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      1. Author :
        Yigit, M. V.; Ghosh, S. K.; Kumar, M.; Petkova, V.; Kavishwar, A.; Moore, A.; Medarova, Z.
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2012
      5. Publication :
        Oncogene
      6. Products :
      7. Volume :
        N/A
      8. Issue :
        N/A
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        MDA-MB-231-luc-D3H2Ln, D3H2Ln, Bioware, IVIS
      12. Abstract :
        Metastases, and not the primary tumor from which they originate, are the main reason for mortality from carcinoma. Although the molecular mechanisms behind metastasis are poorly understood, it is clear that epigenetic dysregulation at the level of microRNA expression is a key characteristic of the metastatic process that can be exploited for therapy. Here, we describe an miRNA-targeted therapeutic approach for the prevention and arrest of lymph node metastasis. Therapy relies on the inhibition of the pro-metastatic microRNA-10b. It is delivered to primary and lymph node metastatic tumor cells using an imaging-capable nanodrug that is designed to specifically home to these tissues. Treatment of invasive human breast tumor cells (MDA-MB-231) with the nanodrug in vitro downregulates miR-10b and abolishes the invasion and migration of the tumor cells. After intravenous delivery to mice bearing orthotopic MDA-MB-231-luc-D3H2LN tumors, the nanodrug accumulates in the primary tumor and lymph nodes. When treatment is initiated before metastasis to lymph nodes, metastasis is prevented. Treatment after the formation of lymph node metastases arrests the metastatic process without a concomitant effect on primary tumor growth raising the possibility of a context-dependent variation in miR-10b breast oncogenesis.Oncogene advance online publication, 14 May 2012; doi:10.1038/onc.2012.173.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/22580603
      14. Call Number :
        PKI @ kd.modi @ 9
      15. Serial :
        10505
      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 :
      3. Type :
        Journal Article
      4. Year :
        2012
      5. Publication :
        Angiogenesis
      6. Products :
      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 :
        Cheng, H. H.; Kuo, C. C.; Yan, J. L.; Chen, H. L.; Lin, W. C.; Wang, K. H.; Tsai, K. K.; Guven, H.; Flaberg, E.; Szekely, L.; Klein, G.; Wu, K. K.
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2012
      5. Publication :
        Proc Natl Acad Sci U S A
      6. Products :
      7. Volume :
        109
      8. Issue :
        N/A
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        A549-luc-C8, A549-luc, IVIS, Bioware, Acetylserotonin O-Methyltransferase/metabolism; Animals; Biocatalysis/drug effects; Cell Line, Tumor; Cell Movement/drug effects; Cell Proliferation/drug effects; Cell Transformation, Neoplastic/drug effects/*pathology; Cyclooxygenase 2/*metabolism; Cyclooxygenase 2 Inhibitors/pharmacology; Fibroblasts/drug effects/metabolism; Humans; Metabolic Networks and Pathways/drug effects; Metabolomics; Mice; Neoplasm Metastasis; Solubility/drug effects; Subcellular Fractions/drug effects/metabolism; Tryptophan/*analogs & derivatives/biosynthesis/metabolism/pharmacology; Tryptophan Hydroxylase/metabolism; Xenograft Model Antitumor Assays
      12. Abstract :
        Cyclooxygenase-2 (COX-2) expression is induced by mitogenic and proinflammatory factors. Its overexpression plays a causal role in inflammation and tumorigenesis. COX-2 expression is tightly regulated, but the mechanisms are largely unclear. Here we show the control of COX-2 expression by an endogenous tryptophan metabolite, 5-methoxytryptophan (5-MTP). By using comparative metabolomic analysis and enzyme-immunoassay, our results reveal that normal fibroblasts produce and release 5-MTP into the extracellular milieu whereas A549 and other cancer cells were defective in 5-MTP production. 5-MTP was synthesized from L-tryptophan via tryptophan hydroxylase-1 and hydroxyindole O-methyltransferase. 5-MTP blocked cancer cell COX-2 overexpression and suppressed A549 migration and invasion. Furthermore, i.p. infusion of 5-MTP reduced tumor growth and cancer metastasis in a murine xenograft tumor model. We conclude that 5-MTP synthesis represents a mechanism for endogenous control of COX-2 overexpression and is a valuable lead for new anti-cancer and anti-inflammatory drug development.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/22851770
      14. Call Number :
        PKI @ kd.modi @ 4
      15. Serial :
        10521
      1. Author :
        Rocks, N.; Bekaert, S.; Coia, I.; Paulissen, G.; Gueders, M.; Evrard, B.; Van Heugen, J. C.; Chiap, P.; Foidart, J. M.; Noel, A.; Cataldo, D.
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2012
      5. Publication :
        Br J Cancer
      6. Products :
      7. Volume :
        107
      8. Issue :
        N/A
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        LL/2-luc-M38, LL/2-luc, Lewis Lung Carcinoma, IVIS
      12. Abstract :
        BACKGROUND: Overall clinical outcome for advanced lung cancer remains very disappointing despite recent advances in treatment. Curcumin has been reported as potentially active against cancer. METHODS: Owing to poor curcumin solubility, we have used cyclodextrins (CD) as an excipient allowing a considerable increase of aqueous solubility and bioavailability of curcumin. The effects of solubilised curcumin have been evaluated in cell cultures as well as in an in vivo orthotopic lung tumour mouse model. RESULTS: Cell proliferation was reduced while apoptosis rates were increased when lung epithelial tumour cells were cultured in the presence of curcumin-CD complexes. For in vivo experiments, cells were grafted into lungs of C57Bl/6 mice treated by an oral administration of a non-soluble form of curcumin, CDs alone or curcumin-CD complexes, combined or not with gemcitabine. The size of orthotopically implanted lung tumours was reduced upon curcumin complex administration as compared with treatments with placebo or non-solubilised curcumin. Moreover, curcumin potentiated the gemcitabine-mediated antitumour effects. CONCLUSION: Our data demonstrate that curcumin, when given orally in a CD-solubilised form, reduces lung tumour size in vivo. In vitro experiments show impaired tumour cell proliferation and increased cell apoptosis. Moreover, our data underline a potential additive effect of curcumin with gemcitabine thus providing an efficient therapeutic option for antilung cancer therapy.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/22929882
      14. Call Number :
        PKI @ kd.modi @ 3
      15. Serial :
        10545
      1. Author :
        Wallis de Vries BM, van Dam GM, Tio RA, Hillebrands JL, Slart RH and Zeebregts CJ
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2008
      5. Publication :
        Journal of Vascular Surgery
      6. Products :
      7. Volume :
        48
      8. Issue :
        6
      9. Page Numbers :
        N/A
      10. Research Area :
        Cardiovascular Research
      11. Keywords :
        In vivo imaging; MMPSense; atherosclerotic carotid plaque
      12. Abstract :
        BACKGROUND: There is increasing evidence that plaque vulnerability, rather than the degree of stenosis, is important in predicting the occurrence of subsequent cerebral ischemic events in patients with carotid artery stenosis. The many imaging modalities currently available have different properties with regard to the visualization of the extent of vulnerability in carotid plaque formation.

        METHODS: Original published studies were identified using the MEDLINE database (January 1966 to March 2008). Manual cross-referencing was also performed.

        RESULTS: There is no single imaging modality that can produce definitive information about the state of vulnerability of an atherosclerotic plaque. Each has its own specific drawbacks, which may be the use of ionizing radiation or nephrotoxic contrast agents, an invasive character, low patient tolerability, or simply the paucity of information obtained on plaque vulnerability. Functional molecular imaging techniques such as positron emission tomography (PET), single photon emission-computed tomography (SPECT) and near infra-red spectroscopy (NIRS) do seem able accurately to visualize and even quantify features of plaque vulnerability and its pathophysiologic processes. Promising new techniques like near infra-red fluorescence imaging are being developed and may be beneficial in this field.

        CONCLUSION: There is a promising role for functional molecular imaging modalities like PET, SPECT, or NIRS related to improvement of selection criteria for carotid intervention, especially when combined with CT or MRI to add further anatomical details to molecular information. Further information will be needed to define whether and where this functional molecular imaging will fit into a clinical strategy.
      13. URL :
        http://www.jvascsurg.org/article/S0741-5214(08)01146-4/abstract
      14. Call Number :
        PKI @ sarah.piper @
      15. Serial :
        4643
      1. Author :
        Wallis de Vries, B. M.; van Dam, G. M.; Tio, R. A.; Hillebrands, J. L.; Slart, R. H.; Zeebregts, C. J.
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2008
      5. Publication :
        J Vasc Surg
      6. Products :
      7. Volume :
        48
      8. Issue :
        N/A
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        MMPSense, IVIS, Atherosclerosis/complications/*diagnosis; Carotid Stenosis/*diagnosis/etiology; Diagnostic Imaging/*methods; Humans; Reproducibility of Results
      12. Abstract :
        BACKGROUND: There is increasing evidence that plaque vulnerability, rather than the degree of stenosis, is important in predicting the occurrence of subsequent cerebral ischemic events in patients with carotid artery stenosis. The many imaging modalities currently available have different properties with regard to the visualization of the extent of vulnerability in carotid plaque formation. METHODS: Original published studies were identified using the MEDLINE database (January 1966 to March 2008). Manual cross-referencing was also performed. RESULTS: There is no single imaging modality that can produce definitive information about the state of vulnerability of an atherosclerotic plaque. Each has its own specific drawbacks, which may be the use of ionizing radiation or nephrotoxic contrast agents, an invasive character, low patient tolerability, or simply the paucity of information obtained on plaque vulnerability. Functional molecular imaging techniques such as positron emission tomography (PET), single photon emission-computed tomography (SPECT) and near infra-red spectroscopy (NIRS) do seem able accurately to visualize and even quantify features of plaque vulnerability and its pathophysiologic processes. Promising new techniques like near infra-red fluorescence imaging are being developed and may be beneficial in this field. CONCLUSION: There is a promising role for functional molecular imaging modalities like PET, SPECT, or NIRS related to improvement of selection criteria for carotid intervention, especially when combined with CT or MRI to add further anatomical details to molecular information. Further information will be needed to define whether and where this functional molecular imaging will fit into a clinical strategy.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/18804942
      14. Call Number :
        PKI @ kd.modi @ 6
      15. Serial :
        10464
      1. Author :
        Albanesi, M.; Mancardi, D. A.; Macdonald, L. E.; Iannascoli, B.; Zitvogel, L.; Murphy, A. J.; Leusen, J. H.; Bruhns, P.
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2012
      5. Publication :
        J Immunol
      6. Products :
      7. Volume :
        189
      8. Issue :
        N/A
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        B16-F10-luc2, B16F10-luc2, IVIS
      12. Abstract :
        mAb therapy for experimental metastatic melanoma relies on activating receptors for the Fc portion of IgG (FcgammaR). Opposing results on the respective contribution of mouse FcgammaRI, FcgammaRIII, and FcgammaRIV have been reported using the gp75-expressing B16 melanoma and the protective anti-gp75 mAb TA99. We analyzed the contribution of FcgammaRs to this therapy model using bioluminescent measurement of lung metastases loads, novel mouse strains, and anti-FcgammaR blocking mAbs. We found that the TA99 mAb-mediated effects in a combination therapy using cyclophosphamide relied on activating FcgammaRs. The combination therapy, however, was not more efficient than mAb therapy alone. We demonstrate that FcgammaRI and, unexpectedly, FcgammaRIII contributed to TA99 mAb therapeutic effects, whereas FcgammaRIV did not. Therefore, FcgammaRIII and FcgammaRI are, together, responsible for anti-gp75 mAb therapy of B16 lung metastases. Our finding that mouse FcgammaRIII contributes to Ab-induced tumor reduction correlates with clinical data on its human functional equivalent human FcgammaRIIIA (CD16A).
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/23150715
      14. Call Number :
        PKI @ kd.modi @ 8
      15. Serial :
        10482
      1. Author :
        Balibar, Carl J; Shen, Xiaoyu; McGuire, Dorothy; Yu, Donghui; McKenney, David; Tao, Jianshi
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2010
      5. Publication :
        Microbiology (Reading, England)
      6. Products :
      7. Volume :
        156
      8. Issue :
        Pt 5
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        Animals; Anti-Bacterial Agents; Bacterial Proteins; Bacteriolysis; Bioware; Cell Wall; Gene Expression Profiling; Gene Knockout Techniques; Genes, Reporter; Lysostaphin; Mice; Microbial Sensitivity Tests; Sepsis; Staphylococcus aureus; Virulence; Xen29
      12. Abstract :
        Transcriptional profiling data accumulated in recent years for the clinically relevant pathogen Staphylococcus aureus have established a cell wall stress stimulon, which comprises a coordinately regulated set of genes that are upregulated in response to blockage of cell wall biogenesis. In particular, the expression of cwrA (SA2343, N315 notation), which encodes a putative 63 amino acid polypeptide of unknown biological function, increases over 100-fold in response to cell wall inhibition. Herein, we seek to understand the biological role that this gene plays in S. aureus. cwrA was found to be robustly induced by all cell wall-targeting antibiotics tested – vancomycin, oxacillin, penicillin G, phosphomycin, imipenem, hymeglusin and bacitracin – but not by antibiotics with other mechanisms of action, including ciprofloxacin, erythromycin, chloramphenicol, triclosan, rifampicin, novobiocin and carbonyl cyanide 3-chlorophenylhydrazone. Although a DeltacwrA S. aureus strain had no appreciable shift in MICs for cell wall-targeting antibiotics, the knockout was shown to have reduced cell wall integrity in a variety of other assays. Additionally, the gene was shown to be important for virulence in a mouse sepsis model of infection.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/20167623
      14. Call Number :
        PKI @ catherine.lautenschlager @
      15. Serial :
        9037
      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 :
      3. Type :
        Journal Article
      4. Year :
        2012
      5. Publication :
        Neoplasia
      6. Products :
      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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