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ALK阳性非小细胞肺癌靶向治疗耐药机制及预后标志物的研究进展

Echinoderm microtubule-associated protein like 4-anaplastic lymphoma kinase (EML4-ALK) fusion accounts for 3%-5% of non-small cell lung cancer (NSCLC) patients. With the in-depth study of the EML4-ALK driver gene, ALK inhibitors represented by crizotinib have been gradually developed and applied in...

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Detalles Bibliográficos
Formato: Online Artículo Texto
Lenguaje:English
Publicado: 中国肺癌杂志编辑部 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7679215/
https://www.ncbi.nlm.nih.gov/pubmed/33203201
http://dx.doi.org/10.3779/j.issn.1009-3419.2020.101.44
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collection PubMed
description Echinoderm microtubule-associated protein like 4-anaplastic lymphoma kinase (EML4-ALK) fusion accounts for 3%-5% of non-small cell lung cancer (NSCLC) patients. With the in-depth study of the EML4-ALK driver gene, ALK inhibitors represented by crizotinib have been gradually developed and applied in the clinic. However, the response to ALK-targeted therapy is heterogeneous among different patients. Most patients with ALK-targeted therapy will inevitably develop drug resistance, leading to tumor progression. Monitoring the efficacy of patients with prognostic markers to change the treatment in time, and selecting individualized follow-up treatment according to the mechanism of drug resistance, can effectively improve the prognosis of patients. This article will review the mechanism of ALK tyrosine kinase inhibitor (ALK-TKI) resistance and related prognostic markers to discuss the prediction for ALK-targeted therapy and the choice of subsequent treatment for drug-resistant patients.
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spelling pubmed-76792152020-12-03 ALK阳性非小细胞肺癌靶向治疗耐药机制及预后标志物的研究进展 Zhongguo Fei Ai Za Zhi 综述 Echinoderm microtubule-associated protein like 4-anaplastic lymphoma kinase (EML4-ALK) fusion accounts for 3%-5% of non-small cell lung cancer (NSCLC) patients. With the in-depth study of the EML4-ALK driver gene, ALK inhibitors represented by crizotinib have been gradually developed and applied in the clinic. However, the response to ALK-targeted therapy is heterogeneous among different patients. Most patients with ALK-targeted therapy will inevitably develop drug resistance, leading to tumor progression. Monitoring the efficacy of patients with prognostic markers to change the treatment in time, and selecting individualized follow-up treatment according to the mechanism of drug resistance, can effectively improve the prognosis of patients. This article will review the mechanism of ALK tyrosine kinase inhibitor (ALK-TKI) resistance and related prognostic markers to discuss the prediction for ALK-targeted therapy and the choice of subsequent treatment for drug-resistant patients. 中国肺癌杂志编辑部 2020-11-20 /pmc/articles/PMC7679215/ /pubmed/33203201 http://dx.doi.org/10.3779/j.issn.1009-3419.2020.101.44 Text en 版权所有©《中国肺癌杂志》编辑部2020 This is an open access article distributed in accordance with the terms of the Creative Commons Attribution (CC BY 3.0) License. See: https://creativecommons.org/licenses/by/3.0/.
spellingShingle 综述
ALK阳性非小细胞肺癌靶向治疗耐药机制及预后标志物的研究进展
title ALK阳性非小细胞肺癌靶向治疗耐药机制及预后标志物的研究进展
title_full ALK阳性非小细胞肺癌靶向治疗耐药机制及预后标志物的研究进展
title_fullStr ALK阳性非小细胞肺癌靶向治疗耐药机制及预后标志物的研究进展
title_full_unstemmed ALK阳性非小细胞肺癌靶向治疗耐药机制及预后标志物的研究进展
title_short ALK阳性非小细胞肺癌靶向治疗耐药机制及预后标志物的研究进展
title_sort alk阳性非小细胞肺癌靶向治疗耐药机制及预后标志物的研究进展
topic 综述
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7679215/
https://www.ncbi.nlm.nih.gov/pubmed/33203201
http://dx.doi.org/10.3779/j.issn.1009-3419.2020.101.44
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