Intermittent high-dose treatment with erlotinib enhances therapeutic efficacy in EGFR-mutant lung cancer

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2015 nî lūn-bûn

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2015年の論文

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2015年論文

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2015年論文

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2015年論文

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2015年論文

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2015年論文

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2015年论文

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2015年论文

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2015年论文

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name

Intermittent high-dose treatme ...... acy in EGFR-mutant lung cancer

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Intermittent high-dose treatme ...... acy in EGFR-mutant lung cancer

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Intermittent high-dose treatme ...... acy in EGFR-mutant lung cancer

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P1476

Intermittent high-dose treatme ...... acy in EGFR-mutant lung cancer

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P2093

Alexandra Florin

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Caroline Volz

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Dennis Plenker

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Dennis Rokitta

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Felix Dietlein

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Jakob Schöttle

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Johannes M Heuckmann

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Katharina König

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Kerstin Albus

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Maike Siobal

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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

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

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

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

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

Gefitinib or carboplatin-paclitaxel in pulmonary adenocarcinoma

Activating mutations in the epidermal growth factor receptor underlying responsiveness of non-small-cell lung cancer to gefitinib

PTEN loss contributes to erlotinib resistance in EGFR-mutant lung cancer by activation of Akt and EGFR

Novel D761Y and common secondary T790M mutations in epidermal growth factor receptor-mutant lung adenocarcinomas with acquired resistance to kinase inhibitors

Modelling vemurafenib resistance in melanoma reveals a strategy to forestall drug resistance

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38458-38468

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scholarly article

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10.18632/ONCOTARGET.6276

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English

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2015-11-02T00:00:00Z

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283513966

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26540572

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4770714

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