Open AccessMolecular and clinical analysis of Chinese patients with anaplastic lymphoma kinase ( ALK )‐rearranged non‐small cell lung cancer
Author(s) -
Zhou Xiaoyun,
Shou Jiawei,
Sheng Jin,
Xu Chunwei,
Ren Shengxiang,
Cai Xiuyu,
Chu Qian,
Wang Wenxian,
Zhen Qinhong,
Zhou Yuefen,
Li Wenfeng,
Pan Hong,
Li Hongsen,
Sun Tao,
Cheng Huanqing,
Wang Huina,
Lou Feng,
Rao Chuangzhou,
Cao Shanbo,
Pan Hongming,
Fang Yong
Publication year - 2019
Publication title -
cancer science
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.035
H-Index - 141
eISSN - 1349-7006
pISSN - 1347-9032
DOI - 10.1111/cas.14177
Subject(s) - anaplastic lymphoma kinase , lung cancer , epidermal growth factor receptor , cancer research , medicine , fusion gene , lymphoma , population , cancer , oncology , pathology , biology , gene , genetics , malignant pleural effusion , environmental health
Anaplastic lymphoma kinase ( ALK ) fusions have been recognized as a therapeutic target in non‐small cell lung cancer ( NSCLC ). However, molecular signatures and clinical characteristics of the Chinese population with ALK ‐rearranged NSCLC are not well elucidated. In the present study, we carried out targeted next‐generation sequencing on tissue and plasma ct DNA samples in 1688 patients with NSCLC . Overall, ALK fusions were detected in 70 patients (4.1%), and the frequencies of ALK fusions detected in tissue and plasma samples were 5.1% and 3.3%, respectively. Additionally, the prevalence of breakpoint locations for EML 4‐ ALK fusions in ct DNA was significantly correlated with that in tumor tissues ( R 2 = .91, P = .045). According to age, the incidence rates of ALK fusions among young (age <45 years), middle‐aged (between 45 and 70 years) and elderly (>70 years) patients were significantly different ( P < .001). In 70 ALK ‐rearranged cases, coexistence of epidermal growth factor receptor ( EGFR ) alterations and ALK fusions was detected in 12 cases (17.1%) and EGFR mutations tended to coexist with non‐ EML 4‐ ALK rearrangements. Notably, novel ALK fusion partners, including TRIM 66 , SWAP 70 , WNK 3 , ERC 1 , TCF 12 and FBN 1 were identified in the present study. Among EML 4 ‐ ALK fusion variants, patients with variant V1 were younger than patients with variant V3 ( P = .023), and TP 53 mutations were more frequently concurrent with variant V3 compared with variant V1 ( P = .009). In conclusion, these findings provide new insights into the molecular‐clinical profiles of patients with ALK ‐rearranged NSCLC that may improve the treatment strategy of this population.