转化为神经内分泌癌作为对 lorlatinib 的耐药机制。
Transformation to neuroendocrine carcinoma as a resistance mechanism to lorlatinib.
机构信息
Lung Unit, The Royal Marsden Hospital, 203 Fulham Rd, Chelsea, London, SW3 6JJ, United Kingdom.
Department of Histopathology, The Royal Marsden Hospital, 203 Fulham Rd, Chelsea, London, SW3 6JJ, United Kingdom.
出版信息
Lung Cancer. 2019 Aug;134:117-120. doi: 10.1016/j.lungcan.2019.05.025. Epub 2019 Jun 6.
OBJECTIVES
Small cell transformation is a well-recognized mechanism of resistance to EGFR-TKI therapy in EGFR-mutant NSCLC, yet it remains a poorly-described phenomenon in ALK-rearranged NSCLC.
MATERIAL AND METHODS
Chart and literature review.
RESULTS
We report a case of a patient with ALK-rearranged lung cancer progressing on three-lines of ALK-targeted therapies, with development of acquired resistance to lorlatinib, with both transformation to a neuroendocrine carcinoma, and acquisition of ALK 1196 M.
CONCLUSIONS
Given the inevitable development of resistance in ALK + NSCLC, if feasible, re-biopsy on progression should be standard over liquid biopsy. Neuroendocrine carcinoma transformation remains an important mechanism of acquired resistance to lorlatinib.
目的
小细胞转化是 EGFR 突变型 NSCLC 患者对 EGFR-TKI 治疗产生耐药的一种公认机制，但在 ALK 重排型 NSCLC 中，这一现象仍描述不足。
材料与方法
图表和文献回顾。
结果
我们报告了一例 ALK 重排型肺癌患者，该患者在接受三线 ALK 靶向治疗后进展，对 lorlatinib 产生获得性耐药，同时发生神经内分泌癌转化，并获得 ALK 1196M 突变。
结论
鉴于 ALK+NSCLC 必然会产生耐药性，如果可行，进展时应通过再次活检而非液体活检来进行标准检测。神经内分泌癌转化仍然是对 lorlatinib 获得性耐药的重要机制。
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