Ensartinib is effective in the treatment of advanced non-small-cell lung cancer with MET amplification after multi-line ALK-TKIs resistance: a case report.

IF 1.8 4区 医学 Q3 ONCOLOGY Anti-Cancer Drugs Pub Date : 2024-03-01 Epub Date: 2023-12-13 DOI:10.1097/CAD.0000000000001559
Yanping Yang, Xincheng He, Wenxuan Xiao, Jun Bai, Yi Liu
{"title":"Ensartinib is effective in the treatment of advanced non-small-cell lung cancer with MET amplification after multi-line ALK-TKIs resistance: a case report.","authors":"Yanping Yang, Xincheng He, Wenxuan Xiao, Jun Bai, Yi Liu","doi":"10.1097/CAD.0000000000001559","DOIUrl":null,"url":null,"abstract":"<p><p>Although patients with ALK-positive non-small cell lung cancer (NSCLC) are initially effective on treatment with ALK tyrosine kinase inhibitors (TKIs), resistance will inevitably develop. Of these patients, 2/3 will develop ALK-independent resistance and little is known about the mechanisms of ALK-independent resistance. In pre-clinical studies, the activation of several bypass signaling pathways has been implicated in the development of resistance, including the MET, EGFR, SRC and IGF1R pathways. Among these, the MET pathway is one of the signaling pathways that has recently been extensively studied, and activation of this pathway is one of the mechanisms of ALK-independent drug resistance. Here, we report a successful case of an advanced NSCLC patient who was resistant to treatment with ALK TKIs and developed MET amplification, who achieved 23 months of progression-free survival after post-line treatment with ensartinib.</p>","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":null,"pages":null},"PeriodicalIF":1.8000,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10833182/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Anti-Cancer Drugs","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1097/CAD.0000000000001559","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2023/12/13 0:00:00","PubModel":"Epub","JCR":"Q3","JCRName":"ONCOLOGY","Score":null,"Total":0}
引用次数: 0

Abstract

Although patients with ALK-positive non-small cell lung cancer (NSCLC) are initially effective on treatment with ALK tyrosine kinase inhibitors (TKIs), resistance will inevitably develop. Of these patients, 2/3 will develop ALK-independent resistance and little is known about the mechanisms of ALK-independent resistance. In pre-clinical studies, the activation of several bypass signaling pathways has been implicated in the development of resistance, including the MET, EGFR, SRC and IGF1R pathways. Among these, the MET pathway is one of the signaling pathways that has recently been extensively studied, and activation of this pathway is one of the mechanisms of ALK-independent drug resistance. Here, we report a successful case of an advanced NSCLC patient who was resistant to treatment with ALK TKIs and developed MET amplification, who achieved 23 months of progression-free survival after post-line treatment with ensartinib.

查看原文
分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
恩沙替尼对多线ALK-TKIs耐药后MET扩增的晚期非小细胞肺癌治疗有效:病例报告。
虽然ALK阳性非小细胞肺癌(NSCLC)患者在接受ALK酪氨酸激酶抑制剂(TKIs)治疗后初期疗效显著,但不可避免地会产生耐药性。在这些患者中,2/3 的患者会出现 ALK 非依赖性耐药,而人们对 ALK 非依赖性耐药的机制知之甚少。在临床前研究中,一些旁路信号通路的激活被认为与耐药性的产生有关,包括 MET、表皮生长因子受体、SRC 和 IGF1R 通路。其中,MET通路是最近被广泛研究的信号通路之一,该通路的激活是ALK依赖性耐药的机制之一。在此,我们成功报道了一例对ALK TKIs治疗耐药并出现MET扩增的晚期NSCLC患者,该患者在接受恩沙替尼线后治疗后获得了23个月的无进展生存期。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 去求助
来源期刊
Anti-Cancer Drugs
Anti-Cancer Drugs 医学-药学
CiteScore
3.80
自引率
0.00%
发文量
244
审稿时长
3 months
期刊介绍: Anti-Cancer Drugs reports both clinical and experimental results related to anti-cancer drugs, and welcomes contributions on anti-cancer drug design, drug delivery, pharmacology, hormonal and biological modalities and chemotherapy evaluation. An internationally refereed journal devoted to the fast publication of innovative investigations on therapeutic agents against cancer, Anti-Cancer Drugs aims to stimulate and report research on both toxic and non-toxic anti-cancer agents. Consequently, the scope on the journal will cover both conventional cytotoxic chemotherapy and hormonal or biological response modalities such as interleukins and immunotherapy. Submitted articles undergo a preliminary review by the editor. Some articles may be returned to authors without further consideration. Those being considered for publication will undergo further assessment and peer-review by the editors and those invited to do so from a reviewer pool.
期刊最新文献
Donafenib inhibits PARP1 expression and induces DNA damage, in combination with PARP1 inhibitors promotes apoptosis in liver cancer cells. Hyper-late major response after 5 years of nivolumab: role of treatment beyond progression in head and neck cancer. Individualized medication of venetoclax based on therapeutic drug monitoring in Chinese acute myeloid leukemia patients using an HPLC method. Complete and durable regression of leptomeningeal involvement during lorlatinib treatment in a patient with lung cancer. Dermatological toxicity associated with the use of gilteritinib in relapsed acute myeloid leukemia with FLT3 mutation: a case report.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
已复制链接
已复制链接
快去分享给好友吧!
我知道了
×
扫码分享
扫码分享
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1