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Relevant bibliographies by topics / Receptor MET

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Academic literature on the topic 'Receptor MET'

Author: Grafiati

Published: 4 June 2021

Last updated: 18 February 2022

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Journal articles on the topic "Receptor MET"

1

Faoro, Leonardo, Gustavo M. Cervantes, Essam El-Hashani, and Ravi Salgia. "MET Receptor Tyrosine Kinase." Journal of Thoracic Oncology 4, no. 11 (November 2009): S1064—S1065. http://dx.doi.org/10.1097/01.jto.0000361752.86918.09.

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Safaie Qamsari, Elmira, Sepideh Safaei Ghaderi, Bahareh Zarei, Ruhollah Dorostkar, Salman Bagheri, Farhad Jadidi-Niaragh, Mohammad Hossein Somi, and Mehdi Yousefi. "The c-Met receptor: Implication for targeted therapies in colorectal cancer." Tumor Biology 39, no. 5 (May 2017): 101042831769911. http://dx.doi.org/10.1177/1010428317699118.

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c-Met (mesenchymal–epithelial transition factor) is a tyrosine kinase receptor activated by hepatocyte growth factor and regulates multiple biological processes, such as cell scattering, survival, and proliferation. Aberrant c-Met signaling has been implicated in a variety of cancer types, including colorectal cancer. c-Met is genetically altered through various mechanisms that is associated with colorectal cancer progression and metastasis. Especially, in colorectal cancer, preclinical evidence for the aberrant activation of the c-Met signaling exists. Accordingly, molecular targeting of c-Met receptor could be a promising strategy, in the treatment of colorectal cancer patients. Recently, it was also shown that crosstalk between c-Met and other cell surface receptors attributes to tumorigenesis and development of therapeutic resistance. Characterization of the molecular mechanisms through which c-Met crosstalks with other receptors in favor of tumor formation and progression remains to explore. This review will describe the mechanisms of aberrant c-Met signaling in colorectal cancer and discuss on additional roles for c-Met receptor through crosstalk with other tyrosine kinase receptors and cell surface proteins in colorectal cancer. Novel therapeutic approaches for c-Met pathway targeting will also be discussed.

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Clague, M. J. "Met Receptor: A Moving Target." Science Signaling 4, no. 190 (September 6, 2011): pe40. http://dx.doi.org/10.1126/scisignal.2002422.

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Lai, Andrea Z., Jasmine V. Abella, and Morag Park. "Crosstalk in Met receptor oncogenesis." Trends in Cell Biology 19, no. 10 (October 2009): 542–51. http://dx.doi.org/10.1016/j.tcb.2009.07.002.

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Carter, Stephanie, Sylvie Urbé, and Michael J. Clague. "The Met Receptor Degradation Pathway." Journal of Biological Chemistry 279, no. 51 (October 5, 2004): 52835–39. http://dx.doi.org/10.1074/jbc.m407769200.

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Goldoni, Silvia, Ashley Humphries, Alexander Nyström, Sampurna Sattar, Rick T. Owens, David J. McQuillan, Keith Ireton, and Renato V. Iozzo. "Decorin is a novel antagonistic ligand of the Met receptor." Journal of Cell Biology 185, no. 4 (May 11, 2009): 743–54. http://dx.doi.org/10.1083/jcb.200901129.

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Decorin, a member of the small leucine-rich proteoglycan gene family, impedes tumor cell growth by down-regulating the epidermal growth factor receptor. Decorin has a complex binding repertoire, thus, we predicted that decorin would modulate the bioactivity of other tyrosine kinase receptors. We discovered that decorin binds directly and with high affinity (Kd = ∼1.5 nM) to Met, the receptor for hepatocyte growth factor (HGF). Binding of decorin to Met is efficiently displaced by HGF and less efficiently by internalin B, a bacterial Met ligand. Interaction of decorin with Met induces transient receptor activation, recruitment of the E3 ubiquitin ligase c-Cbl, and rapid intracellular degradation of Met (half-life = ∼6 min). Decorin suppresses intracellular levels of β-catenin, a known downstream Met effector, and inhibits Met-mediated cell migration and growth. Thus, by antagonistically targeting multiple tyrosine kinase receptors, decorin contributes to reduction in primary tumor growth and metastastic spreading.

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Bolanos-Garcia, Victor Martin. "MET meet adaptors: Functional and structural implications in downstream signalling mediated by the Met receptor." Molecular and Cellular Biochemistry 276, no. 1-2 (August 2005): 149–57. http://dx.doi.org/10.1007/s11010-005-3696-6.

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Sachs, M., K. M. Weidner, V. Brinkmann, I. Walther, A. Obermeier, A. Ullrich, and W. Birchmeier. "Motogenic and morphogenic activity of epithelial receptor tyrosine kinases." Journal of Cell Biology 133, no. 5 (June 1, 1996): 1095–107. http://dx.doi.org/10.1083/jcb.133.5.1095.

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Receptor tyrosine kinases play essential roles in morphogenesis and differentiation of epithelia. Here we examined various tyrosine kinase receptors, which are preferentially expressed in epithelia (c-met, c-ros, c-neu, and the keratin growth factor [KGF] receptor), for their capacity to induce cell motility and branching morphogenesis of epithelial cells. We exchanged the ligand-binding domain of these receptors by the ectodomain of trkA and could thus control signaling by the new ligand, NGF. We demonstrate here that the tyrosine kinases of c-met, c-ros, c-neu, the KGF receptor, and trkA, but not the insulin receptor, induced scattering and increased motility of kidney epithelial cells in tissue culture. Mutational analysis suggests that SHC binding is essential for scattering and increased cell motility induced by trkA. The induction of motility in epithelial cells is thus an important feature of various receptor tyrosine kinases, which in vivo play a role in embryogenesis and metastasis. In contrast, only the c-met receptor promoted branching morphogenesis of kidney epithelial cells in three-dimensional matrices, which resemble the formation of tubular epithelia in development. Interestingly, the ability of c-met to induce morphogenesis could be transferred to trkA, when in a novel receptor hybrid COOH-terminal sequences of c-met (including Y14 to Y16) were fused to the trkA kinase domain. These data demonstrate that tubulogenesis of epithelia is a restricted activity of tyrosine kinases, as yet only demonstrated for the c-met receptor. We predict the existence of specific substrates that mediate this morphogenesis signal.

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Short, Ben. "Decorin has Met a new receptor." Journal of Cell Biology 185, no. 4 (May 11, 2009): 566. http://dx.doi.org/10.1083/jcb.1854iti3.

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Niemann, Hartmut H. "Structural insights into Met receptor activation." European Journal of Cell Biology 90, no. 11 (November 2011): 972–81. http://dx.doi.org/10.1016/j.ejcb.2010.11.014.

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Dissertations / Theses on the topic "Receptor MET"

1

Anderson, Ian Paul. "Met receptor signalling." Thesis, University of Liverpool, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.526784.

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Carter, Stephanie. "Met receptor dynamics and signalling." Thesis, University of Liverpool, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.404701.

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Kamikura, Darren M. "Structurefunction analysis of the met receptor oncoprotein, Tpr-met." Thesis, McGill University, 1999. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=37575.

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The Met protooncogene encodes a receptor tyrosine kinase that is deregulated by point mutation, and overexpression/amplification in a number of human tumours. The Met receptor is also oncogenically activated following genomic rearrangement which generates a cytoplasmic, constitutively activated fusion protein, Tpr-Met. In addition to autophosphorylation sites within the catalytic domain, the carboxy terminus of Tpr-Met/Met contains a single major site of autophosphorylation, tyrosine 489. This tyrosine residue represents a unique multisubstrate binding site, capable of binding numerous intracellular proteins, and is critical for the biological activities of both the Met receptor and Tpr-Met oncoprotein. Addition of the c-src myristoylation sequence to the amino terminus of the normally cytoplasmic Tpr-Met, localizes Tpr-Met to plasma membranes and enhances cellular transformation, in vitro invasion, and tumourigenicity. Furthermore, a membrane targetted Tpr-Met is localized to a similar subcellular compartment as the Met receptor, and alters the complement of signalling proteins required for efficient transformation. In this respect, a membrane localized Tpr-Met resembles oncogenic forms of the transmembrane Met receptor, and provides a model with which to study transformation by Met receptor oncoproteins. Significantly, membrane localization of Tpr-Met induces a phosphoinositide 3' kinase (PI3' K) dependent autocrine loop, involving the production of hyaluronic acid (HA), and post-translational modification of the cell surface receptor for HA, CD44. PI3'K activity and the HA/CD44 autocrine loop, are dependent on the multisubstrate binding site, tyrosine 489, and tyrosine residue 498, a residue with no previously described biochemical function. Although the exact mechanisms by which PI3'K regulates HA production are unclear, the induction of a HA/CD44 autocrine loop may represent a novel mechanism by which deregulated receptor tyrosine kinases increase their onco

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Kamikura, Darren M. "Structure/function analysis of the Met receptor oncoprotein, Tpr-Met." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape7/PQDD_0019/NQ55343.pdf.

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Sirulnik, Leonardo Andres. "Studies on the human c-Met receptor." Thesis, University of Cambridge, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.362813.

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Cheung, Man-ting, and 張敏婷. "Expression of met receptor tyrosine kinase in hepatocellularcarcinoma." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2011. http://hub.hku.hk/bib/B4669965X.

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Paliouras, Grigorios. "Regulation of met receptor tyrosine kinase signalling and biology." Thesis, McGill University, 2010. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=86661.

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Growth factor receptor tyrosine kinases (RTKs) are critical initiators of signal transduction pathways necessary for cell growth, differentiation, migration and survival. Many of these signals are coordinated through scaffold proteins that are phosphorylated upon their recruitment to the activated receptor complex. This provides binding sites for multiple proteins to activate and generate distinct biological responses. The amplitude and duration of a signal is regulated via dephosphorylation and degradation of target proteins. Signal regulation in this manner acts to promote the formation and disassembly of multi-protein complexes and diversify and localize signals downstream from RTKs.
The Met RTK and its ligand, hepatocyte growth factor (HGF), are positive regulators of epithelial morphogenesis, scatter, and survival. However little was known regarding the proteins responsible for attenuating Met receptor activation. In Chapter II, I demonstrated that the Met receptor was hyperphopshorylated in PTP1B-null mice in response to Fas-induced liver damage. Inhibition of Met signaling with PHA665752, removed protection from liver failure in PTP1B-null hepatocytes, demonstrating that PTP1B was a negative regulator of the Met RTK and its removal promoted cell survival against Fas-induced hepatic failure.
In response to Met receptor stimulation, the Gab1 scaffold protein is the prominent protein recruited and phosphorylated downstream from Met and is critical in mediating Met-dependent biological responses. In chapters III and IV, I identified the serine/threonine kinase Pak4 and the microtubule-bound guanine nucleotide exchange factor GEF-H1 as novel proteins recruited to Gab1 following Met receptor activation. I demonstrate that Gab1 and Pak4 synergize to enhance migration and invasion following HGF stimulation. Furthermore, the recruitment of Pak4 to Gab1 is important for its subcellular localization to lamellipodia and critical for epithelial cell dispersal and morphogenesis downstream from Met. In addition, GEF-H1 is important in focal adhesion formation and turnover and this correlates with the ability of GEF-H1 to promote epithelial migration and invasion downstream from Met.
Overall, these studies investigate molecular mechanisms regulating Met-dependent signals and demonstrate for the first time that the Met receptor is a substrate for PTP1B and identify Pak4 and GEF-H1 as key integrators of Met dependent cellular migration and invasion.
Les récepteurs tyrosine kinase aux facteurs de croissance sont des initiateurs critiques des voies de signalisation nécessaires à la croissance, la différentiation, la migration et la survie cellulaire. Beaucoup de ces signaux sont coordonnés par des protéines d'échafaudage qui sont phosphorylées au cours de leur recrutement au complexe de récepteurs activés. Ceci fournit des sites de liaison à de multiples protéines permettant l'activation et la génération de différentes réponses biologiques. L'amplitude et la durée d'un signal est régulée via la déphosphorylation et la dégradation des protéines cibles. De cette façon, la régulation du signal agit pour promouvoir la formation et le désassemblage de complexes protéiques et pour diversifier et localiser les signaux en aval des récepteurs tyrosine kinase.
Le récepteur Met et son ligand HGF (Hepatocyte Growth Factor) sont des régulateurs de la morphogenèse, la dispersion et la survie des cellules épithéliales. Toutefois, peu d'informations sont disponibles sur les protéines responsables de l'extinction des signaux issus du récepteur Met. Dans le chapitre II, je démontre que le récepteur Met est hyperphosphorylé dans les souris knock-out pour PTP1B en réponse aux dommages induits par Fas. L'inhibition par le composé PHA665752 de la signalisation par Met, relève la protection contre les crises hépatiques dans les souris KO pour PTP1B. Ceci démontre que PTP1B est un régulateur négatif de Met et son retrait permet la survie cellulaire contre les crises hépatiques induites par Fas.
En réponse à la stimulation du récepteur Met, la protéine d'échafaudage Gab1 est la plus importante des protéines recrutées et phosphorylées en aval de Met et cette protéine est critique dans la médiation des réponses biologiques dépendantes de Met. Dans les chapitres III et IV, j'ai identifié la kinase Ser/Thr Pak4 et le facteur d'échange de guanine lié aux microtubules (GEF-H1) en tant que nouvelles protéines recrutées à Gab1 suite à l'activation de Met. Je démontre que Gab1 et Pak4 agissent de façon synergique pour promouvoir la migration et l'invasion suite à la stimulation par HGF. De plus, le recrutement de Pak4 à Gab1 est important pour sa localisation cellulaire dans les lamellipodes et est critique pour la dispersion et la morphogenèse des cellules épithéliales en aval de Met. En outre, GEF-H1 est important pour la formation et le roulement des points d'adhésion focaux ce qui est en corrélation avec la capacité de GEF-H1 de promouvoir la migration et l'invasion épithéliale en aval de Met.
Ces études ont pour but d'investiguer les mécanismes moléculaires régulant les signaux dépendants de Met et démontrent pour la première fois que le récepteur Met est un substrat pour PTP1B. Finalement, Pak4 et GEF-H1 sont identifiés comme des intégrateurs clés de la migration et l'invasion cellulaire dépendante de Met.

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Yamamoto, Brent Joseph. "Norleual, an angiotensin IV receptor ligand and C-Met antagonist." Online access for everyone, 2006. http://www.dissertations.wsu.edu/Dissertations/Summer2006/B%5FYamamoto%5F071206.pdf.

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9

Petkiewicz, Stephanie L. "The Met receptor tyrosine kinase in mammary gland tumorigenesis and development /." Thesis, McGill University, 2007. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=103278.

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The Met receptor tyrosine kinase (RTK) is expressed in the mammary gland under both normal and neoplastic conditions. Overexpression of the Met receptor is found in 15--20% of human breast cancers and is correlated with shortened disease-free interval and overall survival. In order to explore the role of dysregulated Met receptor signaling on the development of mammary tumors I have characterized a transgenic mouse model that expresses either wild type or a dysregulated Met receptor in the mammary epithelium under the control of the mouse mammary tumor virus promoter/enhancer (MMTV-Met). The Met receptor variants contained a mutation that results in decreased receptor ubiquitination and prolonged receptor signaling (Y1003F) or an activating mutation that was originally observed in patients with papillary renal carcinoma (M1250T) or both mutations (YF/MT). In vitro and in vivo transformation assays demonstrated that each mutation singly is weakly transforming, however, there was an additive effect on transformation when both mutations were present. This additive effect was observed in the transgenic mice where multiparous MMTV-Met-YF/MT mice developed tumors earlier and with much greater penetrance than did mice expressing either of the single mutants. This provides the first in vivo model that demonstrates a role for ubiquitination in suppression of transforming activity of an RTK. MMTV-Met-YF/MT tumors displayed a range of histological phenotypes but were mainly comprised of luminal lineage cells. Notably, MMTV-Met-M1250T tumors contained cells from both the basal and luminal populations, suggesting transformation of a progenitor cell. Progenitor cell transformation in RTK transgenic mouse models is uncommon and highlights distinct signaling differences and potentially lineage specificity of the two Met mutants.
Through assays of overexpression in vivo and inhibition in vitro, Met receptor signaling has been correlated with the development of the mammary gland. To examine the effects of loss of Met receptor signaling on mammary gland development I have utilized the Cre/LoxP1 recombination system to knock-out the Met receptor from the mammary epithelium. Mammary-specific Cre recombinase efficiently excised floxed DNA as visualized by activation of a beta-galactosidase reporter In Met+/+ glands, however, few beta-galactosidase positive cells are retained In the Mefl/fl glands and an intermediate number are retained in the Met fl/+ glands. This indicates that Met-null cells are selected against and supports a role for Met in the development of the mammary gland.

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Luzac, Michal Leonie. "Small Molecules as Potential Inhibitors of the Met Tyrosine Kinase Receptor." Thesis, University College London (University of London), 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.498510.

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Books on the topic "Receptor MET"

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Somerset, David Alan. Hepatocyte growth factor (HGF) and its receptor c-met, in healthy and pathological human placentae. Birmingham: University of Birmingham, 2001.

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To, Christine Ting Ting. Overexpression of hepatocyte growth factor receptor/Met suppresses tumorigenecity of NCI-H1264 lung squamous carcimona cells. Ottawa: National Library of Canada, 1998.

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Spijker, Anke. Eten met plezier: Dieetinformatie en recepten voor nierpatiënten. 6th ed. Wormer: Inmerc, 2006.

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Rhoer, Sonja van de. Oranje Boven: Een culinaire geschiedenis met vorstelijke recepten. Houten: Van Dishoeck, 1997.

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Wouters, Valeer. Lekker West-Vlaanderen: Historische recepten met hedendaagse ingrediënten. Antwerpen: CODA, 1994.

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Bergman, Anneliese, Immy Timmerman, Miranda Castelein, and Annelène van Eijndhoven. Streep je slank..: Met 170 recepten & 70 tips & 40 oefeningen. 2nd ed. Hoofddorp: Sanoma, 2004.

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Koolsbergen, Titi. Vechten met gerechten tegen hoofdpijn en migraine: Voedingswijzer, recepten en adviezen. 's-Graveland: Fontaine Uitgevers, 2005.

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Hennie, Franssen-Seebregts, and efef com, eds. 500 chocoladegerechten: Heerlijke recepten voor groot en klein gebak met chocolade in de hoofdrol. Utrecht: Veltman Uitgevers, 2008.

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Boros, Peter. Hepatocyte growth factor: The basic principles. Austin: R.G. Landes, 1999.

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Gustave, Flaubert. Madame Bovary: Contexts, critical reception. Edited by Margaret Cohen. 2nd ed. New York, USA: W.W. Norton & Co., 2004.

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Book chapters on the topic "Receptor MET"

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Gao, ChongFeng, and George F. Vande Woude. "The MET Receptor Family." In Receptor Tyrosine Kinases: Family and Subfamilies, 321–58. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-11888-8_8.

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Hammond, D. E., S. Carter, and M. J. Clague. "Met Receptor Dynamics and Signalling." In Current Topics in Microbiology and Immunology, 21–44. Berlin, Heidelberg: Springer Berlin Heidelberg, 2004. http://dx.doi.org/10.1007/978-3-540-69494-6_2.

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Joffre, Carine, Rachel Barrow, Ludovic Ménard, and Stéphanie Kermorgant. "RTKs as Models for Trafficking Regulation: c-Met/HGF Receptor-c-Met Signalling in Cancer—Location Counts." In Vesicle Trafficking in Cancer, 261–77. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-6528-7_13.

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Wortinger, Mark, Jonathan Tetreault, Nick Loizos, and Ling Liu. "MET and RON Receptor Tyrosine Kinases as Therapeutic Antibody Targets for Cancer." In Extracellular Targeting of Cell Signaling in Cancer, 199–227. Chichester, UK: John Wiley & Sons, Ltd, 2018. http://dx.doi.org/10.1002/9781119300229.ch7.

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Gaziova, Ivana, Robert A. Davey, and Lisa A. Elferink. "Identification of Factors Regulating MET Receptor Endocytosis by High-Throughput siRNA Screening." In Membrane Trafficking, 381–94. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-2309-0_26.

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Streit, Andrea C. E., and Claudio D. Stern. "Competence for Neural Induction: HGF/SF, HGFl/MSP and the c-Met Receptor." In Ciba Foundation Symposium 212 - Plasminogen-Related Growth Factors, 155–68. Chichester, UK: John Wiley & Sons, Ltd., 2007. http://dx.doi.org/10.1002/9780470515457.ch10.

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Lokker, Nathalie A., Melanie R. Mark, and Paul J. Godowski. "Structure-Function Analysis of Hepatocyte Growth Factor and its Tyrosine-Kinase Receptor c-Met." In Tyrosine Phosphorylation/Dephosphorylation and Downstream Signalling, 99–102. Berlin, Heidelberg: Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-642-78247-3_8.

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Rodrigues, Gerard A., and Morag Park. "Oncogenic Activation of the Met/HGF Receptor Tyrosine Kinase is Promoted by Leucine Zipper Mediated Dimerization." In Tyrosine Phosphorylation/Dephosphorylation and Downstream Signalling, 103–6. Berlin, Heidelberg: Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-642-78247-3_9.

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Birchmeier, Carmen, Friedhelm Bladt, and Tomoichiro Yamaai. "The Functions of HGF/SF and its Receptor, the c-Met Tyrosine Kinase, in Mammalian Development." In Ciba Foundation Symposium 212 - Plasminogen-Related Growth Factors, 169–82. Chichester, UK: John Wiley & Sons, Ltd., 2007. http://dx.doi.org/10.1002/9780470515457.ch11.

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Löf, Christoffer, Tero Viitanen, Pramod Sukumaran, and Kid Törnquist. "TRPC2: Of Mice But Not Men." In Transient Receptor Potential Channels, 125–34. Dordrecht: Springer Netherlands, 2010. http://dx.doi.org/10.1007/978-94-007-0265-3_6.

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Conference papers on the topic "Receptor MET"

1

DaSilva, John. "Abstract 34: A MET x MET bispecific antibody that induces receptor degradation potently inhibits the growth of MET-addicted tumor xenografts." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-34.

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Yam, Judy Wai Ping, and Sze Keong Tey. "Abstract 5266: Role of nuclear Met receptor in hepatocellular carcinoma." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-5266.

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Lai, Andrea, and Morag Park. "Abstract 4688: Met receptor tyrosine kinase cross-talk in tumorigenesis." 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.am2011-4688.

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Bordeaux, Jennifer, Jason A. Hanna, Seema Agarwal, and David L. Rimm. "Abstract 280: Met (the HGF receptor) localizes to the nucleus in wound healing." 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.am10-280.

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Cantelmo, Anna Rita, Ilaria Sogno, Douglas M. Noonan, Chiara Focaccetti, Elisa Principi, and Adriana Albini. "Abstract 2328: Targeting angiogenesis: Anti-docking site peptides to Met receptor and nanotechnology." 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.am2012-2328.

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Bell, Emily S., Dongmei Zuo, and Morag Park. "Abstract 3453: Autophagic regulation of the Met receptor tyrosine kinase in breast cancer." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-3453.

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Huang, Luying, Fuhao Wang, Haibo Tong, Atsushi Mizokami, Evan T. Keller, Yi Lu, and Jian Zhang. "Abstract 5896: Downregulation of calcium-sensing receptor enhances MET-mediated prostate cancer chemosensitivity." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-5896.

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Miekus, Katarzyna, Marta Pawlowska, and Marcin Majka. "Abstract 237: MET receptor is a potential new target for cervical carcinoma treatment." 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.am2011-237.

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Goetsch, Liliane, Matthieu Broussas, Stéphanie Fabre-Lafay, Alain Robert, Anne-Marie Lepecquet, Alexandra Gonzalez, Thierry Wurch, Christian Bailly, and Nathalie Corvaia. "Abstract 2448: h224G11, a humanized whole antibody targeting the c-Met receptor, induces c-Met down-regulation and triggers ADCC functions." 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.am10-2448.

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Stern, Yaakov E., Andrea Z. Lai, and Morag Park. "Abstract LB-77: The Met receptor tyrosine kinase drives signaling through EGFR and ErbB3 in Met-amplified non-small-cell lung cancer." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-lb-77.

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Reports on the topic "Receptor MET"

1

Bordeaux, Jennifer. Met (HGF Receptor) in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, September 2010. http://dx.doi.org/10.21236/ada535659.

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Bordeaux, Jennifer. Met (HGF Receptor) in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, September 2009. http://dx.doi.org/10.21236/ada515399.

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Deo, Salil, David McAllister, Naveed Sattar, and Jill Pell. The time-varying cardiovascular benefits of glucagon like peptide-1 agonist (GLP-RA)therapy in patients with type 2 diabetes mellitus: A meta-analysis of multinational randomized trials. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, July 2021. http://dx.doi.org/10.37766/inplasy2021.7.0097.

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Abstract:

Review question / Objective: P - patients with type 2 diabetes melllitus already receiving routine medical therapy; I - patients receiving glucagon like peptide 1 receptor agonist (GLP1 receptor agonist) therapy (semaglutide, dulaglutide, liraglutide, exenatide, lixisenatide, efpeglenatide, abiglutide); C - patients receiving standard therapy for diabetes mellitus but not receiving GLP1 agonist therapy; O - composite end point as per invididual trial, cardiovascular mortality, all-cause mortality, myocardial infarction, stoke. Condition being studied: Type 2 diabetes mellitus. Study designs to be included: Randomised controlled trials which enroll a large number of patients (defined as > 500) and are multinational in origin. Studies included will need to have published Kaplan and Meier curves for the end-points presented in the manuscript.

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Qiu, Mei, Liang-Liang Ding, and Hai-Rong Zhou. Impact of SGLT2 inhibitors and GLP1 receptor agonists on respiratory infections: a meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, January 2021. http://dx.doi.org/10.37766/inplasy2021.1.0092.

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Feng, Yu. Renal Safety and Efficacy of Angiotensin Receptor-neprilysin Inhibitor : a meta-analysis of Randomized Controlled Trials. INPLASY - International Platform of Registered Systematic Review Protocols, April 2020. http://dx.doi.org/10.37766/inplasy2020.4.0115.

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Conrad, Susan E. A Role for MEK-Interacting Protein 1 (MP1) in Hormone Responsiveness of Estrogen Receptor-Positive Breast Cancer Cells. Fort Belvoir, VA: Defense Technical Information Center, July 2008. http://dx.doi.org/10.21236/ada491116.

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Zhang, Yong, An-Jun Wang, Bo Wang, Heng Zhang, Shou-Liang Hu, Yan-Hong Tuo, and Tian Li. Efficacy and Safety of Mineralocorticoid Receptor Antagonists for Chronic Dialysis Patients: a Meta-Analysis of Randomized Controlled Studies. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, December 2020. http://dx.doi.org/10.37766/inplasy2020.12.0143.

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Qiu, Mei, Liang-Liang Ding, and Hai-Rong Zhou. Effects of SGLT2 inhibitors and GLP1 receptor agonists on risk of various arrhythmias: a meta-analysis of large randomized trials. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, January 2021. http://dx.doi.org/10.37766/inplasy2021.1.0102.

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Qiu, Mei, Liang-Liang Ding, and Hai-Rong Zhou. Effects of SGLT2 inhibitors and GLP1 receptor agonists on risk of various fractures: a meta-analysis of large randomized trials. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, January 2021. http://dx.doi.org/10.37766/inplasy2021.1.0103.

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Ma, Xiaocong, Liying Lu, Yan Tang, Weisheng Luo, Jianxiang Li, and Meiwen Tang. Association between Toll-like receptor gene polymorphisms and risk of Helicobacter pylori infection: A protocol for systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, March 2021. http://dx.doi.org/10.37766/inplasy2021.3.0009.

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