Relevant bibliographies by topics / AZD8055

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Academic literature on the topic 'AZD8055'

Author: Grafiati
Published: 4 June 2021
Last updated: 2 February 2022

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Journal articles on the topic "AZD8055"

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Marshall, Gayle, Zoe Howard, Jonathan Dry, et al. "Benefits of mTOR kinase targeting in oncology: pre-clinical evidence with AZD8055." Biochemical Society Transactions 39, no. 2 (2011): 456–59. http://dx.doi.org/10.1042/bst0390456.

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AZD8055 is a small-molecule inhibitor of mTOR (mammalian target of rapamycin) kinase activity. The present review highlights molecular and phenotypic differences between AZD8055 and allosteric inhibitors of mTOR such as rapamycin. Biomarkers, some of which are applicable to clinical studies, as well as biological effects such as autophagy, growth inhibition and cell death are compared between AZD8055 and rapamycin. Potential ways to develop rational combinations with mTOR kinase inhibitors are also discussed. Overall, AZD8055 may provide a better therapeutic strategy than rapamycin and analogu
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Cirstea, Diana, Teru Hideshima, Loredana Santo, et al. "Rational Combination Treatment of a Novel Selective mTOR Kinase Inhibitor AZD8055 with IGF-1R Inhibitors in Multiple Myeloma." Blood 120, no. 21 (2012): 4023. http://dx.doi.org/10.1182/blood.v120.21.4023.4023.

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Abstract Abstract 4023 Background: mTOR kinase-targeted therapy is in the early phase of clinical evaluation in multiple myeloma (MM). Despite promising preclinical results with mTOR inhibitors, resistance to this class of drugs in MM patients may occur due to feedback Akt activation by mTORC1. This led to the development of mTORC1/2 inhibition strategies in the treatment for MM, predicated upon the rationale that mTORC2 inhibitors prevent inhibition of mTORC1 blockade-induced feedback AKT activation by mTORC1 inhibitors. Indeed, our previous studies using a novel dual mTORC1 and mTORC2 select
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Cosimo, Emilio, Anuradha Tarafdar, Ailsa Holroyd, Karen Dunn, Mark Catherwood, and Alison M. Michie. "The ATP-Competitive mTOR Inhibitor AZD8055 Reduces Cell Proliferation and Tumour Load in Chronic Lymphocytic Leukaemia." Blood 126, no. 23 (2015): 5287. http://dx.doi.org/10.1182/blood.v126.23.5287.5287.

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Abstract Chronic lymphocytic leukaemia (CLL), often diagnosed in the elderly, is incurable with current therapeutic regimes. Recent studies demonstrate that the microenvironment within CLL patient lymphoid organs protects leukaemic cells from chemotherapy induced apoptosis. This highlights the need for novel therapies that can overcome such cytoprotective signals. Serine/threonine protein kinase mammalian target for rapamycin (mTOR) is a key regulator of cell survival and proliferation and is commonly deregulated in cancer. mTOR is active in two complexes mTORC1 and mTORC2. We demonstrate that
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Zhuo, Fengping, Fangjie Xiong, Kexuan Deng, Zhengguo Li, and Maozhi Ren. "Target of Rapamycin (TOR) Negatively Regulates Ethylene Signals in Arabidopsis." International Journal of Molecular Sciences 21, no. 8 (2020): 2680. http://dx.doi.org/10.3390/ijms21082680.

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Target of rapamycin (TOR) acts as a master regulator in coordination of cell growth with energy and nutrient availability. Despite the increased appreciation of the essential role of the TOR complex in interaction with phytohormone signaling, little is known about its function on ethylene signaling. Here, through expression analysis, genetic and biochemical approaches, we reveal that TOR functions in the regulation of ethylene signals. Transcriptional analysis indicates that TOR inhibition by AZD8055 upregulated senescence- and ethylene-related genes expression. Furthermore, ethylene insensiti
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Cirstea, Diana, Teru Hideshima, Loredana Santo, et al. "Disruption of DEPTOR/mTORC1/mTORC2 Signaling Cascade Using a Novel Selective mTOR Kinase Inhibitor AZD8055 Results In Growth Arrest and Apoptosis In Multiple Myeloma Cells." Blood 116, no. 21 (2010): 791. http://dx.doi.org/10.1182/blood.v116.21.791.791.

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Abstract Abstract 791 Targeting PI3K/Akt/mTOR signaling is among one of the promising therapeutic strategies in multiple myeloma (MM), since it facilitates MM cell survival and development of drug resistance in the context of the bone marrow microenvironment. Specifically, regulation of PI3K activity, which mediates MM cell growth and drug resistance, by mTOR complex 1 (mTORC1) provides the rationale for use of rapamycin analogs for MM treatment. However, rapamycin alone fails to overcome bone marrow-induced proliferation of MM cells, at least in part, because of the mTORC1-dependent feedback
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Pelloski, Christopher E., Rita Kaplon, Mersiha Hadziahmetovic, et al. "The application of radiotherapy to the pediatric preclinical testing program: Results of a pilot study." Journal of Clinical Oncology 30, no. 15_suppl (2012): 9544. http://dx.doi.org/10.1200/jco.2012.30.15_suppl.9544.

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9544 Background: The Pediatric Preclinical Testing Program (PPTP) has been successfully utilized to determine the efficacy of novel agents by testing via its mouse-flank in vivo model. We report on the feasibility and biologic outcomes of a pilot study using rhabdomyosarcoma (RMS) xenograft lines treated with radiotherapy (RT) alone and concurrently with the mTOR tyrosine kinase inhibitor, AZD8055, using the PPTP model. Methods: We developed a mouse flank irradiation device for daily delivery of RT in clinically relevant doses (2 Gy per fraction up to 40 Gy).Two RMS xenograft lines of the PPTP
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Guo, Zhixin, Keyu Zhao, Xue Feng та ін. "mTORC2 Regulates Lipogenic Gene Expression through PPARγ to Control Lipid Synthesis in Bovine Mammary Epithelial Cells". BioMed Research International 2019 (16 травня 2019): 1–11. http://dx.doi.org/10.1155/2019/5196028.

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The mechanistic target of rapamycin complex 2 (mTORC2) primarily functions as an effector of insulin/PI3K signaling to regulate cell proliferation and is associated with cell metabolism. However, the function of mTORC2 in lipid metabolism is not well understood. In the present study, mTORC2 was inactivated by the ATP-competitive mTOR inhibitor AZD8055 or shRNA targeting RICTOR in primary bovine mammary epithelial cells (pBMECs). MTT assay was performed to examine the effect of AZD8055 on cell proliferation. ELISA assay and GC-MS analysis were used to determine the content of lipid. The mRNA an
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Cirstea, Diana, Teru Hideshima, Loredana Santo, et al. "DEPTOR Is a Regulator of Response to mTOR Kinase Inhibitors in Multiple Myeloma." Blood 118, no. 21 (2011): 2916. http://dx.doi.org/10.1182/blood.v118.21.2916.2916.

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Abstract Abstract 2916 Inhibition of the PI3K/mTOR pathway is a promising therapeutic strategy in targeting multiple myeloma (MM) cells in the bone marrow (BM) microenvironment, which abnormally activates PI3K/mTOR signaling cascade mediating proliferation, anti-apoptosis and drug resistance. Exploring the targeting of PI3K/mTOR pathway has led to the development of different therapeutic approaches; however, mTORC1 inhibitors (i.e., temsirolimus and everolimus) have demonstrated only modest activity as single agents. In this regard, several mechanisms underlying rapamycin resistance, including
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Faber, Anthony C., Anna F. Farago, Carlotta Costa, et al. "Assessment of ABT-263 activity across a cancer cell line collection leads to a potent combination therapy for small-cell lung cancer." Proceedings of the National Academy of Sciences 112, no. 11 (2015): E1288—E1296. http://dx.doi.org/10.1073/pnas.1411848112.

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BH3 mimetics such as ABT-263 induce apoptosis in a subset of cancer models. However, these drugs have shown limited clinical efficacy as single agents in small-cell lung cancer (SCLC) and other solid tumor malignancies, and rational combination strategies remain underexplored. To develop a novel therapeutic approach, we examined the efficacy of ABT-263 across >500 cancer cell lines, including 311 for which we had matched expression data for select genes. We found that high expression of the proapoptotic gene Bcl2-interacting mediator of cell death (BIM) predicts sensitivity to ABT-263. In p
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Du, Juan, Anli Tong, Fen Wang, et al. "The Roles of PI3K/AKT/mTOR and MAPK/ERK Signaling Pathways in Human Pheochromocytomas." International Journal of Endocrinology 2016 (2016): 1–8. http://dx.doi.org/10.1155/2016/5286972.

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Objectives. The roles of PI3K/AKT/mTOR and MAPK/ERK pathways involved in the pathogenesis of pheochromocytoma and paraganglioma (PPGL) were demonstrated mostly by in vitro studies with rat or mouse cells and were mainly studied at transcriptional level. This study aimed to investigate the effect of these pathways on the proliferation of human PPGL cells and the activation of these pathways in PPGLs. Methods. Human PPGL cells were treated with sunitinib and inhibitors of PI3K (LY294002), MEK1/2 (U0126), and mTORC1/2 (AZD8055). Cell proliferation was detected by MTT assay. Protein phosphorylatio
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Dissertations / Theses on the topic "AZD8055"

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Harchouni, Seddik. "Manipulation des voies de signalisation de l'énergie pour améliorer la production des biocarburants chez les organismes photosynthétiques." Thesis, Aix-Marseille, 2018. http://www.theses.fr/2018AIXM0498.

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Les triacylglycérol (TAG) est un métabolite hautement énergétique qui peut être facilement converti en biodiesel. Les TAG peuvent être produits à partir de plantes et de microalgues. L'étude des voies de signalisation de l'énergie peut offrir de nouvelles stratégies pour améliorer l'accumulation de biomasse et de TAG sans compromettre la croissance. Dans cette thèse, j'ai étudié le rôle de deux voies principales de signalisation énergétique: la voie du de guanosine ppGpp (guanosine penta(tétra) phosphate) dans le chloroplaste et la voie de TOR (Target of rapamycin) dans le cytosol. J'ai choisi
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Willems, Lise. "Implication de la glutamine dans l’activation de mTORC1 dans les leucémies aiguës myéloïdes et inhibition ciblée." Thesis, Paris 5, 2012. http://www.theses.fr/2012PA05S016/document.

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Dans les leucémies aiguës myéloïdes (LAM), l’activation anormale de nombreuses voies de signalisation intracellulaires favorise la croissance et la survie des cellules tumorales. L’amélioration des connaissances biologiques de ces pathologies hétérogènes, dont le pronostic est réservé, devrait permettre le développement de thérapies ciblées. La kinase oncogénique mTOR est présente au sein de deux complexes, parmi lesquels mTORC1, activé constitutivement dans la majorité des blastes primaires de patients porteurs de LAM, qui contrôle la synthèse protéique, et mTORC2 activé constitutivement dans
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Corriea, Grinal. "THERAPEUTIC EFFICACY OF COMBINATION OF MTOR INHIBITORS AND AMPK ACTIVATORS IN NON-SMALL CELL LUNG CANCER." VCU Scholars Compass, 2014. http://scholarscompass.vcu.edu/etd/3558.

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Pemetrexed (PTX), an antifolate drug, has been approved by the US FDA for first line therapy of mesothelioma and non-small cell lung cancer. In addition to its primary site of action on thymidylate synthase (TS), PTX also inhibits the second folate-dependent enzyme of purine biosynthesis aminoimidazolecarboxamide ribonucleotide formyltransferase (AICART). The accumulation of the substrate for AICART, ZMP, in PTX-inhibited cancer cells leads to activation of AMP-activated protein kinase (AMPK) with subsequent inhibition of mammalian target of rapamycin (mTOR) and hypophosphorylation of its down
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Willems, Lise. "Implication de la glutamine dans l'activation de mTORC1 dans les leucémies aiguës myéloïdes et inhibition ciblée." Phd thesis, Université René Descartes - Paris V, 2012. http://tel.archives-ouvertes.fr/tel-00868018.

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Dans les leucémies aiguës myéloïdes (LAM), l'activation anormale de nombreuses voies de signalisation intracellulaires favorise la croissance et la survie des cellules tumorales. L'amélioration des connaissances biologiques de ces pathologies hétérogènes, dont le pronostic est réservé, devrait permettre le développement de thérapies ciblées. La kinase oncogénique mTOR est présente au sein de deux complexes, parmi lesquels mTORC1, activé constitutivement dans la majorité des blastes primaires de patients porteurs de LAM, qui contrôle la synthèse protéique, et mTORC2 activé constitutivement dans
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Lee, Cheng-Hung, and 李政鴻. "In vitro and in vivo antitumor effect of mammalian target of rapamycin (mTOR) inhibitor AZD8055 in colon cancer cell line." Thesis, 2016. http://ndltd.ncl.edu.tw/handle/91344979666397450491.

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碩士<br>元智大學<br>生物科技與工程研究所<br>104<br>Cancer is the leading cause of death in Taiwan. Among all kinds of cancers, the incidence of colon cancer is highest. How to improve survival after treatment for colon cancer becomes an important issue. In recent decade, the overall survival rate has been improved due to new drugs development and application. Therefore, many research studies have been focused on other effective drugs. Mammalian target of rapamycin (mTOR) is regulatory center for cell proliferation and survival. Inhibition of mTOR as anti-cancer effect has been proven. Currently first generat
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Conference papers on the topic "AZD8055"

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Sabnis, Gauri J., Armina Kazi, Olga Goloubeva, et al. "Abstract 2919: Effect of selumetinib and AZD8055 on the growth of anastrozole resistant tumors." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-2919.

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Dai, Yao, and Dietmar Siemann. "Abstract 4495: Treatment effects of the novel mTOR kinase inhibitor AZD8055 in prostate cancer cell models." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-4495.

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Dai, Yao, and Dietmar W. Siemann. "Abstract 3761: Efficacy of the ATP-competitive mTOR inhibitor AZD8055 in PTEN-wild type cancer cells." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-3761.

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Houghton, Peter J., John M. Maris, Josh Courtright, et al. "Abstract C57: Pediatric Preclinical Testing Program (PPTP) Stage 1 evaluation of AZD8055 an inhibitor of mTOR Kinase." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Nov 15-19, 2009; Boston, MA. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/1535-7163.targ-09-c57.

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Naing, Aung, Carol Aghajanian, Eric Raymond, et al. "Abstract A168: First results from a phase I trial of AZD8055, a dual mTORC1 and mTORC2 inhibitor." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Nov 12-16, 2011; San Francisco, CA. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1535-7163.targ-11-a168.

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Keen, Heather, Sally‐Ann Ricketts, Juliana Bales, et al. "Abstract A225: The mTOR kinase inhibitor AZD8055 modulates18F‐FDG uptakein vivoin the human glioma xenograft model U87‐MG." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Nov 15-19, 2009; Boston, MA. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/1535-7163.targ-09-a225.

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Serova, Maria, Jacqueline Koumaravel, Ivan Bieche, et al. "Abstract B141: Effects of AZD8055, a novel mTOR kinase inhibitor, in human cancer cells developing resistance to rapamycin." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Nov 15-19, 2009; Boston, MA. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/1535-7163.targ-09-b141.

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Jiang, Qun, Jonathan M. Weiss, John R. Ortaldo, et al. "Abstract 5596: Enhanced anti-tumor effect of combination therapy with anti-CD40 antibody and the mTOR kinase inhibitor AZD8055." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-5596.

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Vaughan, Lynsey S., Karen Barker, Hannah Webber, et al. "Abstract 4345: AZD8055, a combined TORC1/TORC2 inhibitor regulates Mycn protein expression and prevents neuroblastoma growth in vitro and in vivo." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-4345.

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Rodrik-Outmezguine, Vanessa S., Nen Cao, Sarat Chandarlapaty, et al. "Abstract 5038: AZD8055 is an effective inhibitor of mTOR kinase signaling and breast cancer growth while relieving feedback inhibition of HER-kinase signaling." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-5038.

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