Takuma Sho, Inoue Yusuke, Karayama Masato, Tsuchiya Kazuo, Tsukui Hiroe, Hozumi Hironao, Suzuki Yuzo, Furuhashi Kazuki, Enomoto Noriyuki, Fujisawa Tomoyuki, Nakamura Yutaro, Inui Naoki, Suda Takafumi
Second Division, Department of Internal Medicine, Hamamatsu University School of Medicine, Hamamatsu, Japan.
Department of Clinical Pharmacology and Therapeutics, Hamamatsu University School of Medicine, Hamamatsu, Japan.
JTO Clin Res Rep. 2021 Dec 4;3(1):100264. doi: 10.1016/j.jtocrr.2021.100264. eCollection 2022 Jan.
Lineage transformation from lung adenocarcinoma (LUAD) to SCLC is associated with resistance to EGFR tyrosine kinase inhibitors. In addition to loss of p53 and RB, transformed SCLCs are usually not dependent on EGFR signaling, which renders the tumors unresponsive to EGFR tyrosine kinase inhibitors. Here, we present a case of spontaneous transformation from -mutant LUAD with loss of p53 and RB to EGFR expression-positive SCLC and neuroendocrine-differentiated LUAD, which was successfully treated with osimertinib.
肺腺癌（LUAD）向小细胞肺癌（SCLC）的谱系转化与对表皮生长因子受体（EGFR）酪氨酸激酶抑制剂的耐药性相关。除了p53和视网膜母细胞瘤（RB）缺失外，转化后的SCLC通常不依赖EGFR信号传导，这使得肿瘤对EGFR酪氨酸激酶抑制剂无反应。在此，我们报告一例自发转化病例，即伴有p53和RB缺失的 - 突变LUAD转化为EGFR表达阳性的SCLC和神经内分泌分化的LUAD，该病例用奥希替尼成功治疗。
