various human tumors having different responses to TMZ. EXPERIMENTAL DESIGN ABT-888+TMZ efficacy in xenograft tumors implanted in subcutaneous, orthotopic, and metastatic sites was assessed by tumor burden, expression of poly(ADP-ribose) polymer, and O(6)-methylguanine methyltransferase (MGMT). RESULTS Varying levels of ABT-888+TMZ sensitivity were evident across a broad histologic spectrum of models (55-100% tumor growth inhibition) in B-cell lymphoma, small cell lung carcinoma, non-small cell lung carcinoma, pancreatic, ovarian, breast, and prostate xenografts, including numerous regressions. Combination efficacy in otherwise TMZ nonresponsive tumors suggests that TMZ resistance may be overcome by poly(ADP-ribose) polymerase inhibition. Profound ABT-888+TMZ efficacy was seen in experimental metastases models that acquired resistance to TMZ. Moreover, TMZ resistance was overcome in crossover treatments, indicating that combination therapy may overcome acquired TMZ resistance. Neither tumor MGMT, mismatch repair, nor poly(ADP-ribose) polymer correlated with the degree of sensitivity to ABT-888+TMZ. CONCLUSIONS Robust ABT-888+TMZ efficacy is observed across a spectrum of tumor types, including orthotopic and metastatic implantation. As many TMZ nonresponsive tumors proved sensitive to ABT-888+TMZ, this novel combination may broaden the clinical use of TMZ beyond melanoma and glioma. Although TMZ resistance may be influenced by MGMT, neither MGMT nor other mechanisms of TMZ resistance (mismatch repair) precluded sensitivity to ABT-888+TMZ. Underlying mechanisms of TMZ resistance in these models are not completely understood but likely involve mechanisms independent of MGMT.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/19934293
      14. Call Number :
        PKI @ catherine.lautenschlager @
      15. Serial :
        8954
      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 :
        Contrasting effects of sunitinib within in vivo models of metastasis
      3. Type :
        Journal Article
      4. Year :
        2012
      5. Publication :
        Angiogenesis
      6. Products :

        Bioware cell linesIVIS Imaging Systems

      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 :
        Hensley, H. H.; Roder, N. A.; O'Brien, S. W.; Bickel, L. E.; Xiao, F.; Litwin, S.; Connolly, D. C.
      2. Title :
        Combined in vivo molecular and anatomic imaging for detection of ovarian carcinoma-associated protease activity and integrin expression in mice
      3. Type :
        Journal Article
      4. Year :
        2012
      5. Publication :
        Neoplasia
      6. Products :

        ProSenseAnnexin VivoIVIS Imaging SystemsIntegriSenseMMPSenseFMT Imaging Systems

      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 :
        Rao, S. M.; Auger, J. L.; Gaillard, P.; Weissleder, R.; Wada, E.; Torres, R.; Kojima, M.; Benoist, C.; Mathis, D.; Binstadt, B. A.
      2. Title :
        The neuropeptide neuromedin U promotes autoantibody-mediated arthritis
      3. Type :
        Journal Article
      4. Year :
        2012
      5. Publication :
        Arthritis Res Ther
      6. Products :

        AngioSense

      7. Volume :
        14
      8. Issue :
        N/A
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        AngioSense, Animals; Arthritis/genetics/*immunology/metabolism; Autoantibodies/*immunology; Bone Marrow Cells/immunology/metabolism/pathology; Calcium/immunology/metabolism; Female; Male; Mast Cells/immunology/metabolism/pathology; Mice; Mice, Inbred C57BL; Mice, Inbred NOD; Mice, Knockout; Mice, Transgenic; Neuropeptides/deficiency/genetics/*immunology; Protein Isoforms/deficiency/genetics/immunology; Receptors, Neurotensin/deficiency/genetics/immunology; Receptors, Neurotransmitter/deficiency/genetics/*immunology; Spleen/immunology/metabolism/pathology
      12. Abstract :
        INTRODUCTION: Neuromedin U (NMU) is a neuropeptide with pro-inflammatory activity. The primary goal of this study was to determine if NMU promotes autoantibody-induced arthritis. Additional studies addressed the cellular source of NMU and sought to define the NMU receptor responsible for its pro-inflammatory effects. METHODS: Serum containing arthritogenic autoantibodies from K/BxN mice was used to induce arthritis in mice genetically lacking NMU. Parallel experiments examined whether NMU deficiency impacted the early mast-cell-dependent vascular leak response induced by these autoantibodies. Bone-marrow chimeric mice were generated to determine whether pro-inflammatory NMU is derived from hematopoietic cells or stromal cells. Mice lacking the known NMU receptors singly and in combination were used to determine susceptibility to serum-transferred arthritis and in vitro cellular responses to NMU. RESULTS: NMU-deficient mice developed less severe arthritis than control mice. Vascular leak was not affected by NMU deficiency. NMU expression by bone-marrow-derived cells mediated the pro-arthritogenic effect. Deficiency of all of the known NMU receptors, however, had no impact on arthritis severity and did not affect the ability of NMU to stimulate intracellular calcium flux. CONCLUSIONS: NMU-deficient mice are protected from developing autoantibody-induced inflammatory arthritis. NMU derived from hematopoietic cells, not neurons, promotes the development of autoantibody-induced inflammatory arthritis. This effect is mediated by a receptor other than the currently known NMU receptors.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/22314006
      14. Call Number :
        PKI @ kd.modi @ 13
      15. Serial :
        10438
      1. Author :
        Hsieh, C. H.; Chang, H. T.; Shen, W. C.; Shyu, W. C.; Liu, R. S.
      2. Title :
        Imaging the impact of Nox4 in cycling hypoxia-mediated U87 glioblastoma invasion and infiltration
      3. Type :
        Journal Article
      4. Year :
        2012
      5. Publication :
        Mol Imaging Biol
      6. Products :

        MMPSenseIVIS Imaging Systems

      7. Volume :
        14
      8. Issue :
        N/A
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        MMPSense, IVIS, Animals; Cell Hypoxia; Cell Line, Tumor; Cell Movement; Enzyme Activation; Extracellular Signal-Regulated MAP Kinases/metabolism; Gene Knockdown Techniques; Glioblastoma/*enzymology/*pathology; Humans; JNK Mitogen-Activated Protein Kinases/metabolism; Matrix Metalloproteinase 9/metabolism; Mice; Mice, SCID; Molecular Imaging/*methods; NADPH Oxidase/*metabolism; NF-kappa B/metabolism; Neoplasm Invasiveness; Reactive Oxygen Species/metabolism; Tumor Microenvironment; Xenograft Model Antitumor Assays
      12. Abstract :
        PURPOSE: We determined the impact of the cycling hypoxia tumor microenvironment on tumor cell invasion and infiltration in U87 human glioblastoma cells and investigated the underlying mechanisms using molecular bio-techniques and imaging. PROCEDURES: The invasive phenotype of U87 cells and xenografts exposed to experimentally imposed cycling hypoxic stress in vitro and in vivo was determined by the matrigel invasion assay in vitro and dual optical reporter gene imaging in vivo. RNAi-knockdown technology was utilized to study the role of the NADPH oxidase subunit 4 (Nox4) on cycling hypoxia-mediated tumor invasion. RESULTS: Cycling hypoxic stress significantly promoted tumor invasion in vitro and in vivo. However, Nox4 knockdown inhibited this effect. Nox4-generated reactive oxygen species (ROS) are required for cycling hypoxia-induced invasive potential in U87 cells through the activation of NF-kappaB- and ERK-mediated stimulation of MMP-9. CONCLUSIONS: Cycling hypoxia-induced ROS via Nox4 should be considered for therapeutic targeting of tumor cell invasion and infiltration in glioblastoma.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/21870211
      14. Call Number :
        PKI @ kd.modi @ 5
      15. Serial :
        10461
      1. Author :
        Phillips, W. T.; Goins, B.; Bao, A.; Vargas, D.; Guttierez, J. E.; Trevino, A.; Miller, J. R.; Henry, J.; Zuniga, R.; Vecil, G.; Brenner, A. J.
      2. Title :
        Rhenium-186 liposomes as convection-enhanced nanoparticle brachytherapy for treatment of glioblastoma
      3. Type :
        Journal Article
      4. Year :
        2012
      5. Publication :
        Neuro Oncol
      6. Products :

        Bioware cell linesIVIS Imaging Systems

      7. Volume :
        14
      8. Issue :
        N/A
      9. Page Numbers :
        416-25
      10. Research Area :
        N/A
      11. Keywords :
        U-87 MG-luc2, U-87-MG-luc2, Glioma, Bioware, IVIS, Animals; Brachytherapy/*methods; Brain Neoplasms/pathology/*radiotherapy; Convection; Glioblastoma/pathology/*radiotherapy; Glioma/pathology/*radiotherapy; Liposomes; Nanoparticles/therapeutic use; Radioisotopes/*therapeutic use; Rats; Rhenium/*therapeutic use; Tumor Burden; Xenograft Model Antitumor Assays
      12. Abstract :
        Although external beam radiation is an essential component to the current standard treatment of primary brain tumors, its application is limited by toxicity at doses more than 80 Gy. Recent studies have suggested that brachytherapy with liposomally encapsulated radionuclides may be of benefit, and we have reported methods to markedly increase the specific activity of rhenium-186 ((186)Re)-liposomes. To better characterize the potential delivery, toxicity, and efficacy of the highly specific activity of (186)Re-liposomes, we evaluated their intracranial application by convection-enhanced delivery in an orthotopic U87 glioma rat model. After establishing an optimal volume of 25 microL, we observed focal activity confined to the site of injection over a 96-hour period. Doses of up to 1850 Gy were administered without overt clinical or microscopic evidence of toxicity. Animals treated with (186)Re-liposomes had a median survival of 126 days (95% confidence interval [CI], 78.4-173 days), compared with 49 days (95% CI, 44-53 days) for controls. Log-rank analysis between these 2 groups was highly significant (P = .0013) and was even higher when 100 Gy was used as a cutoff (P < .0001). Noninvasive luciferase imaging as a surrogate for tumor volume showed a statistically significant separation in bioluminescence by 11 days after 100 Gy or less treatment between the experimental group and the control animals (chi(2)[1, N= 19] = 4.8; P = .029). MRI also supported this difference in tumor size. Duplication of tumor volume differences and survival benefit was possible in a more invasive U251 orthotopic model, with clear separation in bioluminescence at 6 days after treatment (chi(2)[1, N= 9] = 4.7; P = .029); median survival in treated animals was not reached at 120 days because lack of mortality, and log-rank analysis of survival was highly significant (P = .0057). Analysis of tumors by histology revealed minimal areas of necrosis and gliosis. These results support the potential efficacy of the highly specific activity of brachytherapy by (186)Re-liposomes convection-enhanced delivery in glioma.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/22427110
      14. Call Number :
        PKI @ kd.modi @ 2
      15. Serial :
        10500
      1. Author :
        Domanska, U. M.; Timmer-Bosscha, H.; Nagengast, W. B.; Oude Munnink, T. H.; Kruizinga, R. C.; Ananias, H. J.; Kliphuis, N. M.; Huls, G.; De Vries, E. G.; de Jong, I. J.; Walenkamp, A. M.
      2. Title :
        CXCR4 inhibition with AMD3100 sensitizes prostate cancer to docetaxel chemotherapy
      3. Type :
        Journal Article
      4. Year :
        2012
      5. Publication :
        Neoplasia
      6. Products :

        Bioware cell linesIVIS Imaging Systems

      7. Volume :
        14
      8. Issue :
        N/A
      9. Page Numbers :
        709-18
      10. Research Area :
        N/A
      11. Keywords :
        PC-3-luc2, Prostate Cancer, Bioware, IVIS
      12. Abstract :
        Several in vitro and in vivo models have revealed the key role of CXCR4/CXCL12 axis in tumor-stroma interactions. Stromal cells present in the tumor microenvironment express high levels of CXCL12 protein, directly stimulating proliferation and migration of CXCR4-expressing cancer cells. This specific prosurvival influence of stromal cells on tumor cells is thought to protect them from cytotoxic chemotherapy and is postulated as a possible explanation for the minimal residual disease in hematological and solid cancers. Therefore, CXCR4/CXCL12 signaling is an attractive therapeutic target in cancer, as proven in preclinical leukemia mouse models, where CXCR4 inhibition sensitized cancer cells to conventional chemotherapy. This study investigates whether inhibition of CXCR4 with the specific inhibitor AMD3100 sensitizes human prostate cancer cells to docetaxel. We showed that both mouse and human stromal cell lines have a protective effect on PC3-luc cells by promoting their survival after chemotherapy. Furthermore, we demonstrated that AMD3100 sensitizes PC3-luc cells to docetaxel. In a subcutaneous xenograft mouse model of human prostate carcinoma, we showed that a combination of docetaxel and AMD3100 exerts increased antitumor effect compared with docetaxel alone. We concluded that CXCR4 inhibition chemosensitizes prostate cancer cells, both in vitro and in vivo. To explore the relevance of these findings, we analyzed CXCR4 expression levels in human prostate cancer samples. We found that cancer cells present in bone metastatic lesions express higher CXCR4 levels relative to the cells present in primary tumors and lymph node metastatic lesions. These findings underscore the potential of CXCR4 inhibitors as chemosensitizing agents.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/22952424
      14. Call Number :
        PKI @ kd.modi @ 1
      15. Serial :
        10507
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