Epidermal growth factor receptor (EGFR) is highly conserved in pancreatic cancer. - Wikidata - awgldk - TriplyDB

Epidermal growth factor receptor (EGFR) is highly conserved in pancreatic cancer.

Epidermal growth factor receptor (EGFR) is highly conserved in pancreatic cancer.

http://www.wikidata.org/entity/Q33279891

about

Systemic therapies for pancreatic cancer--the role of pharmacogenetics Pan-Bcl-2 inhibitor AT-101 enhances tumor cell killing by EGFR targeted T cells CHIP is a novel tumor suppressor in pancreatic cancer through targeting EGFR Mutational profiling of kinases in human tumours of pancreatic origin identifies candidate cancer genes in ductal and ampulla of vater carcinomas.A new drug delivery method of bispecific ligand-directed toxins, which reduces toxicity and promotes efficacy in a model of orthotopic pancreatic cancer.Ligand stimulation of ErbB4 and a constitutively-active ErbB4 mutant result in different biological responses in human pancreatic tumor cell lines.The relative expression of Mig6 and EGFR is associated with resistance to EGFR kinase inhibitors.Targeting ErbB3-mediated stromal-epithelial interactions in pancreatic ductal adenocarcinoma.A microRNA gene expression signature predicts response to erlotinib in epithelial cancer cell lines and targets EMT.A deimmunized bispecific ligand-directed toxin that shows an impressive anti-pancreatic cancer effect in a systemic nude mouse orthotopic model.A phase I study evaluating the role of the anti-epidermal growth factor receptor (EGFR) antibody cetuximab as a radiosensitizer with chemoradiation for locally advanced pancreatic cancer.Erlotinib is effective in pancreatic cancer with epidermal growth factor receptor mutations: a randomized, open-label, prospective trial Insights into erlotinib action in pancreatic cancer cells using a combined experimental and mathematical approach.Evaluation of phosphatidylinositol-3-kinase catalytic subunit (PIK3CA) and epidermal growth factor receptor (EGFR) gene mutations in pancreaticobiliary adenocarcinoma.Molecular targeted therapies for pancreatic cancer.Epidermal growth factor receptor in pancreatic cancer.Biologic therapies for advanced pancreatic cancer.Erlotinib in the treatment of advanced pancreatic cancer Genetically designing a more potent antipancreatic cancer agent by simultaneously co-targeting human IL13 and EGF receptors in a mouse xenograft model.Challenges of drug resistance in the management of pancreatic cancer.Cetuximab: still an option in the treatment of pancreatic cancer?LncRNA XIST Promotes Pancreatic Cancer Proliferation Through miR-133a/EGFR.The TGFβ-miR200-MIG6 pathway orchestrates the EMT-associated kinase switch that induces resistance to EGFR inhibitors Epidermal growth factor receptor and insulinlike growth factor 1 receptor expression predict poor survival in pancreatic ductal adenocarcinoma.Angiogenin/Ribonuclease 5 Is an EGFR Ligand and a Serum Biomarker for Erlotinib Sensitivity in Pancreatic Cancer.

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P2860

Epidermal growth factor receptor (EGFR) is highly conserved in pancreatic cancer.

http://www.wikidata.org/entity/Q33279891

description

2007 nî lūn-bûn

@nan

2007 թուականի Յունուարին հրատարակուած գիտական յօդուած

@hyw

2007 թվականի հունվարին հրատարակված գիտական հոդված

@hy

2007年の論文

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2007年論文

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2007年論文

@zh-hant

2007年論文

@zh-hk

2007年論文

@zh-mo

2007年論文

@zh-tw

2007年论文

@wuu

name

Epidermal growth factor receptor (EGFR) is highly conserved in pancreatic cancer.

@ast

Epidermal growth factor receptor (EGFR) is highly conserved in pancreatic cancer.

@en

type

label

Epidermal growth factor receptor (EGFR) is highly conserved in pancreatic cancer.

@ast

Epidermal growth factor receptor (EGFR) is highly conserved in pancreatic cancer.

@en

prefLabel

Epidermal growth factor receptor (EGFR) is highly conserved in pancreatic cancer.

@ast

Epidermal growth factor receptor (EGFR) is highly conserved in pancreatic cancer.

@en

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P356

J.SURG.2006.09.009

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P1476

Epidermal growth factor receptor (EGFR) is highly conserved in pancreatic cancer.

@en

P2093

Andrey Frolov

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Ching-Wei D Tzeng

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Donald J Buchsbaum

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J Harrison Howard

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J Pablo Arnoletti

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Martin J Heslin

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Natalya Frolova

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Nirag C Jhala

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Selwyn M Vickers

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P304

464-469

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scholarly article

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10.1016/J.SURG.2006.09.009

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4

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141

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2007-01-22T00:00:00Z

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17383523

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