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。

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
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引用次数: 0

摘要

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。
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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.

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.

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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.
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