About: The Met/HGF receptor is over-expressed in human osteosarcomas and is activated by either a paracrine or an autocrine circuit

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About: The Met/HGF receptor is over-expressed in human osteosarcomas and is activated by either a paracrine or an autocrine circuit Goto Sponge NotDistinct Permalink

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scientific article published on 01 February 1995

Attributes	Values
rdf:type	Item
description	wetenschappelijk artikel (nl) наукова стаття, опублікована в лютому 1995 (uk) article scientifique publié en 1995 (fr) im Februar 1995 veröffentlichter wissenschaftlicher Artikel (de) artículu científicu espublizáu en febreru de 1995 (ast) artikull shkencor i botuar më 01 shkurt 1995 (sq) scientific article published on 01 February 1995 (en)
publication date	wds:Q72560868-54E952E0-2C74-4DEB-8220-8E4E00227F71
publication date	1995-02-01 00:00:00Z (xsd:dateTime)
language of work or name	wds:Q72560868-D2A78308-FCBB-4D9E-979D-760FB97ACAB5
language of work or name	English
author name string	wds:Q72560868-2A9E143B-3F1C-4E0E-994C-C33E7748FB86 wds:Q72560868-37AD3A00-2AAA-4EB4-942D-A3D7EF2F4258 wds:Q72560868-8E15A144-C9ED-4D24-9DB2-E5E7808C3780 wds:Q72560868-A3640BC1-E35A-4F7A-A76A-8D4EDF00BFFB wds:Q72560868-B0328CC7-E7CD-40AC-A159-678B1FB2D36F wds:Q72560868-B61CA918-00F8-4172-B092-EE6A3469E244 wds:Q72560868-E68C6B58-0C31-4B54-99CF-8317AAF7541D
author name string	Comoglio PM Cremona O Baldini N Campanacci M Di Renzo MF Olivero M Ferracini R
rdfs:label	The Met/HGF receptor is over-expressed in human osteosarcomas and is activated by either a paracrine or an autocrine circuit (en) The Met/HGF receptor is over-expressed in human osteosarcomas and is activated by either a paracrine or an autocrine circuit (nl) The Met/HGF receptor is over-expressed in human osteosarcomas and is activated by either a paracrine or an autocrine circuit (sq)
skos:prefLabel	The Met/HGF receptor is over-expressed in human osteosarcomas and is activated by either a paracrine or an autocrine circuit (en) The Met/HGF receptor is over-expressed in human osteosarcomas and is activated by either a paracrine or an autocrine circuit (nl) The Met/HGF receptor is over-expressed in human osteosarcomas and is activated by either a paracrine or an autocrine circuit (sq)
name	The Met/HGF receptor is over-expressed in human osteosarcomas and is activated by either a paracrine or an autocrine circuit (en) The Met/HGF receptor is over-expressed in human osteosarcomas and is activated by either a paracrine or an autocrine circuit (nl) The Met/HGF receptor is over-expressed in human osteosarcomas and is activated by either a paracrine or an autocrine circuit (sq)
author	wds:Q72560868-23A7CDE6-A152-4B99-A649-6300FDC7023B wds:Q72560868-EF2FBAD3-2492-4710-93C0-2C6F2908A7A4
author	Pier-Luigi Lollini Katia Scotlandi
title	wds:Q72560868-B2D3DB2E-981F-458F-9E32-5BD4AAC5BC40
title	The Met/HGF receptor is over-expressed in human osteosarcomas and is activated by either a paracrine or an autocrine circuit (en)
page(s)	wds:Q72560868-255CC621-7A73-43A4-98D2-1DA4833E16CD
page(s)	739-749
instance of	wds:Q72560868-C568975C-AC7A-4E99-8760-53F486B08F61
instance of	scholarly article
PubMed ID	wds:Q72560868-9EB7DA4A-015F-4C44-8C54-25FCEF146936
PubMed ID	http://rdf.ncbi.nlm.nih.gov/pubchem/reference/7862451
PubMed ID	7862451
published in	wds:Q72560868-47268E30-EE3A-48BD-B6A7-262D6C2CC8B8
published in	Oncogene
issue	wds:Q72560868-61C7116B-8188-4D88-A3F2-4E9A681DA13A
volume	wds:Q72560868-A3C55411-5C5F-4699-9D5A-9406CD961270
issue	4
volume	10
is about of	https://www.wikidata.org/wiki/Special:EntityData/Q72560868
is cites work of	MET: a promising anticancer therapeutic target RON (MST1R) is a novel prognostic marker and therapeutic target for gastroesophageal adenocarcinoma A natural hepatocyte growth factor/scatter factor autocrine loop in myoblast cells and the effect of the constitutive Met kinase activation on myogenic differentiation Growth factor-dependent activation of alphavbeta3 integrin in normal epithelial cells: implications for tumor invasion Hepatocyte growth factor is a coupling factor for osteoclasts and osteoblasts in vitro. Disassociation of met-mediated biological responses in vivo: the natural hepatocyte growth factor/scatter factor splice variant NK2 antagonizes growth but facilitates metastasis Genetic alterations in primary osteosarcoma from 54 children and adolescents by targeted allelotyping The MET axis as a therapeutic target Enhanced tumorigenicity and invasion-metastasis by hepatocyte growth factor/scatter factor-met signalling in human cells concomitant with induction of the urokinase proteolysis network Diverse tumorigenesis associated with aberrant development in mice overexpressing hepatocyte growth factor/scatter factor Non-autocrine, constitutive activation of Met in human anaplastic thyroid carcinoma cells in culture ErbB2 and bone sialoprotein as markers for metastatic osteosarcoma cells. Hepatocyte growth factor/scatter factor-Met signaling in tumorigenicity and invasion/metastasis Hepatocyte growth factor/scatter factor-induced intracellular signalling c-MET expression in myofibroblasts: role in autocrine activation and prognostic significance in lung adenocarcinoma Systemic treatment of soft-tissue sarcoma-gold standard and novel therapies Dysregulation of Met receptor tyrosine kinase activity in invasive tumors Role of the MET/HGF receptor in proliferation and invasive behavior of osteosarcoma Overexpression of the hepatocyte growth factor (HGF) receptor (Met) and presence of a truncated and activated intracellular HGF receptor fragment in locally aggressive/malignant human musculoskeletal tumors. Role of cancer cell-stroma interaction in invasive growth of cancer cells Oncogenic mutants of RON and MET receptor tyrosine kinases cause activation of the beta-catenin pathway Osteosarcoma development and stem cell differentiation Activation of the urokinase plasminogen activator/urokinase plasminogen activator receptor system and redistribution of E-cadherin are associated with hepatocyte growth factor-induced motility of pancreas tumor cells overexpressing Met. Chromosomal amplification of leucine-rich repeat kinase-2 (LRRK2) is required for oncogenic MET signaling in papillary renal and thyroid carcinomas The Met oncogene and basal-like breast cancer: another culprit to watch out for? PHA665752, a small-molecule inhibitor of c-Met, inhibits hepatocyte growth factor-stimulated migration and proliferation of c-Met-positive neuroblastoma cells Targeting RTK Signaling Pathways in Cancer Frzb, a secreted Wnt antagonist, decreases growth and invasiveness of fibrosarcoma cells associated with inhibition of Met signaling Imatinib and Dasatinib Inhibit Hemangiosarcoma and Implicate PDGFR-β and Src in Tumor Growth Prkar1a is an osteosarcoma tumor suppressor that defines a molecular subclass in mice c-Met and hepatocyte growth factor: potential as novel targets in cancer therapy C-MET as a new therapeutic target for the development of novel anticancer drugs An orthotopic model of murine osteosarcoma with clonally related variants differing in pulmonary metastatic potential Predominant formation of heavily pigmented dermal melanocytomas resembling 'animal-type' melanomas in hepatocyte growth factor (C57BL/6 x C3H)F1 mice following neonatal UV irradiation In the clinic: ongoing clinical trials evaluating c-MET-inhibiting drugs Personalized comprehensive molecular profiling of high risk osteosarcoma: Implications and limitations for precision medicine Co-expression of hepatocyte growth factor and its receptor in human prostate cancer Aptamers Binding to c-Met Inhibiting Tumor Cell Migration Specific tyrosine kinase inhibitors regulate human osteosarcoma cells in vitro The role of the c-Met pathway in lung cancer and the potential for targeted therapy Constitutively active c-Met kinase in PC-3 cells is autocrine-independent and can be blocked by the Met kinase inhibitor BMS-777607. Activation of c-Met in colorectal carcinoma cells leads to constitutive association of tyrosine-phosphorylated beta-catenin DNA triplex-mediated inhibition of MET leads to cell death and tumor regression in hepatoma. Alternative proteolytic processing of hepatocyte growth factor during wound repair Involvement of MET/TWIST/APC combination or the potential role of ossification factors in pediatric high-grade osteosarcoma oncogenesis

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