Acquired resistance to gefitinib: the contribution of mechanisms other than the T790M, MET, and HGF status.
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Summary
The T790M mutation in the EGFR is relatively common in the patients with acquired resistance to gefitinib, however, mechanisms other than T790m, MET, and HGF status are involved in resistance togefit inib.
- Type
- article
- Published
- 2010-05-01
- Cited by
- 149
- References
- 43
- OpenAlex
- https://openalex.org/W1967249248
- Semantic Scholar
- https://api.semanticscholar.org/CorpusID:5322400
Keywords
Medicine, Gefitinib, T790M, Resistance (ecology), Oncology
References
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- TNM Classification of Malignant Tumours, 7th Edition
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- Resistance to gefitinib
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- “Rapid-Impact Interventions”: How a Policy of Integrated Control for Africa's Neglected Tropical Diseases Could Benefit the Poor
- EKB-569, a new irreversible epidermal growth factor receptor tyrosine kinase inhibitor, with clinical activity in patients with non-small cell lung cancer with acquired resistance to gefitinib.
- MET Amplification Leads to Gefitinib Resistance in Lung Cancer by Activating ERBB3 Signaling
- Acquired Resistance of Lung Adenocarcinomas to Gefitinib or Erlotinib Is Associated with a Second Mutation in the EGFR Kinase Domain
- EGFR mutation and resistance of non-small-cell lung cancer to gefitinib.
- Epidermal growth factor receptor mutations are associated with gefitinib sensitivity in non-small cell lung cancer in Japanese.
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- Comparison of EGFR and K-RAS gene status between primary tumours and corresponding metastases in NSCLC
- Activating mutations in the epidermal growth factor receptor underlying responsiveness of non-small-cell lung cancer to gefitinib.
- Determinants of tumor response and survival with erlotinib in patients with non--small-cell lung cancer.
- Met gene copy number predicts the prognosis for completely resected non‐small cell lung cancer
- Gefitinib response of erlotinib-refractory lung cancer involving meninges—role of EGFR mutation
- Allelic dilution obscures detection of a biologically significant resistance mutation in EGFR-amplified lung cancer.
- Mutations within the tyrosine kinase domain of EGFR gene specifically occur in lung adenocarcinoma patients with a low exposure of tobacco smoking
Cited by
- Expression of selected gene for acquired drug resistance to EGFR-TKI in lung adenocarcinoma.
- EGFR-TKI resistance in NSCLC patients: mechanisms and strategies.
- 非小细胞肺癌个体化治疗相关分子标记物
- 酪氨酸激酶抑制剂耐药机制及其治疗策略
- 非小细胞肺癌T790M基因突变研究进展
- 45例晚期非小细胞肺癌EGFR-TKIs治疗获益后出现孤立进展后联合局部治疗的回顾性分析
- 非小细胞肺癌中EGFR基因状态的检测对EGFR-TKIs疗效的预测价值
- The novel phosphoinositide 3‐kinase–mammalian target of rapamycin inhibitor, BEZ235, circumvents erlotinib resistance of epidermal growth factor receptor mutant lung cancer cells triggered by hepatocyte growth factor
- Management of hyperglycemia from epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs) targeting T790M-mediated resistance.
- Expression of dysadherin and cytokeratin as prognostic indicators of disease-free survival in patients with stage I NSCLC.
- TS, DHFR and GARFT expression in non-squamous cell carcinoma of NSCLC and malignant pleural mesothelioma patients treated with pemetrexed.
- The expression of Ki-67, but not proliferating cell nuclear antigen, predicts poor disease free survival in patients with adenocarcinoma of the lung.
- Epidermal growth factor receptor exon 20 mutation increased in post-chemotherapy patients with non-small cell lung cancer detected with patients' blood samples.
- Insulin-like growth factor receptor-1 expression predicts postoperative recurrence in adenocarcinoma of the lung.
- Clinical Significance of Epithelial-Mesenchymal Transition-Associated Markers in Malignant Pleural Mesothelioma
- Dual inhibition of Met kinase and angiogenesis to overcome HGF-induced EGFR-TKI resistance in EGFR mutant lung cancer.
- Molecular Testing Guideline for Selection of Lung Cancer Patients for EGFR and ALK Tyrosine Kinase Inhibitors
- Molecular Basis of Drug Resistance: Epidermal Growth Factor Receptor Tyrosine Kinase Inhibitors and Anaplastic Lymphoma Kinase Inhibitors
- c-MET/Phospho-MET Protein Expression and MET Gene Copy Number in Non-small Cell Lung Carcinomas
- Activation of ERK-p53 and ERK-mediated phosphorylation of Bcl-2 are involved in autophagic cell death induced by the c-Met inhibitor SU11274 in human lung cancer A549 cells.
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