Halpenny Darragh F, Riely Gregory J, Hayes Sara, Yu Helena, Zheng Junting, Moskowitz Chaya S, Ginsberg Michelle S
Department of Radiology, Memorial Sloan-Kettering Cancer Center, New York, United States.
Thoracic Oncology Service, Division of Solid Tumor Oncology, Department of Medicine, Memorial Sloan-Kettering Cancer Center, New York, United States.
Lung Cancer. 2014 Nov;86(2):190-4. doi: 10.1016/j.lungcan.2014.09.007. Epub 2014 Sep 17.
5% of lung adenocarcinomas harbor rearrangements of the anaplastic lymphoma kinase (ALK) gene. This study compared computed tomography (CT) imaging features in patients with ALK rearrangements and those with EGFR mutations.
MATERIAL/METHODS: 30 patients with ALK rearrangements were studied. 97 patients with epidermal growth factor receptor (EGFR) mutations were used as controls. Features assessed included size and location of thoracic lymphadenopathy, and the size, contour, consistency and location of the primary tumor.
127 lung adenocarcinomas were examined. 30 (24%) tumors harbored ALK rearrangements, 97 (76%) tumors harbored EGFR mutations. ALK tumors had larger thoracic lymphadenopathy than the control group (p=0.005). Both readers identified 17 (57%) patients in the ALK group with lymph nodes >1.5cm. Reader 1 identified 19 (20%) patients in the EGFR group with lymph nodes >1.5cm, and reader 2 identified 18 (19%) (kappa 0.969). Patients with ALK rearrangements were more likely to have multifocal lymphadenopathy. Reader 1 identified 22 (73%) ALK patients versus 35 (36%) EGFR patients with multifocal thoracic nodal enlargement, while reader 2 identified 20 (67%) ALK patients versus 30 (31%) EGFR patients (kappa 0.953). 92% of ALK positive lesions were solid.
ALK positive lung adenocarcinomas are more likely than EGFR mutant lung adenocarcinomas to be associated with larger volume, multifocal thoracic lymphadenopathy. While routine testing for ALK should be standard, the presence of such characteristics in a solid tumor should further prompt testing for ALK rearrangement.
5%的肺腺癌存在间变性淋巴瘤激酶(ALK)基因重排。本研究比较了ALK基因重排患者与表皮生长因子受体(EGFR)突变患者的计算机断层扫描(CT)影像特征。
材料/方法:对30例ALK基因重排患者进行研究。将97例表皮生长因子受体(EGFR)突变患者作为对照。评估的特征包括胸部淋巴结肿大的大小和位置,以及原发肿瘤的大小、轮廓、质地和位置。
共检查了127例肺腺癌。30例(24%)肿瘤存在ALK基因重排,97例(76%)肿瘤存在EGFR突变。ALK基因重排的肿瘤胸部淋巴结肿大比对照组更大(p=0.005)。两位阅片者均识别出ALK组中有17例(57%)患者的淋巴结>1.5cm。阅片者1识别出EGFR组中有19例(20%)患者的淋巴结>1.5cm,阅片者2识别出18例(19%)(kappa值为0.969)。ALK基因重排的患者更易出现多灶性淋巴结肿大。阅片者1识别出22例(73%)ALK基因重排患者与35例(36%)EGFR突变患者有多灶性胸部淋巴结肿大,阅片者2识别出20例(67%)ALK基因重排患者与30例(31%)EGFR突变患者(kappa值为0.953)。92%的ALK阳性病变为实性。
与EGFR突变的肺腺癌相比,ALK阳性的肺腺癌更易出现更大体积的多灶性胸部淋巴结肿大。虽然ALK的常规检测应成为标准,但实性肿瘤中出现此类特征应进一步促使进行ALK基因重排检测。