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      1. Author :
        Matsumoto, K.; Azami, T.; Otsu, A.; Takase, H.; Ishitobi, H.; Tanaka, J.; Miwa, Y.; Takahashi, S.; Ema, M.
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2012
      5. Publication :
        Genesis
      6. Products :
      7. Volume :
        50
      8. Issue :
        N/A
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        AngioSense, Animals; Blood Vessels/embryology/*physiology; Chromosomes, Artificial, Bacterial; Embryo, Mammalian; Endothelial Cells/cytology/metabolism; Endothelium, Vascular/cytology/embryology/metabolism; Female; Founder Effect; Gene Expression Regulation, Developmental; Genes, Reporter; Mice; *Mice, Transgenic; Microscopy, Fluorescence; Morphogenesis/physiology; *Neovascularization, Pathologic; *Neovascularization, Physiologic; Retina/embryology/*physiology; Vascular Endothelial Growth Factor A/genetics/metabolism; Vascular Endothelial Growth Factor Receptor-1/genetics/*metabolism; Vascular Endothelial Growth Factor Receptor-2/genetics/metabolism
      12. Abstract :
        Blood vessel development and network patterning are controlled by several signaling molecules, including VEGF, FGF, TGF-ss, and Ang-1,2. Among these, the role of VEGF-A signaling in vessel morphogenesis is best understood. The biological activity of VEGF-A depends on its reaction with specific receptors Flt1 and Flk1. Roles of VEGF-A signaling in endothelial cell proliferation, migration, survival, vascular permeability, and induction of tip cell filopodia have been reported. In this study, we have generated Flt1-tdsRed BAC transgenic (Tg) mice to monitor Flt1 gene expression during vascular development. We show that tdsRed fluorescence is observed within blood vessels of adult mice and embryos, indicative of retinal angiogenesis and tumor angiogenesis. Flt1 expression recapitulated by Flt1-tdsRed BAC Tg mice overlapped well with Flk1, while Flt1 was expressed more abundantly in endothelial cells of large blood vessels such as dorsal aorta and presumptive stalk cells in retina, providing a unique model to study blood vessel development.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/22489010
      14. Call Number :
        PKI @ kd.modi @ 10
      15. Serial :
        10437
      1. Author :
        Zhuang, H.; Jiang, W.; Zhang, X.; Qiu, F.; Gan, Z.; Cheng, W.; Zhang, J.; Guan, S.; Tang, B.; Huang, Q.; Wu, X.; Huang, X.; Hu, Q.; Lu, M.; Hua, Z. C.
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2012
      5. Publication :
        J Mol Med (Berl)
      6. Products :
      7. Volume :
        N/A
      8. Issue :
        N/A
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        A549-luc-C8, A549-luc, IVIS, Bioware
      12. Abstract :
        Many cancer cell types are resistant to tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-induced apoptosis. Here, we examined whether HSP70 suppression by small interfering RNA (siRNA) sensitized non-small cell lung cancer (NSCLC) cells to TRAIL-induced apoptosis and the underlying mechanisms. We demonstrated that HSP70 suppression by siRNA sensitized NSCLC cells to TRAIL-induced apoptosis by upregulating the expressions of death receptor 4 (DR4) and death receptor 5 (DR5) through activating NF-kappaB, JNK, and, subsequently, p53, consequently significantly amplifying TRAIL-mediated caspase-8 processing and activity, cytosolic translocation of cytochrome c, and cell death. Consistently, the pro-apoptotic proteins Bad and Bax were upregulated, while the anti-apoptotic protein Bcl-2 was downregulated. The luciferase activity of the DR4 promoter was blocked by a NF-kappaB pathway inhibitor BAY11-7082, suggesting that NF-kappaB activation plays an important role in the transcriptional upregulation of DR4. Additionally, HSP70 suppression inhibited the phosphorylation of ERK, AKT, and PKC, thereby downregulating c-FLIP-L. A549 xenografts in mice receiving HSP70 siRNA showed TRAIL-induced cell death and increased DR4/DR5 levels and reduced tumor growth. The combination of psiHSP70 gene therapy with TRAIL also significantly increased the survival benefits induced by TRAIL therapy alone. Interestingly, HSP27 siRNA and TRAIL together could not suppress tumor growth or prolong the survival of tumor-bearing mice significantly, although the combination could efficiently induce the apoptosis of A549 cells in vitro. Our findings suggest that HSP70 suppression or downregulation might be promising to overcome TRAIL resistance in cancer.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/22948392
      14. Call Number :
        PKI @ kd.modi @ 2
      15. Serial :
        10526
      1. Author :
        Evans, L.; Williams, A. S.; Hayes, A. J.; Jones, S. A.; Nowell, M.
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2011
      5. Publication :
        Arthritis Rheum
      6. Products :
      7. Volume :
        63
      8. Issue :
        N/A
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        MMPSense, IVIS, Acrylamides/pharmacology/*therapeutic use; Animals; Arthritis, Experimental/*drug therapy/metabolism/pathology; Cartilage/*metabolism/pathology; Fibroblasts/metabolism/pathology; Humans; Inflammation/metabolism/pathology; Leukocytes/*drug effects/metabolism/pathology; Mice; Nicotinamide Phosphoribosyltransferase/*antagonists & inhibitors; Piperidines/pharmacology/*therapeutic use
      12. Abstract :
        OBJECTIVE: To assess the ability of pre-B cell colony-enhancing factor (PBEF) to regulate inflammation and degradative processes in inflammatory arthritis, using the small molecule inhibitor APO866 in human fibroblasts in vitro and in murine collagen-induced arthritis (CIA). METHODS: Enzyme-linked immunosorbent assays were used to examine regulation of expression of metalloproteinases and chemokines in human fibroblasts. The role of PBEF was further examined using APO866 in mice with CIA, with effects on disease activity assessed using radiography, histology, in vivo imaging, and quantitative polymerase chain reaction (qPCR). RESULTS: In vitro activation of human fibroblasts with PBEF promoted expression of matrix metalloproteinase 3 (MMP-3), CCL2, and CXCL8, an effect inhibited by APO866. In mice with CIA, early intervention with APO866 inhibited synovial inflammation, including chemokine-directed leukocyte infiltration, and reduced a systemic marker of inflammation, serum hyaluronic acid. APO866 blockade led to reduced expression of MMP-3 and MMP-13 in joint extracts and to a reduction in a systemic marker of cartilage erosion, serum cartilage oligomeric matrix protein. Radiologic images revealed that APO866 protected against bone erosion, while qPCR demonstrated inhibition of RANKL expression. In mice with established disease, APO866 reduced synovial inflammation and cartilage destruction, and halted bone erosion. In addition, APO866 reduced the activity of MMP-3, CCL2, and RANKL in vivo, and inhibited production of CCL2 and RANKL in synovial explants from arthritic mice, a result that was reversed with nicotinamide mononucleotide. CONCLUSION: These findings confirm PBEF to be an important regulator of inflammation, cartilage catabolism, and bone erosion, and highlight APO866 as a promising therapeutic agent for targeting PBEF activity in inflammatory arthritis.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/21400478
      14. Call Number :
        PKI @ kd.modi @ 2
      15. Serial :
        10460
      1. Author :
        Yang, Li; Johansson, Jan; Ridsdale, Ross; Willander, Hanna; Fitzen, Michael; Akinbi, Henry T; Weaver, Timothy E
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2010
      5. Publication :
        Journal of immunology (Baltimore, Md.: 1950)
      6. Products :
      7. Volume :
        184
      8. Issue :
        2
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        Animals; Anti-Bacterial Agents; Bronchoalveolar Lavage Fluid; Hydrogen-Ion Concentration; Immunity, Innate; Klebsiella pneumoniae; Macrophages, Alveolar; Mice; Mice, Transgenic; Protein Precursors; Protein Structure, Tertiary; Proteolipids; Saposins; Staphylococcus aureus; Tissue Distribution; Xen5
      12. Abstract :
        Surfactant protein B (SP-B) proprotein contains three saposin-like protein (SAPLIP) domains: a SAPLIP domain corresponding to the mature SP-B peptide is essential for lung function and postnatal survival; the function of SAPLIP domains in the N-terminal (SP-BN) and C-terminal regions of the proprotein is not known. In the current study, SP-BN was detected in the supernatant of mouse bronchoalveolar lavage fluid (BALF) and in nonciliated bronchiolar cells, alveolar type II epithelial cells, and alveolar macrophages. rSP-BN indirectly promoted the uptake of bacteria by macrophage cell lines and directly killed bacteria at acidic pH, consistent with a lysosomal, antimicrobial function. Native SP-BN isolated from BALF also killed bacteria but only at acidic pH; the bactericidal activity of BALF at acidic pH was completely blocked by SP-BN Ab. Transgenic mice overexpressing SP-BN and mature SP-B peptide had significantly decreased bacterial burden and increased survival following intranasal inoculation with bacteria. These findings support the hypothesis that SP-BN contributes to innate host defense of the lung by supplementing the nonoxidant antimicrobial defenses of alveolar macrophages.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/20007532
      14. Call Number :
        PKI @ catherine.lautenschlager @
      15. Serial :
        9995
      1. Author :
        Tafreshi, N. K.; Huang, X.; Moberg, V. E.; Barkey, N. M.; Sondak, V. K.; Tian, H.; Morse, D. L.; Vagner, J.
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2012
      5. Publication :
        Bioconjug Chem
      6. Products :
      7. Volume :
        23
      8. Issue :
        N/A
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        IVIS, B16-F10-luc-G5, B16F10-luc-G5, B16-F10-luc, B16F10-luc
      12. Abstract :
        The incidence of malignant melanoma is rising more rapidly than that of any other cancer in the United States. The melanocortin 1 receptor (MC1R) is overexpressed in most human melanoma metastases, thus making it a promising target for imaging and therapy of melanomas. We have previously reported the development of a peptidomimetic ligand with high specificity and affinity for MC1R. Here, we have conjugated near-infrared fluorescent dyes to the C-terminus of this ligand via lysine-mercaptopropionic acid linkers to generate MC1R specific optical probes (MC1RL-800, 0.4 nM K(i); and MC1RL-Cy5, 0.3 nM K(i)). Internalization of the imaging probe was studied in vitro by fluorescence microscopy using engineered A375/MC1R cells and B16F10 cells with endogenous MC1R expression. The in vivo tumor targeting of MC1RL-800 was evaluated by intravenous injection of probe into nude mice bearing bilateral subcutaneous A375 xenograft tumors with low MC1R expression and engineered A375/MC1R tumors with high receptor expression. Melanotic B16F10 xenografts were also studied. Fluorescence imaging showed that the agent has higher uptake values in tumors with high expression compared to low (p < 0.05), demonstrating the effect of expression levels on image contrast-to-noise. In addition, tumor uptake was significantly blocked by coinjection of excess NDP-alpha-MSH peptide (p < 0.05). In conclusion, the MC1R-specific imaging probe developed in this study displays excellent potential for the intraoperative detection of regional node involvement and for margin detection during melanoma metastasis resection.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/23116461
      14. Call Number :
        PKI @ kd.modi @ 18
      15. Serial :
        10535
      1. Author :
        Qamri, Zahida; Preet, Anju; Nasser, Mohd W; Bass, Caroline E; Leone, Gustavo; Barsky, Sanford H; Ganju, Ramesh K
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2009
      5. Publication :
        Molecular cancer therapeutics
      6. Products :
      7. Volume :
        8
      8. Issue :
        11
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        Animals; Apoptosis; Benzoxazines; Bioware; Breast Neoplasms; Cannabinoids; Cell Cycle; Cell Growth Processes; Cell Line, Tumor; Cell Movement; Cyclooxygenase 2; Dinoprostone; Female; Humans; Immunohistochemistry; Lung Neoplasms; Male; Mammary Neoplasms, Experimental; MDA-MB-231-D3H2LN cells; Mice; Mice, Inbred C3H; Mice, SCID; Mice, Transgenic; Microscopy, Confocal; Morpholines; Naphthalenes; Neoplasm Metastasis; Neovascularization, Pathologic; Receptor, Cannabinoid, CB1; Receptor, Cannabinoid, CB2; RNA, Small Interfering; Signal Transduction; Transfection; Xenograft Model Antitumor Assays
      12. Abstract :
        Cannabinoids have been reported to possess antitumorogenic activity. Not much is known, however, about the effects and mechanism of action of synthetic nonpsychotic cannabinoids on breast cancer growth and metastasis. We have shown that the cannabinoid receptors CB1 and CB2 are overexpressed in primary human breast tumors compared with normal breast tissue. We have also observed that the breast cancer cell lines MDA-MB231, MDA-MB231-luc, and MDA-MB468 express CB1 and CB2 receptors. Furthermore, we have shown that the CB2 synthetic agonist JWH-133 and the CB1 and CB2 agonist WIN-55,212-2 inhibit cell proliferation and migration under in vitro conditions. These results were confirmed in vivo in various mouse model systems. Mice treated with JWH-133 or WIN-55,212-2 showed a 40% to 50% reduction in tumor growth and a 65% to 80% reduction in lung metastasis. These effects were reversed by CB1 and CB2 antagonists AM 251 and SR144528, respectively, suggesting involvement of CB1 and CB2 receptors. In addition, the CB2 agonist JWH-133 was shown to delay and reduce mammary gland tumors in the polyoma middle T oncoprotein (PyMT) transgenic mouse model system. Upon further elucidation, we observed that JWH-133 and WIN-55,212-2 mediate the breast tumor-suppressive effects via a coordinated regulation of cyclooxygenase-2/prostaglandin E2 signaling pathways and induction of apoptosis. These results indicate that CB1 and CB2 receptors could be used to develop novel therapeutic strategies against breast cancer growth and metastasis.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/19887554
      14. Call Number :
        PKI @ catherine.lautenschlager @
      15. Serial :
        8953
      1. Author :
        N/A
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2010
      5. Publication :
        Journal of immunology (Baltimore, Md.: 1950)
      6. Products :
      7. Volume :
        184
      8. Issue :
        5
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        Amino Acid Sequence; Animals; Antimicrobial Cationic Peptides; Bacterial Infections; Bioware; Cell Line; Cells, Cultured; Chemokine CCL2; Chemokine CCL7; Chemokine CXCL1; Chemokines; Female; Humans; Interleukin-8; Leukocytes; Leukocytes, Mononuclear; Macrophages; Mice; Mice, Inbred C57BL; Molecular Sequence Data; NF-kappa B; p38 Mitogen-Activated Protein Kinases; Phosphatidylinositol 3-Kinases; Phosphorylation; Staphylococcal Infections; Staphylococcus aureus; Xen29, Xen14
      12. Abstract :
        With the rapid rise in the incidence of multidrug resistant infections, there is substantial interest in host defense peptides as templates for production of new antimicrobial therapeutics. Natural peptides are multifunctional mediators of the innate immune response, with some direct antimicrobial activity and diverse immunomodulatory properties. We have previously developed an innate defense regulator (IDR) 1, with protective activity against bacterial infection mediated entirely through its effects on the immunity of the host, as a novel approach to anti-infective therapy. In this study, an immunomodulatory peptide IDR-1002 was selected from a library of bactenecin derivatives based on its substantially more potent ability to induce chemokines in human PBMCs. The enhanced chemokine induction activity of the peptide in vitro correlated with stronger protective activity in vivo in the Staphylococcus aureus-invasive infection model, with a >5-fold reduction in the protective dose in direct comparison with IDR-1. IDR-1002 also afforded protection against the Gram-negative bacterial pathogen Escherichia coli. Chemokine induction by IDR-1002 was found to be mediated through a Gi-coupled receptor and the PI3K, NF-kappaB, and MAPK signaling pathways. The protective activity of the peptide was associated with in vivo augmentation of chemokine production and recruitment of neutrophils and monocytes to the site of infection. These results highlight the importance of the chemokine induction activity of host defense peptides and demonstrate that the optimization of the ex vivo chemokine-induction properties of peptides is a promising method for the rational development of immunomodulatory IDR peptides with enhanced anti-infective activity.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/20107187
      14. Call Number :
        PKI @ catherine.lautenschlager @
      15. Serial :
        9033
      1. Author :
        Nijnik, A.; Madera, L.; Ma, S.; Waldbrook, M.; Elliott, M. R.; Easton, D. M.; Mayer, M. L.; Mullaly, S. C.; Kindrachuk, J.; Jenssen, H.; Hancock, R. E.
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2010
      5. Publication :
        J Immunol
      6. Products :
      7. Volume :
        184
      8. Issue :
        N/A
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        Xen14, Xen 14, E. coli Xen14, IVIS, Amino Acid Sequence; Animals; Antimicrobial Cationic Peptides/chemical synthesis/*pharmacology; Bacterial Infections/*metabolism/microbiology/prevention & control; Cell Line; Cells, Cultured; Chemokine CCL2/metabolism; Chemokine CCL7/metabolism; Chemokine CXCL1/metabolism; Chemokines/*metabolism; Female; Humans; Interleukin-8/metabolism; Leukocytes/cytology/*metabolism; Leukocytes, Mononuclear/cytology/drug effects/metabolism; Macrophages/cytology/drug effects/metabolism; Mice; Mice, Inbred C57BL; Molecular Sequence Data; NF-kappa B/metabolism; Phosphatidylinositol 3-Kinases/metabolism; Phosphorylation/drug effects; Staphylococcal Infections/microbiology/prevention & control; Staphylococcus aureus/drug effects; p38 Mitogen-Activated Protein Kinases/metabolism
      12. Abstract :
        With the rapid rise in the incidence of multidrug resistant infections, there is substantial interest in host defense peptides as templates for production of new antimicrobial therapeutics. Natural peptides are multifunctional mediators of the innate immune response, with some direct antimicrobial activity and diverse immunomodulatory properties. We have previously developed an innate defense regulator (IDR) 1, with protective activity against bacterial infection mediated entirely through its effects on the immunity of the host, as a novel approach to anti-infective therapy. In this study, an immunomodulatory peptide IDR-1002 was selected from a library of bactenecin derivatives based on its substantially more potent ability to induce chemokines in human PBMCs. The enhanced chemokine induction activity of the peptide in vitro correlated with stronger protective activity in vivo in the Staphylococcus aureus-invasive infection model, with a >5-fold reduction in the protective dose in direct comparison with IDR-1. IDR-1002 also afforded protection against the Gram-negative bacterial pathogen Escherichia coli. Chemokine induction by IDR-1002 was found to be mediated through a Gi-coupled receptor and the PI3K, NF-kappaB, and MAPK signaling pathways. The protective activity of the peptide was associated with in vivo augmentation of chemokine production and recruitment of neutrophils and monocytes to the site of infection. These results highlight the importance of the chemokine induction activity of host defense peptides and demonstrate that the optimization of the ex vivo chemokine-induction properties of peptides is a promising method for the rational development of immunomodulatory IDR peptides with enhanced anti-infective activity.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/20107187
      14. Call Number :
        PKI @ kd.modi @ 6
      15. Serial :
        10393
      1. Author :
        Takeshita, Fumitaka; Patrawala, Lubna; Osaki, Mitsuhiko; Takahashi, Ryou-u; Yamamoto, Yusuke; Kosaka, Nobuyoshi; Kawamata, Masaki; Kelnar, Kevin; Bader, Andreas G; Brown, David; Ochiya, Takahiro
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2010
      5. Publication :
        Molecular therapy: the journal of the American Society of Gene Therapy
      6. Products :
      7. Volume :
        18
      8. Issue :
        1
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        Aged; Animals; Bioware; Cell Cycle Proteins; Cell Line, Tumor; Cell Proliferation; Down-Regulation; Humans; Male; Mice; MicroRNAs; Middle Aged; PC-3M-luc; Prostatic Neoplasms; Reverse Transcriptase Polymerase Chain Reaction
      12. Abstract :
        Recent reports have linked the expression of specific microRNAs (miRNAs) with tumorigenesis and metastasis. Here, we show that microRNA (miR)-16, which is expressed at lower levels in prostate cancer cells, affects the proliferation of human prostate cancer cell lines both in vitro and in vivo. Transient transfection with synthetic miR-16 significantly reduced cell proliferation of 22Rv1, Du145, PPC-1, and PC-3M-luc cells. A prostate cancer xenograft model revealed that atelocollagen could efficiently deliver synthetic miR-16 to tumor cells on bone tissues in mice when injected into tail veins. In the therapeutic bone metastasis model, injection of miR-16 with atelocollagen via tail vein significantly inhibited the growth of prostate tumors in bone. Cell model studies indicate that miR-16 likely suppresses prostate tumor growth by regulating the expression of genes such as CDK1 and CDK2 associated with cell-cycle control and cellular proliferation. There is a trend toward lower miR-16 expression in human prostate tumors versus normal prostate tissues. Thus, this study indicates the therapeutic potential of miRNA in an animal model of cancer metastasis with systemic miRNA injection and suggest that systemic delivery of miR-16 could be used to treat patients with advanced prostate cancer.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/19738602
      14. Call Number :
        PKI @ catherine.lautenschlager @
      15. Serial :
        8947
      1. Author :
        Wang, S.; Noberini, R.; Stebbins, J. L.; Das, S.; Zhang, Z.; Wu, B.; Mitra, S.; Billet, S.; Fernandez, A.; Bhowmick, N. A.; Kitada, S.; Pasquale, E. B.; Fisher, P. B.; Pellecchia, M.
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2013
      5. Publication :
        Clin Cancer Res
      6. Products :
      7. Volume :
        19
      8. Issue :
        N/A
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        PC-3M-luc-C6, PC-3M-luc, IVIS, Bioware, Prostate cancer, Bioluminescence
      12. Abstract :
        PURPOSE: YSA is an EphA2-targeting peptide that effectively delivers anticancer agents to prostate cancer tumors. Here, we report on how we increased the drug-like properties of this delivery system. EXPERIMENTAL DESIGN: By introducing non-natural amino acids, we have designed two new EphA2 targeting peptides: YNH, where norleucine and homoserine replace the two methionine residues of YSA, and dYNH, where a D-tyrosine replaces the L-tyrosine at the first position of the YNH peptide. We describe the details of the synthesis of YNH and dYNH paclitaxel conjugates (YNH-PTX and dYNH-PTX) and their characterization in cells and in vivo. RESULTS: dYNH-PTX showed improved stability in mouse serum and significantly reduced tumor size in a prostate cancer xenograft model and also reduced tumor vasculature in a syngeneic orthotopic allograft mouse model of renal cancer compared with vehicle or paclitaxel treatments. CONCLUSION: This study reveals that targeting EphA2 with dYNH drug conjugates could represent an effective way to deliver anticancer agents to a variety of tumor types. Clin Cancer Res; 19(1); 128-37. (c)2012 AACR.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/23155185
      14. Call Number :
        PKI @ kd.modi @ 6
      15. Serial :
        10541