Sunitinib Treatment Enhances Metastasis of Innately Drug-Resistant Breast Tumors. - Wikidata - wikimedia - TriplyDB

Sunitinib Treatment Enhances Metastasis of Innately Drug-Resistant Breast Tumors.

Sunitinib Treatment Enhances Metastasis of Innately Drug-Resistant Breast Tumors.

http://www.wikidata.org/entity/Q37660355

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Hypoxia-Targeting Drug Evofosfamide (TH-302) Enhances Sunitinib Activity in Neuroblastoma Xenograft Models.

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Sunitinib Treatment Enhances Metastasis of Innately Drug-Resistant Breast Tumors.

http://www.wikidata.org/entity/Q37660355

description

article científic

@ca

article scientifique

@fr

articolo scientifico

@it

artigo científico

@pt

bilimsel makale

@tr

scientific article published on 23 December 2016

@en

vedecký článok

@sk

vetenskaplig artikel

@sv

videnskabelig artikel

@da

vědecký článek

@cs

name

Sunitinib Treatment Enhances Metastasis of Innately Drug-Resistant Breast Tumors.

@en

Sunitinib Treatment Enhances Metastasis of Innately Drug-Resistant Breast Tumors.

@nl

type

label

Sunitinib Treatment Enhances Metastasis of Innately Drug-Resistant Breast Tumors.

@en

Sunitinib Treatment Enhances Metastasis of Innately Drug-Resistant Breast Tumors.

@nl

prefLabel

Sunitinib Treatment Enhances Metastasis of Innately Drug-Resistant Breast Tumors.

@en

Sunitinib Treatment Enhances Metastasis of Innately Drug-Resistant Breast Tumors.

@nl

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0008-5472.CAN-16-1982

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Cancer Research

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Sunitinib Treatment Enhances Metastasis of Innately Drug-Resistant Breast Tumors.

@en

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Joseph W Wragg

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Roy Bicknell

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Victoria L Heath

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P2860

NIH Image to ImageJ: 25 years of image analysis

Aquaporin-1 water channel expression in human kidney

Modes of resistance to anti-angiogenic therapy

Randomized phase II study of sunitinib versus standard of care for patients with previously treated advanced triple-negative breast cancer.

Phase III randomized trial of sunitinib versus capecitabine in patients with previously treated HER2-negative advanced breast cancer.

Resistance of renal cell carcinoma to sorafenib is mediated by potentially reversible gene expression.

Antiangiogenic therapy using sunitinib combined with rapamycin retards tumor growth but promotes metastasis.

Development of a resistance-like phenotype to sorafenib by human hepatocellular carcinoma cells is reversible and can be delayed by metronomic UFT chemotherapy.

Up-regulation of delta-like 4 ligand in human tumor vasculature and the role of basal expression in endothelial cell function.

Sunitinib: a VEGF and PDGF receptor protein kinase and angiogenesis inhibitor.

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1008-1020

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scholarly article

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10.1158/0008-5472.CAN-16-1982

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4

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77

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2016-12-23T00:00:00Z

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28011623

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5321582

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