Tsuda Takeshi, Ichikawa Tomomi, Matsumoto Masahiro, Mizusihima Isami, Azechi Kenji, Takata Naoki, Murayama Nozomu, Hayashi Kana, Hirai Takahiro, Seto Zenta, Tokui Kotaro, Masaki Yasuaki, Taka Chihiro, Okazawa Seisuke, Kambara Kenta, Imanishi Shingo, Taniguchi Hirokazu, Miwa Toshiro, Hayashi Ryuji, Matsui Shoko, Inomata Minehiko
Department of Respiratory Medicine, Toyama Prefectural Central Hospital, Toyama City, Japan.
Respiratory and Allergy Medicine, Toyama Red Cross Hospital, Toyama City, Japan.
Discov Oncol. 2024 Aug 29;15(1):382. doi: 10.1007/s12672-024-01046-5.
Pulmonary sarcomatoid carcinoma is a rare tumor that is resistant to cytotoxic agents. This observational study aimed to evaluate the detection rate of driver gene alteration and the efficacy of targeted therapy for pulmonary sarcomatoid carcinoma.
We established a database of patients with pulmonary sarcomatoid carcinoma and their clinical information, including EGFR mutation, ALK fusion gene, ROS1 fusion gene, BRAF mutation, and MET exon 14 skipping mutation. The present study retrieved and analyzed the data of patients with pulmonary sarcomatoid carcinoma in whom driver gene alterations were evaluated, and the survival duration after the initiation of treatment with targeted therapy was examined.
A total of 44 patients were included in the present study. The EGFR mutation, ALK fusion gene, and MET exon 14 skipping mutation were detected in 2/43 patients (4.7%), 2/34 patients (5.9%), and 2/16 patients (12.5%), respectively. The ROS1 fusion gene (0/18 patients) and BRAF mutation (0/15 patients) were not detected. Female patients (P = 0.063, Fisher's exact test) and patients without smoking history (P = 0.025, Fisher's exact test) were the dominant groups in which any driver mutation was detected. Five patients with driver gene alterations were treated with targeted therapy. Progression-free survival (PFS) was 1.3 months and 1.6 months in 2 of the patients treated with gefitinib. Two patients with the ALK fusion gene showed 2.1 and 14.0 months of PFS from the initiation of treatment with crizotinib, and a patient with the MET exon 14 skipping mutation showed 9.7 months of PFS from the initiation of treatment with tepotinib.
The EGFR mutation, ALK fusion gene, and MET exon 14 skipping mutation were detected in patients with pulmonary sarcomatoid carcinoma in clinical practice, and some patients achieved long survival times after receiving targeted therapy. Further investigation is necessary to evaluate the efficacy of targeted therapy for pulmonary sarcomatoid carcinoma.
肺肉瘤样癌是一种对细胞毒性药物耐药的罕见肿瘤。本观察性研究旨在评估驱动基因改变的检出率及肺肉瘤样癌靶向治疗的疗效。
我们建立了一个肺肉瘤样癌患者及其临床信息的数据库，包括表皮生长因子受体（EGFR）突变、间变性淋巴瘤激酶（ALK）融合基因、原癌基因酪氨酸蛋白激酶ROS1（ROS1）融合基因、B-Raf原癌基因（BRAF）突变和MET第14外显子跳跃突变。本研究检索并分析了评估驱动基因改变的肺肉瘤样癌患者的数据，并检查了靶向治疗开始后的生存时间。
本研究共纳入44例患者。EGFR突变、ALK融合基因和MET第14外显子跳跃突变分别在2/43例患者（4.7%）、2/34例患者（5.9%）和2/16例患者（12.5%）中被检测到。未检测到ROS1融合基因（0/18例患者）和BRAF突变（0/15例患者）。女性患者（P = 0.063，Fisher精确检验）和无吸烟史的患者（P = 0.025，Fisher精确检验）是检测到任何驱动突变的主要人群。5例驱动基因改变的患者接受了靶向治疗。接受吉非替尼治疗的2例患者的无进展生存期（PFS）分别为1.3个月和1.6个月。2例ALK融合基因患者从开始使用克唑替尼治疗起的PFS为2.1个月和14.0个月，1例MET第14外显子跳跃突变患者从开始使用替泊替尼治疗起的PFS为9.7个月。
在临床实践中，肺肉瘤样癌患者中检测到了EGFR突变、ALK融合基因和MET第14外显子跳跃突变，部分患者在接受靶向治疗后获得了较长的生存时间。有必要进一步研究评估肺肉瘤样癌靶向治疗的疗效。
