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<p>The transformation of lung adenocarcinoma into large cell neuroendocrine carcinoma (LCNEC) in terms of genotype and histology has been described as a mechanism of acquired resistance to epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TKI). However, this phenomenon is exceedingly rare in anaplastic lymphoma kinase (ALK)-positive lung adenocarcinoma. Here, we report a case of an ALK-positive lung adenocarcinoma patient who developed resistance following sequential treatment with the ALK-TKI alectinib and lorlatinib, accompanied by histological transformation to LCNEC and concurrent genetic alterations including TP53 deletion, CDKN2A deletion, and MYC amplification. This case expands the spectrum of ALK-TKI resistance mechanisms and highlights the potential value of exploring combinatorial approaches incorporating immunotherapy, antiangiogenic therapy, and chemotherapy for the management of such cases.</p>

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Case report: ALK inhibitor-induced transformation of ALK fusion-positive lung adenocarcinoma to large cell neuroendocrine carcinoma

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年1月28日

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  • Rui Zhong,
  • Xinyue Wang,
  • Jinhua Xu,
  • Shuai Wang,
  • Ying Liu,
  • Hui Li

摘要

The transformation of lung adenocarcinoma into large cell neuroendocrine carcinoma (LCNEC) in terms of genotype and histology has been described as a mechanism of acquired resistance to epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TKI). However, this phenomenon is exceedingly rare in anaplastic lymphoma kinase (ALK)-positive lung adenocarcinoma. Here, we report a case of an ALK-positive lung adenocarcinoma patient who developed resistance following sequential treatment with the ALK-TKI alectinib and lorlatinib, accompanied by histological transformation to LCNEC and concurrent genetic alterations including TP53 deletion, CDKN2A deletion, and MYC amplification. This case expands the spectrum of ALK-TKI resistance mechanisms and highlights the potential value of exploring combinatorial approaches incorporating immunotherapy, antiangiogenic therapy, and chemotherapy for the management of such cases.