Cytotoxic activity of tivantinib (ARQ 197) is not due solely to c-MET inhibition. - Wikidata - wikimedia - TriplyDB

Cytotoxic activity of tivantinib (ARQ 197) is not due solely to c-MET inhibition.

Cytotoxic activity of tivantinib (ARQ 197) is not due solely to c-MET inhibition.

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Progress in systemic therapy of advanced hepatocellular carcinoma Non-Invasive Methods to Monitor Mechanisms of Resistance to Tyrosine Kinase Inhibitors in Non-Small-Cell Lung Cancer: Where Do We Stand?State of the art management of metastatic gastroesophageal cancer Research Progress of HGF/c-MET Inhibitor in the Treatment of Non-small Cell Lung Cancer Targeting the epithelial to mesenchymal transition in glioblastoma: the emerging role of MET signaling Profile of tivantinib and its potential in the treatment of hepatocellular carcinoma: the evidence to date From molecular classification to targeted therapeutics: the changing face of systemic therapy in metastatic gastroesophageal cancer Hepatocellular carcinoma: Where there is unmet need Tubulin is a molecular target of the Wnt-activating chemical probe Phase II study of the c-MET inhibitor tivantinib (ARQ 197) in patients with relapsed or relapsed/refractory multiple myeloma.A first-in-human study of AMG 208, an oral MET inhibitor, in adult patients with advanced solid tumors The potential roles of hepatocyte growth factor (HGF)-MET pathway inhibitors in cancer treatment.Systemic treatment of hepatocellular carcinoma: Past, present and future Identification of DW532 as a novel anti-tumor agent targeting both kinases and tubulin.Response to crizotinib in a patient with MET-mutant papillary renal cell cancer after progression on tivantinib.c-Met signaling in the development of tumorigenesis and chemoresistance: potential applications in pancreatic cancer HGF/MET-directed therapeutics in gastroesophageal cancer: a review of clinical and biomarker development.MET and PI3K/mTOR as a potential combinatorial therapeutic target in malignant pleural mesothelioma.Targeting MET Amplification as a New Oncogenic Driver.The c-Met Inhibitor MSC2156119J Effectively Inhibits Tumor Growth in Liver Cancer Models Novel agents in development for advanced non-small cell lung cancer.The evolving genomic classification of lung cancer.Phase 1 trial of tivantinib in combination with sorafenib in adult patients with advanced solid tumors Molecularly targeted therapies in non-small-cell lung cancer annual update 2014 Targeting the pro-survival protein MET with tivantinib (ARQ 197) inhibits growth of multiple myeloma cells.New metastatic model of human small-cell lung cancer by orthotopic transplantation in mice.Aptamers Binding to c-Met Inhibiting Tumor Cell Migration Improved diagnostics targeting c-MET in non-small cell lung cancer: expression, amplification and activation?Impact of MET targeting on tumor-associated angiogenesis and growth of MET mutations-driven models of liver cancer.Tivantinib induces G2/M arrest and apoptosis by disrupting tubulin polymerization in hepatocellular carcinoma.Phase II study of tivantinib (ARQ 197) in patients with metastatic triple-negative breast cancer Understanding drugs in breast cancer through drug sensitivity screening Cytotoxic activity of the MK2 inhibitor CMPD1 in glioblastoma cells is independent of MK2.A randomized, placebo-controlled, phase 1/2 study of tivantinib (ARQ 197) in combination with irinotecan and cetuximab in patients with metastatic colorectal cancer with wild-type KRAS who have received first-line systemic therapy GSK3 alpha and beta are new functionally relevant targets of tivantinib in lung cancer cells Off-target effects of c-MET inhibitors on thyroid cancer cells.Tumor and circulating biomarkers in patients with second-line hepatocellular carcinoma from the randomized phase II study with tivantinib.Imprecision in the Era of Precision Medicine in Non-Small Cell Lung Cancer.Targeting angiogenesis in renal cell carcinoma.Developing biomarkers to predict benefit from HGF/MET pathway inhibitors.

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Cytotoxic activity of tivantinib (ARQ 197) is not due solely to c-MET inhibition.

http://www.wikidata.org/entity/Q37137050

description

article científic

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article scientifique

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articolo scientifico

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artigo científico

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bilimsel makale

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scientific article published on 18 April 2013

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vedecký článok

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vetenskaplig artikel

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videnskabelig artikel

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vědecký článek

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name

Cytotoxic activity of tivantinib (ARQ 197) is not due solely to c-MET inhibition.

@en

Cytotoxic activity of tivantinib

@nl

type

label

Cytotoxic activity of tivantinib (ARQ 197) is not due solely to c-MET inhibition.

@en

Cytotoxic activity of tivantinib

@nl

prefLabel

Cytotoxic activity of tivantinib (ARQ 197) is not due solely to c-MET inhibition.

@en

Cytotoxic activity of tivantinib

@nl

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0008-5472.CAN-12-3256

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Cancer Research

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Cytotoxic activity of tivantinib (ARQ 197) is not due solely to c-MET inhibition

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Aki Aoyama

http://www.w3.org/2001/XMLSchema#string

Jeffrey A Engelman

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Jie Qi

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Naoya Fujita

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Takao Yamori

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Tomoko Oh-hara

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Youngchul Song

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P2860

Amplification of MET may identify a subset of cancers with extreme sensitivity to the selective tyrosine kinase inhibitor PHA-665752

Discovery of a novel mode of protein kinase inhibition characterized by the mechanism of inhibition of human mesenchymal-epithelial transition factor (c-Met) protein autophosphorylation by ARQ 197

MET amplification occurs with or without T790M mutations in EGFR mutant lung tumors with acquired resistance to gefitinib or erlotinib

MET amplification leads to gefitinib resistance in lung cancer by activating ERBB3 signaling.

Activity of crizotinib (PF02341066), a dual mesenchymal-epithelial transition (MET) and anaplastic lymphoma kinase (ALK) inhibitor, in a non-small cell lung cancer patient with de novo MET amplification.

Mechanisms of acquired crizotinib resistance in ALK-rearranged lung Cancers.

Met, metastasis, motility and more

Invasive growth: a MET-driven genetic programme for cancer and stem cells

Developmental roles of HGF/SF and its receptor, the c-Met tyrosine kinase

The NCI60 human tumour cell line anticancer drug screen

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3087-3096

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scholarly article

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10.1158/0008-5472.CAN-12-3256

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10

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73

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Ryohei Katayama

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2013-04-18T00:00:00Z

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23598276

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3759033

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