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病例报告:一名ALK重排肺腺癌患者,其KIF5B-RET融合对阿来替尼耐药,使用普拉替尼进行晚期治疗成功。

Case Report: Successful late-line pralsetinib treatment in an ALK-rearranged lung adenocarcinoma patient with KIF5B-RET fusion resistant to alectinib.

作者信息

Jin Feng, Wang Chenyang, Yang Fang, Wang Shubin, Wang Fen

机构信息

Department of Medical Oncology, Peking University Shenzhen Hospital, Shenzhen, China.

Shenzhen University, Shenzhen, China.

出版信息

Front Genet. 2025 Jun 17;16:1569912. doi: 10.3389/fgene.2025.1569912. eCollection 2025.

Abstract

Anaplastic lymphoma kinase () fusion, an oncogenic driver alteration, accounts for 5%-6% of non-small cell lung cancer (NSCLC) patients. tyrosine kinase inhibitors (TKIs) provide significant clinical benefit in advanced ALK-rearranged NSCLC. However, acquired resistance to TKIs inevitably arises, and the underlying mechanisms remain incompletely elucidated. This report describes a stage IV lung adenocarcinoma (LUAD) patient with -rearranged who developed fusion-mediated resistance following second-line alectinib therapy. The patient achieved a partial response (PR) to third-line pralsetinib, sustained for 4 months. This case highlights fusion as a potential resistance mechanism post alectinib treatment and suggested = pralsetinib, a inhibitor, as a viable therapeutic option in this context. These findings contribute to the evolving understanding of resistance management strategies in -rearranged NSCLC.

摘要

间变性淋巴瘤激酶(ALK)融合是一种致癌驱动改变,在非小细胞肺癌(NSCLC)患者中占5%-6%。ALK酪氨酸激酶抑制剂(TKIs)在晚期ALK重排的NSCLC中提供显著的临床益处。然而,对ALK TKIs的获得性耐药不可避免地出现,其潜在机制仍未完全阐明。本报告描述了一名IV期肺腺癌(LUAD)患者,其ALK重排,在二线阿来替尼治疗后出现了EML4-ALK融合介导的耐药。该患者对三线普拉替尼获得了部分缓解(PR),持续了4个月。本病例突出了EML4-ALK融合作为阿来替尼治疗后潜在的耐药机制,并提示在这种情况下,ALK抑制剂普拉替尼是一种可行的治疗选择。这些发现有助于不断发展对ALK重排NSCLC耐药管理策略的理解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/816c/12209176/aa604788480d/fgene-16-1569912-g001.jpg

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