Yasui Sho, Honda Takayuki, Onishi Iichiro, Ikeda Sadakatsu, Miyazaki Yasunari
Department of Respiratory Medicine, Tokyo Medical and Dental University, Tokyo, JPN.
Department of Pathology, Tokyo Medical and Dental University, Tokyo, JPN.
Cureus. 2024 Feb 23;16(2):e54739. doi: 10.7759/cureus.54739. eCollection 2024 Feb.
The serine-threonine protein kinase B-RAF (BRAF) fusions are rarely observed in non-small cell lung cancer (NSCLC) accounting for less than 1%, and therapeutic evidence for molecular-targeted drugs is lacking, unlike for BRAF V600E mutation by RAF and MEK inhibitors. A 75-year-old female patient with no smoking history and mild renal dysfunction developed recurrent lung adenocarcinoma and was initially treated with pembrolizumab immunotherapy followed by chemotherapy using docetaxel showing a certain efficacy but the disease finally progressed. Comprehensive genome profiling showed a novel SLC44A1-BRAF fusion and the tumor progression was controlled with the MEK inhibitor trametinib. Because of the rarity of NSCLC with BRAF fusion, the description of this case would be helpful for the treatment strategy for such tumors.
丝氨酸 - 苏氨酸蛋白激酶B-RAF(BRAF)融合在非小细胞肺癌(NSCLC)中很少见,占比不到1%,且缺乏分子靶向药物的治疗证据,这与RAF和MEK抑制剂针对BRAF V600E突变的情况不同。一名75岁、无吸烟史且有轻度肾功能不全的女性患者发生复发性肺腺癌,最初接受帕博利珠单抗免疫治疗,随后使用多西他赛化疗,显示出一定疗效,但疾病最终进展。综合基因组分析显示一种新的SLC44A1 - BRAF融合,使用MEK抑制剂曲美替尼控制了肿瘤进展。由于BRAF融合的NSCLC罕见,该病例描述将有助于此类肿瘤的治疗策略制定。