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Relevant bibliographies by topics / MET/HGF

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Academic literature on the topic 'MET/HGF'

Author: Grafiati

Published: 15 June 2024

Last updated: 31 July 2025

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Journal articles on the topic "MET/HGF"

1

Toiyama, Y., K. Tanaka, H. Yasuda, et al. "Use of co-expression of HGF and c-Met to predict peritoneal dissemination established by autocrine HGF/c-Met signaling in gastric cancer." Journal of Clinical Oncology 29, no. 4_suppl (2011): 40. http://dx.doi.org/10.1200/jco.2011.29.4_suppl.40.

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40 Background: Epithelial mesencymal transition (EMT) promotes facilitates migration and invasion of epithelial tumour cells. EMT is induced by growth factors implicated in theses process such as hepatocyte growth factor (HGF). Our aim of this study is whether HGF/c-Met pathway is associated with metastasis of gastric cancer (GC), especially in peritoneal dissemination (PD). Methods: HGF and c-Met expression and EMT related molecules were evaluated using real-time PCR and immunohistochemistry in GC tissues. The role of HGF/c-Met pathway for EMT and anoikis was determined and c-Met TKI (SU11274

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Zhang, Hongli, Qingqing Feng, Wei-Dong Chen, and Yan-Dong Wang. "HGF/c-MET: A Promising Therapeutic Target in the Digestive System Cancers." International Journal of Molecular Sciences 19, no. 11 (2018): 3295. http://dx.doi.org/10.3390/ijms19113295.

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The HGF/c-MET pathway is active in the development of digestive system cancers, indicating that inhibition of HGF/c-MET signaling may have therapeutic potential. Various HGF/c-MET signaling inhibitors, mainly c-MET inhibitors, have been tested in clinical trials. The observed efficacy and adverse events of some c-MET inhibitors were not very suitable for treating digestive system cancers. The development of new HGF/c-MET inhibitors in preclinical studies may bring promising treatments and synergistic combination (traditional anticancer drugs and c-MET inhibitors) strategies provided anacceptab

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Weimar, Iris S., Daphne de Jong, Egbert J. Muller та ін. "Hepatocyte Growth Factor/Scatter Factor Promotes Adhesion of Lymphoma Cells to Extracellular Matrix Molecules Via α4β1 and α5β1 Integrins". Blood 89, № 3 (1997): 990–1000. http://dx.doi.org/10.1182/blood.v89.3.990.

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Abstract Hepatocyte growth factor (HGF )/scatter factor (SF ) is the ligand for a tyrosine kinase cell surface receptor encoded by the MET protooncogene (c-MET). HGF/SF can induce proliferation and motility in epithelial cells and promotes invasion of carcinoma cells and NIH3T3 fibroblasts transfected with both HGF/SF and c-MET genes. Our results show that HGF/SF and c-MET also play a role in adhesion and invasion of human lymphoma cells. c-MET mRNA is expressed in hemopoietic cells, such as hemopoietic progenitor cells (CD34+ cells) in bone marrow (BM) and mobilized peripheral blood, immature

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Gallo, Simona, Valentina Sala, Stefano Gatti, and Tiziana Crepaldi. "Cellular and molecular mechanisms of HGF/Met in the cardiovascular system." Clinical Science 129, no. 12 (2015): 1173–93. http://dx.doi.org/10.1042/cs20150502.

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Met tyrosine kinase receptor, also known as c-Met, is the HGF (hepatocyte growth factor) receptor. The HGF/Met pathway has a prominent role in cardiovascular remodelling after tissue injury. The present review provides a synopsis of the cellular and molecular mechanisms underlying the effects of HGF/Met in the heart and blood vessels. In vivo, HGF/Met function is particularly important for the protection of the heart in response to both acute and chronic insults, including ischaemic injury and doxorubicin-induced cardiotoxicity. Accordingly, conditional deletion of Met in cardiomyocytes result

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De Silva, Dinuka M., Arpita Roy, Takashi Kato, et al. "Targeting the hepatocyte growth factor/Met pathway in cancer." Biochemical Society Transactions 45, no. 4 (2017): 855–70. http://dx.doi.org/10.1042/bst20160132.

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Hepatocyte growth factor (HGF)-induced activation of its cell surface receptor, the Met tyrosine kinase, drives mitogenesis, motogenesis and morphogenesis in a wide spectrum of target cell types and embryologic, developmental and homeostatic contexts. Typical paracrine HGF/Met signaling is regulated by HGF activation at target cell surfaces, HGF binding-induced receptor activation, internalization and degradation. Despite these controls, HGF/Met signaling contributes to oncogenesis, tumor angiogenesis and invasiveness, and tumor metastasis in many types of cancer, leading to the rapid growth o

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Kauma, Scott, Natalie Hayes, and Shannon Weatherford. "The Differential Expression of Hepatocyte Growth Factor and Met in Human Placenta*." Journal of Clinical Endocrinology & Metabolism 82, no. 3 (1997): 949–54. http://dx.doi.org/10.1210/jcem.82.3.3806.

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Abstract Met is the tyrosine kinase receptor for the ligand hepatocyte growth factor (HGF). Met/HGF plays an important role in epithelial cell proliferation, migration, and morphogenesis. HGF also plays a crucial role in placental development in the mouse. To determine whether HGF potentially has a similar role in human placental development, the production and localization of Met and HGF were determined in early second trimester and term placentas. Reverse transcription-PCR using specific primers demonstrated the expression of Met and HGF messenger ribonucleic acid in placental villi. HGF pro

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Yamasaki, Koji, Shoichiro Mukai, Takahiro Nagai, et al. "Matriptase-Induced Phosphorylation of MET is Significantly Associated with Poor Prognosis in Invasive Bladder Cancer; an Immunohistochemical Analysis." International Journal of Molecular Sciences 19, no. 12 (2018): 3708. http://dx.doi.org/10.3390/ijms19123708.

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Hepatocyte growth factor (HGF) plays an important role in cancer progression via phosphorylation of MET (c-met proto-oncogene product, receptor of HGF). HGF-zymogen (pro-HGF) must be processed for activation by HGF activators including matriptase, which is a type II transmembrane serine protease and the most efficient activator. The enzymatic activity is tightly regulated by HGF activator inhibitors (HAIs). Dysregulated pro-HGF activation (with upregulated MET phosphorylation) is reported to promote cancer progression in various cancers. We retrospectively analyzed the expression of matriptase

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Woolf, A. S., M. Kolatsi-Joannou, P. Hardman, et al. "Roles of hepatocyte growth factor/scatter factor and the met receptor in the early development of the metanephros." Journal of Cell Biology 128, no. 1 (1995): 171–84. http://dx.doi.org/10.1083/jcb.128.1.171.

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Several lines of evidence suggest that hepatocyte growth factor/scatter factor (HGF/SF), a soluble protein secreted by embryo fibroblasts and several fibroblast lines, may elicit morphogenesis in adjacent epithelial cells. We investigated the role of HGF/SF and its membrane receptor, the product of the c-met protooncogene, in the early development of the metanephric kidney. At the inception of the mouse metanephros at embryonic day 11, HGF/SF was expressed in the mesenchyme, while met was expressed in both the ureteric bud and the mesenchyme, as assessed by reverse transcription PCR, in situ h

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Tanaka, Ryota, Mizue Terai, Eric Londin, and Takami Sato. "The Role of HGF/MET Signaling in Metastatic Uveal Melanoma." Cancers 13, no. 21 (2021): 5457. http://dx.doi.org/10.3390/cancers13215457.

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Hepatocyte growth factor (HGF)/mesenchymal-epithelial transition factor (MET) signaling promotes tumorigenesis and tumor progression in various types of cancer, including uveal melanoma (UM). The roles of HGF/MET signaling have been studied in cell survival, proliferation, cell motility, and migration. Furthermore, HGF/MET signaling has emerged as a critical player not only in the tumor itself but also in the tumor microenvironment. Expression of MET is frequently observed in metastatic uveal melanoma and is associated with poor prognosis. It has been reported that HGF/MET signaling pathway ac

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Czyz, Malgorzata. "HGF/c-MET Signaling in Melanocytes and Melanoma." International Journal of Molecular Sciences 19, no. 12 (2018): 3844. http://dx.doi.org/10.3390/ijms19123844.

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Hepatocyte growth factor (HGF)/ mesenchymal-epithelial transition factor (c-MET) signaling is involved in complex cellular programs that are important for embryonic development and tissue regeneration, but its activity is also utilized by cancer cells during tumor progression. HGF and c-MET usually mediate heterotypic cell–cell interactions, such as epithelial–mesenchymal, including tumor–stroma interactions. In the skin, dermal fibroblasts are the main source of HGF. The presence of c-MET on keratinocytes is crucial for wound healing in the skin. HGF is not released by normal melanocytes, but

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Dissertations / Theses on the topic "MET/HGF"

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Ding, Shunli. "Rôle du couple HGF/C-MET dans l'angiogenèse." Paris 7, 2004. http://www.theses.fr/2004PA077188.

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Moore, Amy Elizabeth. "The role of HGF/Met signalling in colorectal tumorigenesis." Thesis, University of Bristol, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.544331.

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Besret, Soizic. "Ligations chimiques : synthèse d'inhibiteurs extracellulaires de la signalisation HGF/SF-MET." Phd thesis, Université du Droit et de la Santé - Lille II, 2011. http://tel.archives-ouvertes.fr/tel-00630962.

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Les peptides constituent une famille de biomolécules dont l'utilisation dans différents domaines thérapeutiques (cancer, diabète, sida) s'est fortement développée ces dernières années. Le défi pour les chimistes consiste à y accéder grâce à de nouvelles méthodes fiables et efficaces. La première partie de notre travail a d'abord été orientée vers le développement deux méthodes de ligations non natives efficaces et complémentaires de celles existant. La première méthode, appelée ligation thiocarbamate, permet d'obtenir des peptides alkylthiocarbamate avec de très bons rendements, alors que la s

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Murat, Cahue de Bernardis. "Estudo molecular dos componentes da via de sinalização HGF/MET em insulinomas." Universidade de São Paulo, 2013. http://www.teses.usp.br/teses/disponiveis/5/5135/tde-03102013-110107/.

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Os insulinomas são os tumores neuroendócrinos pancreáticos funcionantes mais frequentes, entretanto, os aspectos moleculares envolvidos em sua tumorigênese precisam ser melhor esclarecidos. As características morfológicas e histoquímicas dos insulinomas não conseguem predizer completamente seu comportamento biológico, apenas o fenótipo invasivo local e a presença de metástase são as formas confiáveis do diagnóstico maligno. A presente investigação teve por objetivos analisar a expressão gênica por reação em cadeia da polimerase (PCR) em tempo real e a expressão protéica por imuno-histoquímica

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Mekki, Meriem Sarah. "Conséquences de l'hypoxie sur la régulation de la signalisation HGF/SF-MET." Thesis, Lille 2, 2015. http://www.theses.fr/2015LIL2S047/document.

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Le récepteur à activité tyrosine kinase MET et son ligand le facteur de croissance des hepatocytes (Hepatocyte Growth Factor/Scattor Factor (HGF/SF)) sont essentiels pour la migration, la morphogenèse et la survie des cellules épithéliales. En plus de son implication et son importance physiologiques, la dérégulation de la signalisation de MET favorise la progression et l’invasion tumorales dans plusieurs types de cancers. Au sein des tumeurs, l’hypoxie est également un phénomène crucial qui induit une réponse adaptative menant à l’invasion, la métastase cancéreuses et la résistance aux traitem

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Tjin, Esther Pit Mien. "The HGF/MET and WNT signaling pathways in B cell differentiation and neoplasia." [S.l. : Amsterdam : s.n.] ; Universiteit van Amsterdam [Host}, 2005. http://dare.uva.nl/document/17835.

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Stefan, Monica. "Identifizierung eines neuen Interaktionspartners des HGF-Rezeptors c-Met SHIP-1 spielt eine Schlüsselrolle bei der Vermittlung der HGF-induzierten Tubulogenese von Epithelzellen /." [S.l.] : [s.n.], 2001. http://deposit.ddb.de/cgi-bin/dokserv?idn=961707232.

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Arlt, Franziska. "Das neu identifizierte Gen MACC1 ist ein Regulator des HGF/Met-Signalweges und ist prognostisch für die Metastasierung des Kolonkarzinoms." Doctoral thesis, Humboldt-Universität zu Berlin, Mathematisch-Naturwissenschaftliche Fakultät I, 2009. http://dx.doi.org/10.18452/15974.

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Das Kolonkarzinom ist eine der häufigsten Tumorerkrankungen weltweit. Etwa 50 % der Patienten entwickeln Fernmetastasen. Diese haben eine sehr schlechte Überlebensprognose. Deshalb fokussiert die Forschung auf die Identifizierung neuer, molekularer Marker für eine verbesserte Metastasierungsvorhersage. Identifizierte Hochrisiko-Patienten könnten somit rechtzeitig eine individualisierte, intensivere Therapie erhalten. MACC1 (Metastasis-associated in colon cancer 1) ist ein neu identifiziertes Gen, das in Kolonkarzinomen und deren Fernmetastasen überexprimiert wird. Die Domänenstruktur von MACC

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Rocha, Angélica Gomes 1989. "Estudo da expressão proteica da via HGF/c-Met/STAT3 no carcinoma diferenciado da tiroide." [s.n.], 2014. http://repositorio.unicamp.br/jspui/handle/REPOSIP/310289.

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Orientadores: Laura Sterian Ward, Antônio Hugo José Fróes Marques Campos<br>Dissertação (mestrado) - Universidade Estadual de Campinas, Faculdade de Ciências Médicas<br>Made available in DSpace on 2018-08-26T01:02:11Z (GMT). No. of bitstreams: 1 Rocha_AngelicaGomes_M.pdf: 1644333 bytes, checksum: e3503fb6e2c8209f7a6696df111d6a78 (MD5) Previous issue date: 2014<br>Resumo: Marcadores de malignidade, especialmente capazes de distinguir lesões de padrão folicular, que sejam de fácil implantação na rotina do diagnóstico de nódulos tireoidianos, continuam sendo extremamente necessários, dado o cre

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Chmielowiec, Jolanta. "The role of the Met tyrosine kinase receptor in skin maintenance and regeneration." Doctoral thesis, Humboldt-Universität zu Berlin, Mathematisch-Naturwissenschaftliche Fakultät I, 2007. http://dx.doi.org/10.18452/15690.

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Met und der korrespondierende Ligand HGF/SF sind im hyperproliferativen Epithelium von Hautwunden exprimiert. Aus diesem Grund ist es wahrscheinlich, dass der Rezeptor und sein Ligand in autokriner Weise wechselwirken und wichtige Funktionen für den Heilungsprozess der Haut besitzen. Unter Verwendung der Keratin 14 Cre-Rekombinase konnte ein „Knockout“ des Met-Rezeptors spezifisch in der Epidermis erzielt werden. In der Tat zeigten die Ergebnisse, dass Met für die Re-epithelisierung in Wundschlussprozessen essentiell ist, da in den an der Wundheilung beteiligten Keratinozyten keine Rekombinati

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Books on the topic "MET/HGF"

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1948-, Goldberg I. D., and Rosen E. M, eds. Hepatocyte growth factor-scatter factor (HGF-SF) and the C-met receptor. Birkhäuser, 1992.

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

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Alami, Jennifer. The role of HGF and met in Wilms tumour. 2004.

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Jung, Waltraud. Expression des "Hepatocyte-Growth-Factors" (HGF) und des c-met/HGF-Rezeptors in Leber, Gehirn und weissen Blutzellen. 1994.

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Long, Isolde Marie Seiden. Functional relationships between hepatocyte growth factor receptor (HGF)/Met signaling and Ki-ras oncogenic mutation in colon carcinoma cells. 2005.

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Book chapters on the topic "MET/HGF"

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Ray, Mandira, J. G. Garcia, and Ravi Salgia. "HGF/c-MET Signaling in Advanced Cancers." In Cancer Genome and Tumor Microenvironment. Springer New York, 2009. http://dx.doi.org/10.1007/978-1-4419-0711-0_12.

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Vande Woude, G. F., M. Jeffers, J. Cortner, G. Alvord, I. Tsarfaty, and J. Resau. "Met-HGF/SF: Tumorigenesis, Invasion and Metastasis." In Ciba Foundation Symposium 212 - Plasminogen-Related Growth Factors. John Wiley & Sons, Ltd., 2007. http://dx.doi.org/10.1002/9780470515457.ch8.

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Thewke, Douglas P., Jianqun Kou, Makenzie L. Fulmer, and Qian Xie. "The HGF/MET Signaling and Therapeutics in Cancer." In Current Human Cell Research and Applications. Springer Singapore, 2017. http://dx.doi.org/10.1007/978-981-10-7296-3_8.

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Zambelli, Alberto, Giuseppe Biamonti, and Angela Amato. "HGF/c-Met Signalling in the Tumor Microenvironment." In Advances in Experimental Medicine and Biology. Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-47189-7_2.

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Karsten, Ruud, and Joost Roeters. "Behandeling Van Een PatiëNt Met Erfelijke Of Idiopathische Gingivafibromatose (HGF)." In Tandheelkundige casuïstiek. Bohn Stafleu van Loghum, 2008. http://dx.doi.org/10.1007/978-90-313-8811-0_92.

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Abounader, Roger, and John Laterra. "HGF/c-Met Signaling and Targeted Therapeutics in Brain Tumors." In CNS Cancer. Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60327-553-8_39.

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Chandel, Vaishali, Sibi Raj, Ramesh Choudhari, and Dhruv Kumar. "Role of c-Met/HGF Axis in Altered Cancer Metabolism." In Cancer Cell Metabolism: A Potential Target for Cancer Therapy. Springer Singapore, 2020. http://dx.doi.org/10.1007/978-981-15-1991-8_7.

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Corso, Simona, and Silvia Giordano. "Mechanisms of Resistance to Molecular Therapies Targeting the HGF/MET Axis." In Resistance to Targeted Anti-Cancer Therapeutics. Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67932-7_4.

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Cortner, J., G. F. Vande Woude, and S. Rong. "The Met-HGF/SF autocrine signaling mechanism is involved in sarcomagenesis." In Experientia Supplementum. Birkhäuser Basel, 1995. http://dx.doi.org/10.1007/978-3-0348-9070-0_6.

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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. Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-6528-7_13.

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Conference papers on the topic "MET/HGF"

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Chen, Dawei, Ziyong Sun, Likun Zhang, et al. "Abstract 747: Paracrine c-MET/HGF HCC PDX: evaluation of a biologics targeting c-MET." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-747.

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Wortinger, Mark A., Wei Zeng, Wei Jennifer Yang, et al. "Abstract 695: LA480, a c-Met antibody with neutralization and internalization properties, inhibits HGF-dependent and HGF-independent c-Met pathway activation and tumor growth." 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.am10-695.

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Gordon, Marcia, Alexandra Croft, Chi-Ming Li, Sean Taylor, Sean R. Caenepeel, and Kim Quon. "Abstract LB-241: HGF promotes resistance to MET inhibitor AMG337 in MET-amplified gastric cancer cells." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-lb-241.

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Owusu, Benjamin Y., Phanindra K. Venukadasula, Robert A. Galemmo, and Lidija Klampfer. "Abstract 1583: SRI31215, a novel inhibitor of oncogenic HGF/MET signaling." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-1583.

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Yu, Yanlin, Liping Huang, and Glenn Merlino. "Abstract 4114: Blocking Ezrin can inhibit HGF/Met signaling-induced metastasis." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-4114.

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Hughes, Veronica S., and Dietmar W. Siemann. "Abstract 4102: Effect of HGF concentrations on c-Met inhibition investigation." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-4102.

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Vierkant, Robert A., Kimberly R. Kalli, Kristin L. White, et al. "Abstract 893: Associations between HGF, MET, and phospho-MET expression, overall survival, andHGFgenotypes in epithelial ovarian cancer." 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.am2011-893.

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Chen, Dawei, Xiaoming Song, Jie Cai, Taiping Chen, Yiyou Chen, and Henry Q. X. Li. "Abstract 1322: Autocrine c-met/HGF HCC patient derived xenograft (PDX) models for evaluating c-met inhibitors." 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.am2012-1322.

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Taniguchi, Hirokazu, Shinji Takeuchi, Koji Fukuda, et al. "Abstract 4763: Targeted therapy by MET inhibitors against small-cell lung cancer with aberrant activation of HGF/MET pathway." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-4763.

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Hultberg, Anna, Cristina Basilico, Cristophe Blanchetot, et al. "Abstract LB-330: Four individually druggable Met hotspots mediate HGF-driven tumor progression." 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-330.

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Reports on the topic "MET/HGF"

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

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

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