Fiore Michele, Trecca Pasquale, Perrone Giuseppe, Amato Michelina, Righi Daniela, Trodella Lucio, D'Angelillo Rolando M, Ramella Sara
Radiotherapy Unit, Campus Bio-Medico University, Rome, Italy.
Anatomical Pathology Research Unit, Campus Bio-Medico University, Rome, Italy.
Tumori. 2019 Dec;105(6):NP12-NP16. doi: 10.1177/0300891619832261. Epub 2019 Feb 24.
Targeted therapies against epidermal growth factor receptor (EGFR) have revolutionized the treatment of a subset of lung adenocarcinomas that have EGFR-activating mutations; however, all patients treated with EGFR tyrosine kinase inhibitors (TKIs) ultimately develop resistance. Histologic transformation of EGFR-mutant adenocarcinoma to small cell lung cancer (SCLC) is a resistance mechanism rarely reported in the literature.
We describe the case of a woman with metastatic lung cancer adenocarcinoma with mutated EGFR with an initial response to gefitinib and radiation therapy, who progressed after 18 months due to the development of a resistance mechanism. The new biopsy performed after progression highlighted histologic transformation to SCLC, while maintaining the original EGFR mutation.
To better identify patients who progress after TKIs and radiation therapy, it is important to perform tumor rebiopsy and collect data to study mechanisms of acquired EGFR TKI resistance.
针对表皮生长因子受体（EGFR）的靶向治疗彻底改变了对一部分具有EGFR激活突变的肺腺癌的治疗方式；然而，所有接受EGFR酪氨酸激酶抑制剂（TKIs）治疗的患者最终都会产生耐药性。EGFR突变型腺癌组织学转化为小细胞肺癌（SCLC）是一种在文献中很少报道的耐药机制。
我们描述了一名患有转移性肺腺癌且EGFR突变的女性病例，该患者最初对吉非替尼和放射治疗有反应，但在18个月后因出现耐药机制而病情进展。病情进展后进行的新活检显示组织学转化为SCLC，同时保留了原始的EGFR突变。
为了更好地识别在TKIs和放射治疗后病情进展的患者，进行肿瘤再次活检并收集数据以研究获得性EGFR TKI耐药机制非常重要。
