1. Resources
  2. Citations Library

Citation Details

You are viewing citation details. You can save or export citation(s) below, access an article, or start a new search.

141–150 of 499 records found matching your query:
Back to Search
Select All  |  Deselect All

Headers act as filters

      1. Author :
        N/A
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2010
      5. Publication :
        Molecular Imaging and Biology
      6. Products :
      7. Volume :
        N/A
      8. Issue :
        N/A
      9. Page Numbers :
        N/A
      10. Research Area :
        Cancer
      11. Keywords :
        Optical imaging, Image-guided surgery, Molecular imaging, Near-infrared fluorescence
      12. Abstract :
        In cancer surgery, intra-operative assessment of the tumor-free margin, which is critical for the prognosis of the patient, relies on the visual appearance and palpation of the tumor. Optical imaging techniques provide real-time visualization of the tumor, warranting intra-operative image-guided surgery. Within this field, imaging in the near-infrared light spectrum offers two essential advantages: increased tissue penetration of light and an increased signal-tobackground-ratio of contrast agents. In this article, we review the various techniques, contrast agents, and camera systems that are currently used for image-guided surgery. Furthermore, we provide an overview of the wide range of molecular contrast agents targeting specific hallmarks of cancer and we describe perspectives on its future use in cancer surgery.
      13. URL :
        http://www.springerlink.com/content/78233815221t6563/
      14. Call Number :
        PKI @ sarah.piper @
      15. Serial :
        4486
      1. Author :
        Kim DE, Kim JY, Schellingerhout D, Shon SM, Jeong SW, Kim EJ and Kim WK
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2009
      5. Publication :
        Molecular Imaging
      6. Products :
      7. Volume :
        8
      8. Issue :
        5
      9. Page Numbers :
        N/A
      10. Research Area :
        Cardiovascular Research
      11. Keywords :
        ProSense; in vivo imaging
      12. Abstract :
        Inflammation in atherosclerotic plaques causes plaque vulnerability and rupture, leading to thromboembolic complications. Cathepsin B (CatB) proteases secreted by macrophages play a major role in plaque inflammation. We used a CatB-activatable near-infrared fluorescence (NIRF) imaging agent to demonstrate the inflammatory component in mice atheromata and the atherosclerosis- modulating effects of atorvastatin or glucosamine treatments. Apolipoprotein E knockout mice (n = 35) were fed normal chow, a Western diet, a Western diet + atorvastatin, a Western diet + glucosamine, or a Western diet + atorvastatin + glucosamine for 14 weeks. Twenty-four hours after the intravenous injection of a CatB-activatable probe, ex vivo NIRF imaging of the aortas and brains was performed, followed by histology. The CatB-related signal, observed in the aortas but not in the cerebral arteries, correlated very well with protease activity and the presence of macrophages on histology. Animals on Western diets could be distinguished from animals on a normal diet. The antiatherosclerotic effects of atorvastatin and glucosamine could be demonstrated, with reduced CatB-related signal compared with untreated animals. Plaque populations were heterogeneous within individuals, with some plaques showing a high and others a lower CatB-related signal. These differences in signal intensity could not be predicted by visual inspection of the plaques but did correlate with histologic evidence of inflammation in every case. This suggests that vulnerable inflamed plaques can be identified by optical molecular imaging.
      13. URL :
        http://www.bcdecker.com/pubMedLinkOut.aspx?pub=MIO&vol=8&iss=5&page=291
      14. Call Number :
        PKI @ sarah.piper @
      15. Serial :
        4558
      1. Author :
        Shan, Liang; Wang, Songping; Sridhar, Rajagopalan; Bhujwalla, Zaver M; Wang, Paul C
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2007
      5. Publication :
        Molecular imaging
      6. Products :
      7. Volume :
        6
      8. Issue :
        2
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        Animals; Bioware; Breast Neoplasms; Cell Line, Tumor; Fluorescence; Fluorescent Dyes; Humans; Liposomes; Magnetic Resonance Imaging; Magnetics; MDA-MB-231-D3H1 cells; Mice; Mice, Inbred Strains; Microscopy, Confocal; Molecular Probes; Optics and Photonics; Transferrin; Xenograft Model Antitumor Assays
      12. Abstract :
        A dual probe with fluorescent and magnetic reporter groups was constructed by linkage of the near-infrared (NIR) fluorescent transferrin conjugate (Tf(NIR)) on the surface of contrast agent-encapsulated cationic liposome (Lip-CA). This probe was used for magnetic resonance imaging (MRI) and optical imaging of MDA-MB-231-luc breast cancer cells grown as a monolayer in vitro and as solid tumor xenografts in nude mice. Confocal microscopy, optical imaging, and MRI showed a dramatic increase of in vitro cellular uptake of the fluorescent and magnetic reporter groups from the probe compared with the uptake of contrast agent or Lip-CA alone. Pretreatment with transferrin (Tf) blocked uptake of the probe reporters, indicating the importance and specificity of the Tf moiety for targeting. Intravenous administration of the dual probe to nude mice significantly enhanced the tumor contrast in MRI, and preferential accumulation of the fluorescent signal was clearly seen in NIR-based optical images. More interestingly, the contrast enhancement in MRI showed a heterogeneous pattern within tumors, which reflected the tumor's morphologic heterogeneity. These results indicate that the newly developed dual probe enhances the tumor image contrast and is superior to contrast agent alone for identifying the tumor pathologic features on the basis of MRI but also is suitable for NIR-based optical imaging.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/17445503
      14. Call Number :
        PKI @ catherine.lautenschlager @
      15. Serial :
        8992
      1. Author :
        Steve H. Thorne; Yoram Barak; Wenchuan Liang; Michael H. Bachmann; Jianghong Rao; Christopher H. Contag; A. Matin
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2009
      5. Publication :
        Molecular Cancer Therapeutics
      6. Products :
      7. Volume :
        8
      8. Issue :
        2
      9. Page Numbers :
        N/A
      10. Research Area :
        Cancer
      11. Keywords :
        Cancer; in vivo imaging; drug discovery; chemotherapy
      12. Abstract :
        We report the discovery of a new prodrug, 6-chloro-9-nitro-5-oxo-5H-benzo(a)phenoxazine (CNOB). This prodrug is efficiently activated by ChrR6, the highly active prodrug activating bacterial enzyme we have previously developed. The CNOB/ChrR6 therapy was effective in killing several cancer cell lines in vitro. It also efficiently treated tumors in mice with up to 40% complete remission. 9-Amino-6-chloro-5H-benzo(a)phenoxazine-5-one (MCHB) was the only product of CNOB reduction by ChrR6. MCHB binds DNA; at nonlethal concentration, it causes cell accumulation in the S phase, and at lethal dose, it induces cell surface Annexin V and caspase-3 and caspase-9 activities. Further, MCHB colocalizes with mitochondria and disrupts their electrochemical potential. Thus, killing by CNOB involves MCHB, which likely induces apoptosis through the mitochondrial pathway. An attractive feature of the CNOB/ChrR6 regimen is that its toxic product, MCHB, is fluorescent. This feature proved helpful in in vitro studies because simple fluorescence measurements provided information on the kinetics of CNOB activation within the cells, MCHB killing mechanism, its generally efficient bystander effect in cells and cell spheroids, and its biodistribution. The emission wavelength of MCHB also permitted its visualization in live animals, allowing noninvasive qualitative imaging of MCHB in mice and the tumor microenvironment. This feature may simplify exploration of barriers to the penetration of MCHB in tumors and their amelioration.
      13. URL :
        http://mct.aacrjournals.org/content/8/2/333.abstract
      14. Call Number :
        PKI @ sarah.piper @
      15. Serial :
        4500
      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 :
        Beckers, Annelies; Organe, Sophie; Timmermans, Leen; Vanderhoydonc, Frank; Deboel, Ludo; Derua, Rita; Waelkens, Etienne; Brusselmans, Koen; Verhoeven, Guido; Swinnen, Johannes V
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2006
      5. Publication :
        Molecular cancer therapeutics
      6. Products :
      7. Volume :
        5
      8. Issue :
        9
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        Adenosine Triphosphate; Aminoimidazole Carboxamide; AMP-Activated Protein Kinases; Bioware; Breast Neoplasms; Carcinoma, Squamous Cell; Cell Line, Tumor; DNA, Neoplasm; Drug Synergism; Enzyme Activation; Humans; Lipids; Methotrexate; Multienzyme Complexes; Nucleotide Deaminases; PC-3M-luc; Phosphoribosylaminoimidazolecarboxamide Formyltransferase; Phosphoribosylglycinamide Formyltransferase; Protein-Serine-Threonine Kinases; Purines; Ribonucleosides; Ribonucleotides; RNA Interference
      12. Abstract :
        Because of its ability to mimic a low energy status of the cell, the cell-permeable nucleoside 5-aminoimidazole-4-carboxamide (AICA) riboside was proposed as an antineoplastic agent switching off major energy-consuming processes associated with the malignant phenotype (lipid production, DNA synthesis, cell proliferation, cell migration, etc.). Key to the antineoplastic action of AICA riboside is its conversion to ZMP, an AMP mimetic that at high concentrations activates the AMP-activated protein kinase (AMPK). Here, in an attempt to increase the efficacy of AICA riboside, we pretreated cancer cells with methotrexate, an antimetabolite blocking the metabolism of ZMP. Methotrexate enhanced the AICA riboside-induced accumulation of ZMP and led to a decrease in the levels of ATP, which functions as an intrasteric inhibitor of AMPK. Consequently, methotrexate markedly sensitized AMPK for activation by AICA riboside and potentiated the inhibitory effects of AICA riboside on tumor-associated processes. As cotreatment elicited antiproliferative effects already at concentrations of compounds that were only marginally effective when used alone, our findings on the cooperation between methotrexate and AICA riboside provide new opportunities both for the application of classic antimetabolic chemotherapeutics, such as methotrexate, and for the exploitation of the energy-sensing machinery as a target for cancer intervention.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/16985054
      14. Call Number :
        PKI @ catherine.lautenschlager @
      15. Serial :
        8978
      1. Author :
        Mitchell, Dianne; Pobre, Eileen G; Mulivor, Aaron W; Grinberg, Asya V; Castonguay, Roselyne; Monnell, Travis E; Solban, Nicolas; Ucran, Jeffrey A; Pearsall, R Scott; Underwood, Kathryn W; Seehra, Jasbir; Kumar, Ravindra
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2010
      5. Publication :
        Molecular cancer therapeutics
      6. Products :
      7. Volume :
        9
      8. Issue :
        2
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        Activin Receptors, Type II; Animals; Bioware; Bone Morphogenetic Proteins; CHO Cells; Cricetinae; Cricetulus; Endothelial Cells; Endothelium, Vascular; Growth Differentiation Factor 2; Humans; MCF-7-luc-F5 cells; Mice; Neoplasms; Neovascularization, Pathologic; Surface Plasmon Resonance; Telangiectasia, Hereditary Hemorrhagic
      12. Abstract :
        Activin receptor-like kinase-1 (ALK1) is a type I, endothelial cell-specific member of the transforming growth factor-beta superfamily of receptors known to play an essential role in modulating angiogenesis and vessel maintenance. In the present study, we sought to examine the angiogenic and tumorigenic effects mediated upon the inhibition of ALK1 signaling using a soluble chimeric protein (ALK1-Fc). Of 29 transforming growth factor-beta-related ligands screened by surface plasmon resonance, only bone morphogenetic protein (BMP9) and BMP10 displayed high-affinity binding to ALK1-Fc. In cell-based assays, ALK1-Fc inhibited BMP9-mediated Id-1 expression in human umbilical vein endothelial cells and inhibited cord formation by these cells on a Matrigel substrate. In a chick chorioallantoic membrane assay, ALK1-Fc reduced vascular endothelial growth factor-, fibroblast growth factor-, and BMP10-mediated vessel formation. The growth of B16 melanoma explants was also inhibited significantly by ALK1-Fc in this assay. Finally, ALK1-Fc treatment reduced tumor burden in mice receiving orthotopic grafts of MCF7 mammary adenocarcinoma cells. These data show the efficacy of chimeric ALK1-Fc proteins in mitigating vessel formation and support the view that ALK1-Fc is a powerful antiangiogenic agent capable of blocking vascularization.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/20124460
      14. Call Number :
        PKI @ catherine.lautenschlager @
      15. Serial :
        9010
      1. Author :
        Shimomura, Toshiyasu; Hasako, Shinichi; Nakatsuru, Yoko; Mita, Takashi; Ichikawa, Koji; Kodera, Tsutomu; Sakai, Takumi; Nambu, Tadahiro; Miyamoto, Mayu; Takahashi, Ikuko; Miki, Satomi; Kawanishi, Nobuhiko; Ohkubo, Mitsuru; Kotani, Hidehito; Iwasawa, Yoshikazu
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2010
      5. Publication :
        Molecular cancer therapeutics
      6. Products :
      7. Volume :
        9
      8. Issue :
        1
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        Animals; Antineoplastic Agents; Antineoplastic Combined Chemotherapy Protocols; Bioware; Cell Death; Cell Line, Tumor; Cell Proliferation; Cyclohexanecarboxylic Acids; HeLa-luc; Humans; Inhibitory Concentration 50; Mice; Mitosis; Protein kinase inhibitors; Protein-Serine-Threonine Kinases; Rats; Taxoids; Thiazoles; Xenograft Model Antitumor Assays
      12. Abstract :
        Aurora-A kinase is a one of the key regulators during mitosis progression. Aurora-A kinase is a potential target for anticancer therapies because overexpression of Aurora-A, which is frequently observed in some human cancers, results in aberrant mitosis leading to chromosomal instability and possibly tumorigenesis. MK-5108 is a novel small molecule with potent inhibitory activity against Aurora-A kinase. Although most of the Aurora-kinase inhibitors target both Aurora-A and Aurora-B, MK-5108 specifically inhibited Aurora-A kinase in a panel of protein kinase assays. Inhibition of Aurora-A by MK-5108 in cultured cells induced cell cycle arrest at the G(2)-M phase in flow cytometry analysis. The effect was confirmed by the accumulation of cells with expression of phosphorylated Histone H3 and inhibition of Aurora-A autophosphorylation by immunostaining assays. MK-5108 also induced phosphorylated Histone H3 in skin and xenograft tumor tissues in a nude rat xenograft model. MK-5108 inhibited growth of human tumor cell lines in culture and in different xenograft models. Furthermore, the combination of MK-5108 and docetaxel showed enhanced antitumor activities compared with control and docetaxel alone-treated animals without exacerbating the adverse effects of docetaxel. MK-5108 is currently tested in clinical trials and offers a new therapeutic approach to combat human cancers as a single agent or in combination with existing taxane therapies.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/20053775
      14. Call Number :
        PKI @ catherine.lautenschlager @
      15. Serial :
        9006
      1. Author :
        Galina Gabriely, Thomas Wurdinger, Santosh Kesari, Christine C. Esau, Julja Burchard, Peter S. Linsley and Anna M. Krichevsky
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2008
      5. Publication :
        Molecular and Cellular Biology
      6. Products :
      7. Volume :
        28
      8. Issue :
        17
      9. Page Numbers :
        N/A
      10. Research Area :
        Neuroscience
      11. Keywords :
        in vivo imaging; MMPSense; microRNA 21; glioma
      12. Abstract :
        Substantial data indicate that microRNA 21 (miR-21) is significantly elevated in glioblastoma (GBM) and in many other tumors of various origins. This microRNA has been implicated in various aspects of carcinogenesis, including cellular proliferation, apoptosis, and migration. We demonstrate that miR-21 regulates multiple genes associated with glioma cell apoptosis, migration, and invasiveness, including the RECK and TIMP3 genes, which are suppressors of malignancy and inhibitors of matrix metalloproteinases (MMPs). Specific inhibition of miR-21 with antisense oligonucleotides leads to elevated levels of RECK and TIMP3 and therefore reduces MMP activities in vitro and in a human model of gliomas in nude mice. Moreover, downregulation of miR-21 in glioma cells leads to decreases of their migratory and invasion abilities. Our data suggest that miR-21 contributes to glioma malignancy by downregulation of MMP inhibitors, which leads to activation of MMPs, thus promoting invasiveness of cancer cells. Our results also indicate that inhibition of a single oncomir, like miR-21, with specific antisense molecules can provide a novel therapeutic approach for “physiological” modulation of multiple proteins whose expression is deregulated in cancer.
      13. URL :
        http://mcb.asm.org/cgi/content/abstract/28/17/5369
      14. Call Number :
        PKI @ sarah.piper @
      15. Serial :
        4546
      1. Author :
        Fogal, Valentina; Richardson, Adam D; Karmali, Priya P; Scheffler, Immo E; Smith, Jeffrey W; Ruoslahti, Erkki
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2010
      5. Publication :
        Molecular and cellular biology
      6. Products :
      7. Volume :
        30
      8. Issue :
        6
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        Animals; Bioware; Carbon; Carrier Proteins; Cell Death; Cell Line, Tumor; Cell Proliferation; Cell Survival; Electron Transport Complex I; Gene Knockdown Techniques; Humans; Mass Spectrometry; MDA-MB-231-D3H2LN cells; Mice; Mitochondria; Mitochondrial Proteins; Neoplasm Metastasis; Neoplasms; Oxidative Phosphorylation; Protein Biosynthesis; Protein Stability; Rotenone
      12. Abstract :
        p32/gC1qR/C1QBP/HABP1 is a mitochondrial/cell surface protein overexpressed in certain cancer cells. Here we show that knocking down p32 expression in human cancer cells strongly shifts their metabolism from oxidative phosphorylation (OXPHOS) to glycolysis. The p32 knockdown cells exhibited reduced synthesis of the mitochondrial-DNA-encoded OXPHOS polypeptides and were less tumorigenic in vivo. Expression of exogenous p32 in the knockdown cells restored the wild-type cellular phenotype and tumorigenicity. Increased glucose consumption and lactate production, known as the Warburg effect, are almost universal hallmarks of solid tumors and are thought to favor tumor growth. However, here we show that a protein regularly overexpressed in some cancers is capable of promoting OXPHOS. Our results indicate that high levels of glycolysis, in the absence of adequate OXPHOS, may not be as beneficial for tumor growth as generally thought and suggest that tumor cells use p32 to regulate the balance between OXPHOS and glycolysis.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/20100866
      14. Call Number :
        PKI @ catherine.lautenschlager @
      15. Serial :
        8952
Back to Search
Select All  |  Deselect All