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Updated: May 27, 2026

Ultra-Fast Amplicon-Based Next-Generation Sequencing in Non-Squamous Non-Small Cell Lung Cancer
Published on: September 8, 2023
The potential for crizotinib in non-small cell lung cancer: a perspective review
1Department of Internal Medicine, Seoul National University College of Medicine, 101 Daehak-ro, Jongno-gu, Seoul 110-744, Korea.
Abstract:
Tyrosine kinases have a crucial role as key regulators of signaling pathways that influence cell differentiation and growth. Dysregulation of tyrosine kinase-mediated signaling is understood to be an important oncogenic driver. Genetic rearrangements involving the tyrosine kinase anaplastic lymphoma kinase (ALK) gene occur in non-small cell lung cancer (NSCLC), anaplastic large cell lymphomoas, inflammatory myofibroblastic tumors, and other cancers. Cells with abnormal ALK signaling are sensitive to ALK inhibitors such as crizotinib. This review will highlight the discovery of the fusion between echinoderm microtubule-associated protein-like 4 (EML4) and ALK as an oncogenic driver, recognition of other ALK gene rearrangements in NSCLC, and the confirmation that crizotinib is an effective treatment for patients with ALK-positive NSCLC. Work is underway to further define the role for crizotinib in the treatment of ALK-positive lung cancer and other cancers and to investigate the molecular mechanisms for resistance to ALK inhibition with crizotinib.
Insights
Anaplastic lymphoma kinase (ALK) gene rearrangements drive cancer growth. Crizotinib effectively treats ALK-positive non-small cell lung cancer (NSCLC), with ongoing research into resistance mechanisms.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Tyrosine kinases regulate critical cell signaling pathways.
- Dysregulated tyrosine kinase signaling, particularly involving anaplastic lymphoma kinase (ALK), drives oncogenesis.
- ALK gene rearrangements are implicated in non-small cell lung cancer (NSCLC) and other malignancies.
Purpose of the Study:
- To review the discovery of the echinoderm microtubule-associated protein-like 4 (EML4)-ALK fusion oncogene.
- To discuss the identification of various ALK gene rearrangements in NSCLC.
- To summarize the efficacy of crizotinib in treating ALK-positive NSCLC and explore future directions.
Main Methods:
- Literature review focusing on ALK gene rearrangements and targeted therapies.
- Analysis of studies detailing the EML4-ALK fusion and its oncogenic role.
- Examination of clinical trial data on crizotinib in ALK-positive cancers.
Main Results:
- The EML4-ALK fusion was identified as a significant oncogenic driver.
- Multiple ALK gene rearrangements are recognized in NSCLC.
- Crizotinib demonstrated efficacy in patients with ALK-positive NSCLC.
Conclusions:
- ALK rearrangements are key oncogenic drivers in specific cancers.
- Crizotinib is an effective targeted therapy for ALK-positive NSCLC.
- Further research is needed to optimize crizotinib treatment and overcome resistance mechanisms.
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