• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利：CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法，用中文像聊天一样搜索，搜遍4000万医学文献。AI智能推荐，让科研检索更轻松。

立即免费搜索

文件翻译

保留排版，准确专业，支持PDF/Word/PPT等文件格式，支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述，25分钟生成高质量综述，智能提取关键信息，辅助科研写作。

立即免费体验

克唑替尼治疗棘皮动物微管相关蛋白样 4-间变性淋巴瘤激酶融合基因肺癌患者耐药获得成功，可能与间充质上皮转化扩增有关。

Successful Treatment with Crizotinib to Overcome Drug Resistance Possibly Due to Mesenchymal-epithelial Transition Amplification in a Lung Cancer Patient with the Echinoderm Microtubule-associated Protein-like 4-anaplastic Lymphoma Kinase Fusion Gene.

机构信息

Department of Respiratory Medicine, University of Occupational and Environmental Health, Japan.

Department of Thoracic Oncology, National Cancer Center Hospital East, Japan.

出版信息

Intern Med. 2023 Nov 1;62(21):3215-3221. doi: 10.2169/internalmedicine.1164-22. Epub 2023 Mar 15.

DOI:10.2169/internalmedicine.1164-22
PMID:36927974
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10686730/
Abstract

Amplification of the mesenchymal-epithelial transition (MET) gene plays an important role in anticancer drug resistance to anaplastic lymphoma kinase-tyrosine kinase inhibitors (ALK-TKIs) in echinoderm microtubule-associated protein-like 4-anaplastic lymphoma kinase (EML4-ALK)-rearranged lung cancer cells. We encountered an ALK-rearranged lung cancer patient who developed MET amplification after alectinib treatment and showed an effective response to fifth-line crizotinib. First-line alectinib treatment was effective for 2.5 years; however, liver metastases exacerbated. Liver biopsy specimens revealed MET and human epidermal growth factor receptor 2 (HER2) amplifications. Switching to the MET inhibitor crizotinib improved liver metastases. Crizotinib may be effective in ALK-positive patients with MET amplification.

摘要

间质上皮转化 (MET) 基因的扩增在棘皮动物微管相关蛋白样 4-间变性淋巴瘤激酶 (EML4-ALK) 融合肺癌细胞对间变性淋巴瘤激酶酪氨酸激酶抑制剂 (ALK-TKIs) 的抗癌药物耐药中起着重要作用。我们遇到了一位接受艾乐替尼治疗后出现 MET 扩增的 ALK 重排肺癌患者，并且对第五线克唑替尼表现出有效反应。一线艾乐替尼治疗有效 2.5 年；然而，肝转移恶化。肝活检标本显示 MET 和人表皮生长因子受体 2 (HER2) 扩增。改用 MET 抑制剂克唑替尼改善了肝转移。克唑替尼可能对 MET 扩增的 ALK 阳性患者有效。

相似文献

1
Successful Treatment with Crizotinib to Overcome Drug Resistance Possibly Due to Mesenchymal-epithelial Transition Amplification in a Lung Cancer Patient with the Echinoderm Microtubule-associated Protein-like 4-anaplastic Lymphoma Kinase Fusion Gene.克唑替尼治疗棘皮动物微管相关蛋白样 4-间变性淋巴瘤激酶融合基因肺癌患者耐药获得成功，可能与间充质上皮转化扩增有关。
Intern Med. 2023 Nov 1;62(21):3215-3221. doi: 10.2169/internalmedicine.1164-22. Epub 2023 Mar 15.
2
Protocol Design for the Bench to Bed Trial in Alectinib-Refractory Non-Small-Cell Lung Cancer Patients Harboring the EML4-ALK Fusion Gene (ALRIGHT/OLCSG1405).针对携带EML4-ALK融合基因的阿来替尼难治性非小细胞肺癌患者的从实验室到临床研究的方案设计（ALRIGHT/OLCSG1405）
Clin Lung Cancer. 2016 Nov;17(6):602-605. doi: 10.1016/j.cllc.2016.05.005. Epub 2016 Jun 2.
3
ALK inhibitors in the treatment of advanced NSCLC.ALK 抑制剂治疗晚期 NSCLC。
Cancer Treat Rev. 2014 Mar;40(2):300-6. doi: 10.1016/j.ctrv.2013.07.002. Epub 2013 Aug 7.
4
Management of Resistance to First-Line Anaplastic Lymphoma Kinase Tyrosine Kinase Inhibitor Therapy.一线间变性淋巴瘤激酶酪氨酸激酶抑制剂治疗耐药的管理。
Curr Treat Options Oncol. 2018 May 28;19(7):37. doi: 10.1007/s11864-018-0553-x.
5
Clinicopathological features and resistance mechanisms in HIP1-ALK-rearranged lung cancer: A multicenter study.HIP1-ALK 重排肺癌的临床病理特征和耐药机制：一项多中心研究。
Genes Chromosomes Cancer. 2022 Apr;61(4):177-186. doi: 10.1002/gcc.23005. Epub 2021 Nov 1.
6
miR-100-5p confers resistance to ALK tyrosine kinase inhibitors Crizotinib and Lorlatinib in EML4-ALK positive NSCLC.miR-100-5p 赋予 EML4-ALK 阳性 NSCLC 对 ALK 酪氨酸激酶抑制剂克唑替尼和洛拉替尼的耐药性。
Biochem Biophys Res Commun. 2019 Apr 2;511(2):260-265. doi: 10.1016/j.bbrc.2019.02.016. Epub 2019 Feb 18.
7
Differential protein stability and clinical responses of EML4-ALK fusion variants to various ALK inhibitors in advanced ALK-rearranged non-small cell lung cancer.晚期 EML4-ALK 融合变异型非小细胞肺癌中不同蛋白稳定性与各种 ALK 抑制剂的临床反应。
Ann Oncol. 2017 Apr 1;28(4):791-797. doi: 10.1093/annonc/mdw693.
8
Amphiregulin triggered epidermal growth factor receptor activation confers in vivo crizotinib-resistance of EML4-ALK lung cancer and circumvention by epidermal growth factor receptor inhibitors.双调蛋白触发的表皮生长因子受体激活赋予EML4-ALK肺癌体内克唑替尼耐药性以及表皮生长因子受体抑制剂对其的规避。
Cancer Sci. 2017 Jan;108(1):53-60. doi: 10.1111/cas.13111. Epub 2016 Dec 30.
9
Dual ALK and EGFR inhibition targets a mechanism of acquired resistance to the tyrosine kinase inhibitor crizotinib in ALK rearranged lung cancer.双重 ALK 和 EGFR 抑制靶向治疗针对 ALK 重排肺癌对酪氨酸激酶抑制剂克唑替尼获得性耐药的机制。
Lung Cancer. 2014 Jan;83(1):37-43. doi: 10.1016/j.lungcan.2013.09.019. Epub 2013 Oct 14.
10
Hypoxia induces resistance to ALK inhibitors in the H3122 non-small cell lung cancer cell line with an ALK rearrangement via epithelial-mesenchymal transition.缺氧通过上皮-间质转化诱导具有ALK重排的H3122非小细胞肺癌细胞系对ALK抑制剂产生耐药性。
Int J Oncol. 2014 Oct;45(4):1430-6. doi: 10.3892/ijo.2014.2574. Epub 2014 Aug 1.

引用本文的文献

1
Combinatorial therapy is a safe and durable treatment option in -rearranged non-small cell lung cancer with an acquired exon 14 skipping mutation mediated resistance to alectinib: a case report.联合治疗是一种安全且持久的治疗选择，用于治疗具有获得性外显子14跳跃突变介导的对阿来替尼耐药的重排非小细胞肺癌：一例报告。
Transl Lung Cancer Res. 2023 Dec 26;12(12):2558-2564. doi: 10.21037/tlcr-23-613. Epub 2023 Dec 22.
2
Anaplastic lymphoma kinase inhibitors-a review of anticancer properties, clinical efficacy, and resistance mechanisms.间变性淋巴瘤激酶抑制剂——抗癌特性、临床疗效及耐药机制综述
Front Pharmacol. 2023 Oct 25;14:1285374. doi: 10.3389/fphar.2023.1285374. eCollection 2023.

本文引用的文献

1
Beyond epidermal growth factor receptor: MET amplification as a general resistance driver to targeted therapy in oncogene-driven non-small-cell lung cancer.超越表皮生长因子受体：MET 扩增作为驱动基因非小细胞肺癌中靶向治疗的一般耐药驱动因素。
ESMO Open. 2021 Dec;6(6):100319. doi: 10.1016/j.esmoop.2021.100319. Epub 2021 Nov 24.
2
Trastuzumab Deruxtecan in -Mutant Non-Small-Cell Lung Cancer.曲妥珠单抗 deruxtecan 治疗 - 突变型非小细胞肺癌。
N Engl J Med. 2022 Jan 20;386(3):241-251. doi: 10.1056/NEJMoa2112431. Epub 2021 Sep 18.
3
Early Alectinib Resistance From MET Amplification in ALK-Rearranged NSCLC: Response to Crizotinib with Re-Response to Alectinib and Crizotinib.
ALK 重排的非小细胞肺癌中 MET 扩增导致的早期阿来替尼耐药：对克唑替尼的反应及对阿来替尼和克唑替尼的再次反应
Clin Lung Cancer. 2021 Nov;22(6):e851-e855. doi: 10.1016/j.cllc.2021.04.008. Epub 2021 Apr 27.
4
Heterogeneity in MET-Aberrant NSCLC.MET异常的非小细胞肺癌中的异质性。
J Thorac Oncol. 2021 Apr;16(4):504-506. doi: 10.1016/j.jtho.2021.01.1609.
5
Genetic Heterogeneity of MET-Aberrant NSCLC and Its Impact on the Outcome of Immunotherapy.MET 异常非小细胞肺癌的遗传异质性及其对免疫治疗结局的影响。
J Thorac Oncol. 2021 Apr;16(4):572-582. doi: 10.1016/j.jtho.2020.11.017. Epub 2020 Dec 9.
6
Emergence of a -amplified clone during disease progression in an -rearranged NSCLC patient treated with ALK-inhibitors: a case report.一名接受ALK抑制剂治疗的重排非小细胞肺癌（NSCLC）患者疾病进展期间出现α-扩增克隆：病例报告
Transl Lung Cancer Res. 2020 Jun;9(3):787-792. doi: 10.21037/tlcr.2020.04.03.
7
MET-dependent solid tumours - molecular diagnosis and targeted therapy.依赖 MET 的实体瘤——分子诊断与靶向治疗。
Nat Rev Clin Oncol. 2020 Sep;17(9):569-587. doi: 10.1038/s41571-020-0377-z. Epub 2020 Jun 8.
8
Updated overall survival and final progression-free survival data for patients with treatment-naive advanced ALK-positive non-small-cell lung cancer in the ALEX study.在 ALEX 研究中，未经治疗的晚期 ALK 阳性非小细胞肺癌患者的更新总生存和最终无进展生存数据。
Ann Oncol. 2020 Aug;31(8):1056-1064. doi: 10.1016/j.annonc.2020.04.478. Epub 2020 May 11.
9
MET Alterations Are a Recurring and Actionable Resistance Mechanism in ALK-Positive Lung Cancer.MET 改变是 ALK 阳性肺癌中一种反复出现且可采取行动的耐药机制。
Clin Cancer Res. 2020 Jun 1;26(11):2535-2545. doi: 10.1158/1078-0432.CCR-19-3906. Epub 2020 Feb 21.
10
Is there a place for crizotinib in c-MET alterations? A case of efficacy in ALK positive NSCLC patient with secondary c-MET amplification.克唑替尼在c-MET改变中是否有一席之地？1例ALK阳性非小细胞肺癌患者继发c-MET扩增后的疗效病例。
Ann Oncol. 2020 Mar;31(3):440-441. doi: 10.1016/j.annonc.2019.11.016. Epub 2019 Dec 9.