EGFR activation is a potential determinant of primary resistance of hepatocellular carcinoma cells to sorafenib. - Wikidata - wikimedia - TriplyDB

EGFR activation is a potential determinant of primary resistance of hepatocellular carcinoma cells to sorafenib.

EGFR activation is a potential determinant of primary resistance of hepatocellular carcinoma cells to sorafenib.

http://www.wikidata.org/entity/Q39362619

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Role of sorafenib in the treatment of advanced hepatocellular carcinoma: An update Ferroptosis, a new form of cell death, and its relationships with tumourous diseases Aberrant regulation of Wnt signaling in hepatocellular carcinoma Regulation of amphiregulin gene expression by β-catenin signaling in human hepatocellular carcinoma cells: a novel crosstalk between FGF19 and the EGFR system BCRP/ABCG2 inhibition sensitizes hepatocellular carcinoma cells to sorafenib Actionable gene expression-based patient stratification for molecular targeted therapy in hepatocellular carcinoma Antagonism of sorafenib and regorafenib actions by platelet factors in hepatocellular carcinoma cell lines.New knowledge of the mechanisms of sorafenib resistance in liver cancer Virtual target screening: validation using kinase inhibitors.Oncolytic immunotherapy using recombinant vaccinia virus GLV-1h68 kills sorafenib-resistant hepatocellular carcinoma efficiently.Role of anti-angiogenesis therapy in the management of hepatocellular carcinoma: The jury is still out.The Enhanced metastatic potential of hepatocellular carcinoma (HCC) cells with sorafenib resistance Epidermal Growth Factor Receptor-Dependent Mutual Amplification between Netrin-1 and the Hepatitis C Virus.Sorafenib in advanced hepatocellular carcinoma: current status and future perspectives.Inactivation of hypoxia-induced YAP by statins overcomes hypoxic resistance tosorafenib in hepatocellular carcinoma cells.eIF5A2 is an alternative pathway for cell proliferation in cetuximab-treated epithelial hepatocellular carcinoma.Let-7a enhances the sensitivity of hepatocellular carcinoma cells to cetuximab by regulating STAT3 expression.YC-1 enhances the anti-tumor activity of sorafenib through inhibition of signal transducer and activator of transcription 3 (STAT3) in hepatocellular carcinoma.Impact of pretreatment serum cholinesterase level in unresectable advanced hepatocellular carcinoma patients treated with sorafenib.Second line systemic therapy options for advanced hepatocellular carcinoma; a systematic review.MEK 1/2 inhibitors in the treatment of hepatocellular carcinoma.A miR-7/GAS6/TYRO3 axis regulates the growth and invasiveness of sorafenib-resistant cells in human hepatocellular carcinoma.HDAC6-mediated EGFR stabilization and activation restrict cell response to sorafenib in non-small cell lung cancer cells.New Approach for Treatment of Primary Liver Tumors: The Role of Quercetin.Tumour initiating cells and IGF/FGF signalling contribute to sorafenib resistance in hepatocellular carcinoma Sorafenib, a multikinase inhibitor, induces formation of stress granules in hepatocarcinoma cells.A preclinical evaluation of a novel multikinase inhibitor, SKLB-329, as a therapeutic agent against hepatocellular carcinoma.TGFβ signaling confers sorafenib resistance via induction of multiple RTKs in hepatocellular carcinoma cells.Hepatocellular carcinoma treatment: a comparative review of emerging growth factor receptor antagonists.Cellular and molecular targets for the immunotherapy of hepatocellular carcinoma.MicroRNA pharmacogenomics based integrated model of miR-17-92 cluster in sorafenib resistant HCC cells reveals a strategy to forestall drug resistance.Des-gamma-carboxy prothrombin antagonizes the effects of Sorafenib on human hepatocellular carcinoma through activation of the Raf/MEK/ERK and PI3K/Akt/mTOR signaling pathways.Serum cytokine profiles predict survival benefits in patients with advanced hepatocellular carcinoma treated with sorafenib: a retrospective cohort study.Upregulation of UBE2Q1 via gene copy number gain in hepatocellular carcinoma promotes cancer progression through β-catenin-EGFR-PI3K-Akt-mTOR signaling pathway.Heat stress induced, ligand-independent MET and EGFR signalling in hepatocellular carcinoma.MicroRNA-9 enhances sensitivity to cetuximab in epithelial phenotype hepatocellular carcinoma cells through regulation of the eukaryotic translation initiation factor 5A-2.Protein biosynthesis, a target of sorafenib, interferes with the unfolded protein response (UPR) and ferroptosis in hepatocellular carcinoma cells.Evaluation of individual sensitivity of head and neck squamous cell carcinoma to cetuximab by short-term culture of tumor slices.Patient-derived multicellular tumor spheroids towards optimized treatment for patients with hepatocellular carcinoma.Silencing the expression of copine-III enhances the sensitivity of hepatocellular carcinoma cells to the molecular targeted agent sorafenib

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EGFR activation is a potential determinant of primary resistance of hepatocellular carcinoma cells to sorafenib.

http://www.wikidata.org/entity/Q39362619

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2012 nî lūn-bûn

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2012年の論文

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2012年学术文章

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2012年学术文章

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2012年学术文章

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2012年学术文章

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2012年學術文章

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2012年學術文章

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2012年學術文章

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name

EGFR activation is a potential ...... carcinoma cells to sorafenib.

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EGFR activation is a potential ...... carcinoma cells to sorafenib.

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type

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EGFR activation is a potential ...... carcinoma cells to sorafenib.

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EGFR activation is a potential ...... carcinoma cells to sorafenib.

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prefLabel

EGFR activation is a potential ...... carcinoma cells to sorafenib.

@en

EGFR activation is a potential ...... carcinoma cells to sorafenib.

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International Journal of Cancer

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EGFR activation is a potential ...... carcinoma cells to sorafenib.

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P2093

Antoine Galmiche

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Christophe Louandre

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Corinne Godin

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Eric Trécherel

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Jean-Claude Barbare

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Jean-Claude Mazière

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Momar Diouf

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Sébastien Dupont

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Zakaria Ezzoukhry

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P2860

Kinase-dead BRAF and oncogenic RAS cooperate to drive tumor progression through CRAF

Melanomas acquire resistance to B-RAF(V600E) inhibition by RTK or N-RAS upregulation

RAF inhibitors prime wild-type RAF to activate the MAPK pathway and enhance growth

Molecular determinants of the response of glioblastomas to EGFR kinase inhibitors.

Sorafenib in advanced hepatocellular carcinoma

The EGF receptor family: spearheading a merger of signaling and therapeutics

The landscape of somatic copy-number alteration across human cancers.

Hepatocellular carcinoma

RAF inhibitors transactivate RAF dimers and ERK signalling in cells with wild-type BRAF

BAY 43-9006 exhibits broad spectrum oral antitumor activity and targets the RAF/MEK/ERK pathway and receptor tyrosine kinases involved in tumor progression and angiogenesis

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10.1002/IJC.27604

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12

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131

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Bruno Chauffert

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2012-04-30T00:00:00Z

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224708649

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22514082

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