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      1. Author :
        Abrams, T. J.; Murray, L. J.; Pesenti, E.; Holway, V. W.; Colombo, T.; Lee, L. B.; Cherrington, J. M.; Pryer, N. K.
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2003
      5. Publication :
        Molecular Cancer Therapy
      6. Products :
      7. Volume :
        2
      8. Issue :
        N/A
      9. Page Numbers :
        1011
      10. Research Area :
        N/A
      11. Keywords :
        Animals, Antibiotics, Antineoplastic/pharmacology/therapeutic use, Bone Neoplasms/secondary, Breast Neoplasms/*drug therapy, Cell Line, Tumor, Doxorubicin/pharmacology/therapeutic use, Enzyme Inhibitors/*pharmacology, Female, Fluorouracil/therapeutic use, Humans, Indoles/*pharmacology, Mice, Mice, Nude, Mice, Transgenic, Neoplasm Transplantation, Phosphorylation, Pyrroles/*pharmacology, Rats, Rats, Sprague-Dawley, Time Factors IVIS, Xenogen
      12. Abstract :
        SU11248 is an oral multitargeted tyrosine kinase inhibitor with antitumor and antiangiogenic activities through targeting platelet-derived growth factor receptor, vascular endothelial growth factor receptor, KIT, and FLT3, the first three of which are expressed in human breast cancer and/or its supporting tissues. The purpose of the present studies was to demonstrate the potent anticancer activity of SU11248 alone or in combination with conventional cytotoxic agents against several distinct preclinical models of breast cancer. SU11248 was administered as a monotherapy to (1) mouse mammary tumor virus-v-Ha-ras mice and 7,12-dimethylbenz(a)anthracene-treated rats bearing mammary tumors and (2) mice bearing human breast cancer xenografts of s.c. MX-1 tumors and osseous metastasis of a MDA-MB-435-derived cell line (435/HAL-Luc). SU11248 was also administered in combination with docetaxel both in xenograft models and in combination with 5-fluorouracil and doxorubicin in the MX-1 model. SU11248 treatment potently regressed growth of mammary cancers in mouse mammary tumor virus-v-Ha-ras transgenic mice (82% regression) and 7,12-dimethylbenz(a)anthracene-induced mammary tumors in rats (99% regression at the highest dose; P < 0.05 for both). This agent also inhibited MX-1 tumor growth by 52%, with markedly enhanced anticancer effects when administered in combination with docetaxel, 5-fluorouracil, or doxorubicin compared with either agent alone (P < 0.05). SU11248 treatment in combination with docetaxel effectively prolonged survival of mice, with 435/HAL-Luc cancer xenografts established in bone compared with either agent alone (P < 0.05). These results demonstrate that SU11248 is effective in preclinical breast cancer models and suggest that it may be useful in the treatment of breast cancer in the clinic.
      13. URL :
        http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=14578466
      14. Call Number :
        135733
      15. Serial :
        7350
      1. Author :
        Abravanel, Daniel L; Belka, George K; Pan, Tien-chi; Pant, Dhruv K; Collins, Meredith A; Sterner, Christopher J; Chodosh, Lewis A
      2. Title :
        Notch promotes recurrence of dormant tumor cells following HER2/neu-targeted therapy
      3. Type :
        Journal Article
      4. Year :
        2015
      5. Publication :
        The Journal of clinical investigation
      6. Products :
      7. Volume :
        125
      8. Issue :
        6
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        IVIS; IVIS BLI in vivo
      12. Abstract :
        Breast cancer mortality is principally due to recurrent tumors that arise from a reservoir of residual tumor cells that survive therapy. Remarkably, breast cancers can recur after extended periods of clinical remission, implying that at least some residual tumor cells pass through a dormant phase prior to relapse. Nevertheless, the mechanisms that contribute to breast cancer recurrence are poorly understood. Using a mouse model of recurrent mammary tumorigenesis in combination with bioinformatics analyses of breast cancer patients, we have identified a role for Notch signaling in mammary tumor dormancy and recurrence. Specifically, we found that Notch signaling is acutely upregulated in tumor cells following HER2/neu pathway inhibition, that Notch signaling remains activated in a subset of dormant residual tumor cells that persist following HER2/ neu downregulation, that activation of Notch signaling accelerates tumor recurrence, and that inhibition of Notch signaling by either genetic or pharmacological approaches impairs recurrence in mice. Consistent with these findings, meta-analysis of microarray data from over 4,000 breast cancer patients revealed that elevated Notch pathway activity is independently associated with an increased rate of recurrence. Together, these results implicate Notch signaling in tumor recurrence from dormant residual tumor cells and provide evidence that dormancy is a targetable stage of breast cancer progression.
      13. URL :
        N/A
      14. Call Number :
        PKI @ user @ 9475
      15. Serial :
        21059
      1. Author :
        Abu Ammar, Aiman; Raveendran, Raji; Gibson, Dan; Nassar, Taher; Benita, Simon
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2016
      5. Publication :
        Journal of Medicinal Chemistry
      6. Products :
      7. Volume :
        59
      8. Issue :
        19
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        IVIS; IVIS BLI in vivo
      12. Abstract :
        Side effects and acquired resistance by cancer cells limit the use of platinum anticancer drugs. Modification of oxaliplatin (OXA) into a lipophilic Pt(IV) complex [Pt(DACH)(OAc)(OPal)(ox)] (1), containing both lipophilic and hydrophilic axial ligands, was applied to improve performance and facilitate incorporation into polymeric nanoparticles. Complex 1 exhibited unique potency against a panel of cancer cells, including cisplatin-resistant tumor cells. [Pt(DACH)(OAc)(OPal)(ox)] incorporated nanoparticles (2) presented a mean diameter of 146 nm with encapsulation yields above 95% as determined by HPLC. Complexes 1 and 2 showed enhanced in vitro cellular Pt accumulation, DNA platination, and antiproliferative effect compared to OXA. Results of an orthotopic intraperitoneal model of metastatic ovarian cancer (SKOV-3) and a xenograft subcutaneous model of colon (HCT-116) tumor in SCID-bg mice showed that the activity of 1 and 2 significantly decreased tumor growth rates compared to control and OXA treatment groups. Consequently, these findings warrant further development toward clinical translation.
      13. URL :
        http://pubs.acs.org/doi/abs/10.1021/acs.jmedchem.6b00955
      14. Call Number :
        PKI @ user @ 13289
      15. Serial :
        20160
      1. Author :
        Abu Lila, Amr S; Kato, Chihiro; Fukushima, Masakazu; Huang, Cheng-Long; Wada, Hiromi; Ishida, Tatsuhiro
      2. Title :
        Downregulation of thymidylate synthase by RNAi molecules enhances the antitumor effect of pemetrexed in an orthotopic malignant mesothelioma xenograft mouse model
      3. Type :
        Journal Article
      4. Year :
        2016
      5. Publication :
        International Journal of Oncology
      6. Products :
      7. Volume :
        N/A
      8. Issue :
        N/A
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        IVIS; IVIS FLI in vivo
      12. Abstract :
        Malignant pleural mesothelioma (MPM) is an incurable cancer with an increasing incidence. Currently, pemetrexed (PMX)-based chemotherapy is the mainstay of chemotherapy for MPM, however, the outcome of PMX-based chemotherapy in patients with MPM is dismal. RNA interference (RNAi) technology has been considered as an effective tool to substantially enhance the therapeutic efficacy of chemotherapeutic agents in many preclinical and clinical settings. In this study, therefore, we investigated whether non-viral anti-thymidylate synthase RNAi embedded liposome (TS shRNA lipoplex) would effectively guide the downregulation of TS in human malignant mesothelioma MSTO-211H cells. Consequently, it enhanced the antitumor effect of PMX both in vitro and in vivo. TS shRNA effectively enhanced the in vitro cell growth inhibition upon treatment with PMX via downregulating TS expression in the MSTO-211H cell line. In in vivo orthotopic tumor model, the combined treatment of PMX and TS shRNA lipoplex efficiently combated the progression of orthotopic thoracic tumors and as a result prolonged mouse survival, compared to each single treatment. Our findings emphasize the pivotal relevance of RNAi as an effective tool for increasing the therapeutic efficacy of PMX, a cornerstone in the treatment regimens of MPM, and thereby, raising the possibility for the development of a novel therapeutic strategy, combination therapy of TS-shRNA and PMX, that can surpass many of the currently applied, but less effective, therapeutic regimens against lethal MPM.
      13. URL :
        N/A
      14. Call Number :
        PKI @ user @ 10864
      15. Serial :
        20159
      1. Author :
        Acharyya, S.; Villalta, S. A.; Bakkar, N.; Bupha-Intr, T.; Janssen, P. M.; Carathers, M.; Li, Z. W.; Beg, A. A.; Ghosh, S.; Sahenk, Z.; Weinstein, M.; Gardner, K. L.; Rafael-Fortney, J. A.; Karin, M.; Tidball, J. G.; Baldwin, A. S.; Guttridge, D. C.
      2. Title :
        Interplay of IKK/NF-?B signaling in macrophages and myofibers promotes muscle degeneration in Duchenne muscular dystrophy
      3. Type :
        Journal Article
      4. Year :
        2007
      5. Publication :
        Journal of Clinical Investigation
      6. Products :
      7. Volume :
        117
      8. Issue :
        N/A
      9. Page Numbers :
        889
      10. Research Area :
        N/A
      11. Keywords :
        IVIS, Xenogen
      12. Abstract :
        Duchenne muscular dystrophy (DMD) is a lethal X-linked disorder associated with dystrophin deficiency that results in chronic inflammation and severe skeletal muscle degeneration. In DMD mouse models and patients, we find that I?B kinase/NF-?B (IKK/NF-?B) signaling is persistently elevated in immune cells and regenerative muscle fibers. Ablation of 1 allele of the p65 subunit of NF-?B was sufficient to improve pathology in mdx mice, a model of DMD. In addition, conditional deletion of IKK? in mdx mice elucidated that NF-?B functions in activated macrophages to promote inflammation and muscle necrosis and in skeletal muscle fibers to limit regeneration through the inhibition of muscle progenitor cells. Furthermore, specific pharmacological inhibition of IKK resulted in improved pathology and muscle function in mdx mice. Collectively, these results underscore the critical role of NF-?B in the progression of muscular dystrophy and suggest the IKK/NF-?B signaling pathway as a potential therapeutic target for DMD.
      13. URL :
        N/A
      14. Call Number :
        135736
      15. Serial :
        6665
      1. Author :
        Ackler, Scott; Oleksijew, Anatol; Chen, Jun; Chyla, Brenda J; Clarin, Jerry; Foster, Kelly; McGonigal, Thomas; Mishra, Sasmita; Schlessinger, Sally; Smith, Morey L
      2. Title :
        Clearance of systemic hematologic tumors by venetoclax (Abt‐199) and navitoclax
      3. Type :
        Journal Article
      4. Year :
        2015
      5. Publication :
        Pharmacology Research & Perspectives
      6. Products :
      7. Volume :
        3
      8. Issue :
        5
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        Apoptosis,; Bcl-2 family proteins,; bioluminescent imaging,; drug therapy,; leukemia/lymphoma,; systemic engraftment; Pharma; IVIS; IVIS BLI in vitro
      12. Abstract :
        The Bcl-2 family inhibitors venetoclax and navitoclax demonstrated potent antitumor activity in chronic lymphocytic leukemia patients, notably in reducing marrow load and adenopathy. Subsequent trials with venetoclax have been initiated in non-Hodgkin’s lymphoma and multiple myeloma patients. Traditional preclinical models fall short either in faithfully recapitulating disease progression within such compartments or in allowing the direct longitudinal analysis of systemic disease. We show that intravenous inoculation of engineered RS4;11 (acute lymphoblastic leukemia) and Granta 519 (mantle cell lymphoma) bioluminescent reporter cell lines result in tumor engraftment of bone marrow, with additional invasion of the central nervous system in the case of Granta 519. Importantly, apoptosis induction and response of these systemically engrafted tumors to Bcl-2 family inhibitors alone or in combination with standard-of-care agents could be monitored longitudinally with optical imaging, and was more accurately reflective of the observed clinical response.
      13. URL :
        N/A
      14. Call Number :
        PKI @ user @ 10228
      15. Serial :
        21058
      1. Author :
        Acuff, H. B.; Carter, K. J.; Fingleton, B.; Gorden, D. L.; Matrisian, L. M.
      2. Title :
        MMP9 from bone marrow-derived cells contributes to survival but not growth of tumor cells in the lung microenvironment
      3. Type :
        Journal Article
      4. Year :
        2006
      5. Publication :
        Cancer Research
      6. Products :
      7. Volume :
        66
      8. Issue :
        N/A
      9. Page Numbers :
        259
      10. Research Area :
        N/A
      11. Keywords :
        IVIS, Xenogen
      12. Abstract :
        The role of specific stromal-derived MMPs was analyzed in experimental metastasis assays in wildtype and either MMP9, MMP7, or MMP2 null mice. MMP9 null mice showed an 81% reduction in Lewis Lung Carcinoma tumor number, while MMP7 null mice showed a 42% increase in tumor number and there was no difference in tumor number in MMP2 null mice compared to wildtype controls. Similarly, in an orthotopic model of lung cancer, 50% fewer MMP9 null mice were able to establish tumors in the lung compared to control mice, although the size of the tumors was not different. The effect of MMP9 on lung tumor colonization was dependent on the expression of MMP9 from bone marrow-derived cells and is most likely contributed by neutrophils. To examine temporal effects of stromal MMP9, bioluminescence imaging from luciferase expressing human lung cancer-derived A549 cells revealed that there were fewer tumor cells in the lungs of MMP9 null mice as early as 19 hours after injection compared to control mice, with no difference in subsequent growth rates. Six hours after injection of tumor cells, MMP9 null mice showed a four-fold increase in the percent of tumor cells undergoing apoptosis compared to control mice. We conclude that MMP9 from the bone marrow contributes to the early survival and establishment of tumors in the lung and has no effect on subsequent growth. These results provide insights into the failure of MMP inhibitors in clinical trials in patients with late stage lung cancer.
      13. URL :
        N/A
      14. Call Number :
        135742
      15. Serial :
        6904
      1. Author :
        Acuff, HB; Carter, KJ; Fingleton, B; Gorden, DL; Matrisian, LM
      2. Title :
        Matrix Metalloproteinase-9 from Bone Marrow–Derived Cells Contributes to Survival but not Growth of Tumor Cells in the Lung Microenvironment
      3. Type :
        Journal Article
      4. Year :
        2006
      5. Publication :
        Cancer Research
      6. Products :
      7. Volume :
        66
      8. Issue :
        N/A
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        IVIS, Xenogen
      12. Abstract :
        The role of specific stromal-derived matrix metalloproteinases (MMPs) was analyzed in experimental metastasis assays in wild-type and either MMP-9, MMP-7, or MMP-2 null mice. MMP-9 null mice showed an 81% reduction in Lewis lung carcinoma tumor number, whereas MMP-7 null mice showed a 42% increase in tumor number, and there was no difference in tumor number in MMP-2 null mice compared with wild-type controls. Similarly, in an orthotopic model of lung cancer, 50% fewer MMP-9 null mice were able to establish tumors in the lung compared with control mice, although the size of the tumors was not different. The effect of MMP-9 on lung tumor colonization was dependent on the expression of MMP-9 from bone marrow-derived cells and is most likely contributed by neutrophils. To examine temporal effects of stromal MMP-9, bioluminescence imaging from luciferase-expressing human lung cancer-derived A549 cells revealed that there were fewer tumor cells in the lungs of MMP-9 null mice as early as 19 hours after injection compared with control mice, with no difference in subsequent growth rates. Six hours after injection of tumor cells, MMP-9 null mice showed a 4-fold increase in the percent of tumor cells undergoing apoptosis compared with control mice. We conclude that MMP-9 from the bone marrow contributes to the early survival and establishment of tumors in the lung and has no effect on subsequent growth. These results provide insights into the failure of MMP inhibitors in clinical trials in patients with late-stage lung cancer.
      13. URL :
        N/A
      14. Call Number :
        135739
      15. Serial :
        6837
      1. Author :
        Acuff, Nicole V.; Li, Xin; Latha, Krishna; Nagy, Tamas; Watford, Wendy T.
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2017
      5. Publication :
        Infection and Immunity
      6. Products :
      7. Volume :
        N/A
      8. Issue :
        N/A
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        IVIS; IVIS BLI in vivo
      12. Abstract :
        Tumor progression locus 2 (Tpl2) is a serine-threonine kinase that regulates Th1 differentiation, secretion of the inflammatory cytokine IFNγ, and host defense against the intracellular pathogens Toxoplasma gondii, Listeria monocytogenes, and Mycobacterium tuberculosis. However, there is relatively little known about the contribution of Tpl2 to Th17 differentiation and immune cell function during infection with an extracellular pathogen. The goal of this study was to determine whether Tpl2 influences the immune response generated to the extracellular bacterium Citrobacter rodentium, which induces a mixed Th1/Th17 response. During peak infection with C. rodentium, Tpl2-/- mice experienced greater bacterial burdens with evidence of dissemination to the liver and spleen but ultimately cleared the bacteria within three weeks post infection similar to wild type mice. Tpl2-/- mice also recruited fewer neutrophils and monocytes to the colon during peak infection, which correlated with increased bacterial burdens. In mixed bone marrow chimeras, Tpl2 was shown to play a T-cell intrinsic role in promoting both IFNγ and IL-17A production during infection with C. rodentium. However, upon CD4 T cell transfer into Rag-/- mice, Tpl2-/- CD4 T cells were equally protective as wild type CD4 T cells against dissemination of bacteria and mortality. These data indicate that enhanced bacterial burdens in Tpl2-/- mice are not caused primarily by impairments in CD4 T cell function but result from defects in innate immune cell recruitment and function.
      13. URL :
        http://iai.asm.org/content/early/2017/07/25/IAI.00193-17.abstract
      14. Call Number :
        PKI @ catherine.lautenschlager @ 14159
      15. Serial :
        14235
      1. Author :
        Adachi, T; Kawakami, E; Ishimaru, N; Ochiya, T; Hayashi, Y; Ohuchi, H; Tanihara, M; Tanaka, E; Noji, S
      2. Title :
        Delivery of small interfering RNA with a synthetic collagen poly (Pro Hyp Gly) for gene silencing in vitro and in vivo
      3. Type :
        Journal Article
      4. Year :
        2010
      5. Publication :
        Development, Growth & Differentiation
      6. Products :
      7. Volume :
        52
      8. Issue :
        N/A
      9. Page Numbers :
        693
      10. Research Area :
        N/A
      11. Keywords :
        IVIS, Xenogen
      12. Abstract :
        Silencing gene expression by small interfering RNAs (siRNAs) has become a powerful tool for the genetic analysis of many animals. However, the rapid degradation of siRNA and the limited duration of its action in vivo have called for an efficient delivery technology. Here, we describe that siRNA complexed with a synthetic collagen poly(Pro-Hyp-Gly) (SYCOL) is resistant to nucleases and is efficiently transferred into cells in vitro and in vivo, thereby allowing long-term gene silencing in vivo. We found that the SYCOL-mediated local application of siRNA targeting myostatin, coding a negative regulator of skeletal muscle growth, in mouse skeletal muscles, caused a marked increase in the muscle mass within a few weeks after application. Furthermore, in vivo administration of an anti-luciferase siRNA/SYCOL complex partially reduced luciferase expression in xenografted tumors in vivo. These results indicate a SYCOL-based non-viral delivery method could be a reliable simple approach to knockdown gene expression by RNAi in vivo as well as in vitro.
      13. URL :
        N/A
      14. Call Number :
        135745
      15. Serial :
        5847
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