Related Experiment Video
Updated: Sep 12, 2026
Next Generation Sequencing for the Detection of Actionable Mutations in Solid and Liquid Tumors
Published on: September 20, 2016
[Chromosomal imbalance in primary lung squamous cell carcinoma and their relationship with smoking]
Wen-Sheng Yan1, Lan-Ying Song, Wei-Dong Wei
1Research Department, Cancer Center, Sun Yat-sen University, Guangzhou, Guangdong 510-060, P.R. China.
Background & Objective:
Chromosomal imbalance plays an important role in tumorigenesis of lung cancer, and may be influenced by different carcinogens. This study was to examine chromosomal imbalance in primary lung squamous cell carcinoma (LSCC), and their association with smoking.
Methods:
Chromosomal gains and losses in 39 specimens of LSCC were identified by comparative genomic hybridization (CGH), the association between chromosomal imbalances in LSCC and smoking was analyzed.
Results:
The most frequent chromosomal gains of LSCC were detected on chromosomal arms 3q (74.4%, 29/39), 5p (66.7%, 26/39), 1q (43.6%, 17/39), 8q (41.0%, 16/39), 12p (42.6%, 18/39), 2p (38.5%, 15/39), and 18p (33.3%, 13/39), with minimal amplified regions (MAR) at 3q26.2-29 (74.4%, 29/39), 5p14.3-15.3 (66.7%, 26/39), 1q41-44(41.0%, 16/39), 8q23 (41.0%, 16/39), 12p13 (41.0%, 16/39), and 18p11.2 (33.3%, 13/39)u high-copy-number amplification at chromosomal arms 3q, and 5p were found in 15 (38.5%), and 6 (15.4%) patients. Chromosomal losses mainly involved chromosomal arms 3p (56.4%, 22/39), 5q (53.8%, 21/39), 13q (51.3%, 20/39), 8p (46.1%, 18/39), 4p (43.6%, 17/39), 4q (43.6%, 17/39), 1p (41.0%, 16/39), 2q (38.5%, 15/39), 9q (35.9%, 14/39), 13p (35.9%, 14/39), 16p (35.9%, 14/39) ,6p (33.3%, 13/39), and 6q (30.7%, 12/39), with minimal deleted regions (MDR) at 3p14.2-21.2 (51.3%, 20/39), 5q15-22 (51.3%, 20/39), 13q14.2-21.2 (48.7%, 19/39), 8p21.1-22 (43.6%, 17/39), 2q32 (35.9%, 14/39), and 16p12-13.1 (33.3%, 13/39). Amplification rates of chromosomal arms 3q, and 8q in smoking LSCC patients were significantly higher than those in non-smoking LSCC patients (P=0.002,P=0.031). While high incidences of gains at chromosomal arms 5p and 12p, and of losses at chromosomal arms 3p, 4q, and 5q were the common feature of chromosomal changes of smoking and non-smoking LSCC patients.
Conclusion:
3q, 5p, 1q, 8q, 12p, 2p, 18p gains and 3p, 5q, 13q, 8p, 4p, 4q, 1p, 2q, 9q, 13p,16p, 6p, 6q loses might be involved in tumorigenesis and/or progression of LSCC, smoking-induced lung cancer may be associated with 3q, 8q gains.
