Oya Yuko, Yoshida Tatsuya, Uemura Takehiro, Murakami Yoshiko, Inaba Yoshitaka, Hida Toyoaki
Department of Thoracic Oncology, Aichi Cancer Center Hospital, Nagoya, Aichi 464-8681, Japan.
Department of Pathology and Molecular Diagnostics, Aichi Cancer Center Hospital, Nagoya, Aichi 464-8681, Japan.
Oncol Lett. 2018 Oct;16(4):4219-4222. doi: 10.3892/ol.2018.9158. Epub 2018 Jul 17.
The resistance mechanisms to anaplastic lymphoma kinase (ALK) inhibitors comprise ALK gene variations, such as ALK point mutations and copy-number gains, the activation of bypass signaling through the activation of other oncogenes and small cell lung cancer (SCLC) transformation. To date, few studies have investigated whether tumor markers for SCLC correlate with the SCLC transformation in EGFR-mutant NSCLC and ALK-positive non-SCLC (NSCLC). The present case study reported a patient with SCLC transformation after alectinib treatment. The patient exhibited elevation of pro-gastrin-releasing peptide precursor and neuron-specific enolase levels, which may be predictive of SCLC transformation during the resistance to ALK-tyrosine kinase inhibitors.
间变性淋巴瘤激酶(ALK)抑制剂的耐药机制包括ALK基因变异,如ALK点突变和拷贝数增加,通过激活其他致癌基因激活旁路信号以及小细胞肺癌(SCLC)转化。迄今为止,很少有研究调查SCLC的肿瘤标志物是否与EGFR突变型非小细胞肺癌(NSCLC)和ALK阳性非NSCLC(NSCLC)中的SCLC转化相关。本病例研究报告了1例接受阿来替尼治疗后发生SCLC转化的患者。该患者胃泌素释放肽前体和神经元特异性烯醇化酶水平升高,这可能预示着在对ALK酪氨酸激酶抑制剂耐药期间会发生SCLC转化。