ArticleNPJ precision oncology2026
Case report: ALK inhibitor-induced transformation of ALK fusion-positive lung adenocarcinoma to large cell neuroendocrine carcinoma.
Article in NPJ precision oncology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- ALK rearrangements and resistance mutations in non-small cell lung cancer: molecular mechanisms and therapeutic implications.Cancer chemotherapy and pharmacology · 2026Review
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Authors and funding
6 authors.
Funding
Abstract
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.
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