Scholarlink

Background <p>Reports of small-cell lung cancer (SCLC) transdifferentiation in epidermal growth factor receptor tyrosine (<i>EGFR</i>)‑mutant lung adenocarcinoma (LUAD) often reflect pre‑existing combined SCLC or are limited by sampling bias, obscuring true treatment‑induced lineage transformation.</p> Case presentation <p>We report a female patient with EGFR‑mutant LUAD who, during <i>EGFR</i> tyrosine kinase inhibitor therapy, developed SCLC transformation confirmed histopathologically. The patient showed limited response to first‑line SCLC chemoimmunotherapy, and a subsequent biopsy revealed mixed SCLC/LUAD histology with neuroendocrine differentiation and shared genetic alterations between components.</p> Conclusions <p>This case provides strong clinicopathological and molecular evidence supporting neuroendocrine transdifferentiation from LUAD to SCLC, culminating in a mixed phenotypic state. Further research is needed to define optimal therapeutic strategies for this resistant phenotype.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Authentic neuroendocrine transdifferentiation from lung adenocarcinoma to small-cell lung cancer: a case report

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年3月12日

查看全文
  • Mengqian Li,
  • Ping Zhou,
  • Xuexue Wu,
  • Lili Jiang

摘要

Background

Reports of small-cell lung cancer (SCLC) transdifferentiation in epidermal growth factor receptor tyrosine (EGFR)‑mutant lung adenocarcinoma (LUAD) often reflect pre‑existing combined SCLC or are limited by sampling bias, obscuring true treatment‑induced lineage transformation.

Case presentation

We report a female patient with EGFR‑mutant LUAD who, during EGFR tyrosine kinase inhibitor therapy, developed SCLC transformation confirmed histopathologically. The patient showed limited response to first‑line SCLC chemoimmunotherapy, and a subsequent biopsy revealed mixed SCLC/LUAD histology with neuroendocrine differentiation and shared genetic alterations between components.

Conclusions

This case provides strong clinicopathological and molecular evidence supporting neuroendocrine transdifferentiation from LUAD to SCLC, culminating in a mixed phenotypic state. Further research is needed to define optimal therapeutic strategies for this resistant phenotype.