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Updated: Jul 15, 2026
Ultra-Fast Amplicon-Based Next-Generation Sequencing in Non-Squamous Non-Small Cell Lung Cancer
Published on: September 8, 2023
[Distinguishing second primary tumors from lung metastasis in patients with postoperative non-small cell lung cancer
Jie Wang1, Charles Lu, Xu-yi Liu
1Department of Respiratory Medicine, Beijing University School of Oncology, Beijing Cancer Hospital, Beijing 100036, China.
Objective:
In patients with resected early stage non-small cell lung cancer (NSCLC), intrapulmonary solitary tumor represents either second primary tumor (SPT) or a metastasis. This study is to discern SPT from lung metastasis in patients with postoperative NSCLC followed a solitary intrapulmonary tumor by microsatellite analysis.
Methods:
Twenty-one patients with stage I - III(A) NSCLC resected by surgery during 1994.1 - 2002.8 were studied. Paired tumors from 21 patients with NSCLC and a solitary lung nodule were analyzed for their loss of heterozygosity (LOH) on chromosomal arms 3p, 9p and 17p. DNA from microdissected tumors and non-malignant lung tissues was subjected to polymerase chain reaction-based microsatellite analysis using 8 microsatellite markers. An effort was also made to distinguish SPT from lung metastasis on the basis of clinical and histopathologic features.
Results:
The paired tumors from 7 patients had concordant patterns of LOH at all microsatellite loci suggesting the same clonal origin, and supporting metastatic spread, where 4 paired tumors had discordant patterns of at all loci suggesting independent tumor origin. These observations were supported by the clinical and pathologic findings. Additional 6 paired tumors had concordant allelic loss on 3p and discordant loss on the other, clinical characteristics supporting metastatic disease. In contrast, 2 paired tumors had concordant allelic loss on 9p or 17p but discordant loss on the 3p, clinical data supporting SPT.
Conclusions:
The paired tumors from 7 patients had concordant patterns of LOH at all microsatellite loci suggesting the same clonal origin, and supporting metastatic spread, where 4 paired tumors had discordant patterns of at all loci suggesting independent tumor origin. These observations were supported by the clinical and pathologic findings. Additional 6 paired tumors had concordant allelic loss on 3p and discordant loss on the other, clinical characteristics supporting metastatic disease. In contrast, 2 paired tumors had concordant allelic loss on 9p or 17p but discordant loss on the 3p, clinical data supporting SPT.
