Successful crizotinib monotherapy in EGFR-mutant lung adenocarcinoma with acquired MET amplification after erlotinib therapy. - Wikidata - wikimedia - TriplyDB

Successful crizotinib monotherapy in EGFR-mutant lung adenocarcinoma with acquired MET amplification after erlotinib therapy.

Successful crizotinib monotherapy in EGFR-mutant lung adenocarcinoma with acquired MET amplification after erlotinib therapy.

http://www.wikidata.org/entity/Q37660829

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Successful crizotinib monotherapy in EGFR-mutant lung adenocarcinoma with acquired MET amplification after erlotinib therapy.

http://www.wikidata.org/entity/Q37660829

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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 17 February 2017

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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

Successful crizotinib monother ...... ation after erlotinib therapy.

@en

Successful crizotinib monother ...... ation after erlotinib therapy.

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type

label

Successful crizotinib monother ...... ation after erlotinib therapy.

@en

Successful crizotinib monother ...... ation after erlotinib therapy.

@nl

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Successful crizotinib monother ...... ation after erlotinib therapy.

@en

Successful crizotinib monother ...... ation after erlotinib therapy.

@nl

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J.RMCR.2017.02.009

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Respiratory medicine case reports

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Successful crizotinib monother ...... cation after erlotinib therapy

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Haruhiko Sugimura

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Katsuhiro Yoshimura

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Masato Karayama

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Naoki Inui

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Noriyuki Enomoto

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Takafumi Suda

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Tomoyuki Fujisawa

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Yusuke Inoue

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Yutaro Nakamura

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P2860

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

Genotypic and histological evolution of lung cancers acquiring resistance to EGFR inhibitors

Analysis of tumor specimens at the time of acquired resistance to EGFR-TKI therapy in 155 patients with EGFR-mutant lung cancers.

Activation of MET via diverse exon 14 splicing alterations occurs in multiple tumor types and confers clinical sensitivity to MET inhibitors.

Response to MET inhibitors in patients with stage IV lung adenocarcinomas harboring MET mutations causing exon 14 skipping

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

An orally available small-molecule inhibitor of c-Met, PF-2341066, exhibits cytoreductive antitumor efficacy through antiproliferative and antiangiogenic mechanisms.

Response to Crizotinib/Erlotinib Combination in a Patient with a Primary EGFR-Mutant Adenocarcinoma and a Primary c-met-Amplified Adenocarcinoma of the Lung

Hepatocyte growth factor enhances vascular endothelial growth factor-induced angiogenesis in vitro and in vivo.

Crizotinib, a c-Met inhibitor, prevents metastasis in a metastatic uveal melanoma model.

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160-163

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10.1016/J.RMCR.2017.02.009

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