阿列克替尼
医学
肺癌
腺鳞癌
融合基因
肿瘤科
癌
癌症研究
内科学
癌症
间变性淋巴瘤激酶
腺癌
病理
基因
生物
恶性胸腔积液
生物化学
作者
Yanyan Qin,Fei Li,Yuan Tan,Qianqian Duan,Qin Zhang
标识
DOI:10.3389/fonc.2022.998545
摘要
Lung Adenosquamous carcinoma (ASC) is a rare histological subtype of lung cancer accounting for 0.4%-4% of all lung cancers. ASC is generally considered to be an aggressive cancer with poor prognosis. There is no specific standard treatment for ASC, and current treatment of ASC is relied on the guideline for non-small cell lung cancer (NSCLC). To date, only sporadic canonical EML4-ALK fusions have been reported in ASC patients, and the efficiency of ALK-TKI is still unclear in non-canonical ALK fusion positive ASC patients. Here we describe the case of a stage IV ASC patient harboring a novel CPE-ALK fusion detected via 74 genes panel analysis. Interestingly, the TP53 was wild-type and no another somatic mutation was found within 74 genes. In addition, immunohistochemical staining (IHC) also supports an oncogenic role for the CPE-ALK fusion. Based on these findings, the patient received alectinib 600 mg twice daily. After 4 months on treatment the patients achieved a radiological partial response (PR) and his symptoms were significantly relieved. Imaging showed that lesions of the patient were reduced, and the clinical evaluation was partial response (PR). To the best of our knowledge, this is the first report of a dramatic tumor response to alectinib in a patient with ASC harboring a CPE-ALK fusion. In addition, targeted NGS analysis may improve detection of ALK fusion in routine practice.
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