Targeting the tumor-promoting microenvironment in MET-amplified NSCLC cells with a novel inhibitor of pro-HGF activation.

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Targeting the tumor-promoting microenvironment in MET-amplified NSCLC cells with a novel inhibitor of pro-HGF activation.

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2017 nî lūn-bûn

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2017年の論文

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2017年論文

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2017年論文

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2017年論文

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2017年論文

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2017年論文

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2017年论文

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2017年论文

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2017年论文

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Targeting the tumor-promoting ...... hibitor of pro-HGF activation.

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Targeting the tumor-promoting ...... hibitor of pro-HGF activation.

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Targeting the tumor-promoting ...... hibitor of pro-HGF activation.

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P1476

Targeting the tumor-promoting ...... nhibitor of pro-HGF activation

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Benjamin Y Owusu

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Lidija Klampfer

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Phanindra Venukadasula

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Robert A Galemmo

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Shantasia Thomas

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Zhenfu Han

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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

An uncleavable form of pro-scatter factor suppresses tumor growth and dissemination in mice

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

Acquired resistance of lung adenocarcinomas to gefitinib or erlotinib is associated with a second mutation in the EGFR kinase domain

The Evolution of Therapies in Non-Small Cell Lung Cancer

A decade of EGFR inhibition in EGFR-mutated non small cell lung cancer (NSCLC): Old successes and future perspectives

MET: a critical player in tumorigenesis and therapeutic target

EGFR mutations in lung cancer: correlation with clinical response to gefitinib therapy.

EGFR mutation and resistance of non-small-cell lung cancer to gefitinib.

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

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63014-63025

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scholarly article

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10.18632/ONCOTARGET.18260

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English

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James W. Janetka

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2017-05-29T00:00:00Z

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28968967

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5609899

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