|
KMID : 0982820110100020087
|
|
Journal of Lung Cancer
2011 Volume.10 No. 2 p.87 ~ p.93
|
|
|
Clinicopathologic Implications of ALK Gene Copy Number Gain in Non-small Cell Lung Cancer
|
|
Yoo Seol-Bong
Kim Hyo-Jin
Xu Xianhua
Sun Ping-Li
Jin Yan
Paik Jin-Ho
Jheon Sang-Hoon
Lee Choon-Taek
Chung Jin-Haeng
|
|
|
Abstract
|
|
|
Purpose: The anaplastic lymphoma kinase (ALK) gene is a potential molecular target in non-small cell lung carcinoma (NSCLC). The clinicopathologic implication of a change in the ALK gene copy number (GCN) is unclear.
Materials and Methods: A total of 434 primary NSCLC samples were analyzed by fluorescence in situ hybridization (FISH) for ALK GCN.
Results: Ninety-six cases (22.1%) showed ALK GCN gain with amplification in 16 (3.7%) cases. The cases with ALK GCN gain consisted of 47 adenocarcinomas (49.0%), 41 squamous cell carcinomas (42.7%), 5 adenosquamous carcinomas (5.2%) and 3 other NSCLCs (3.1%). ALK gene amplification was identified in 7 adenocarcinomas (43.7%) and 9 squamous cell carcinomas (56.3%). There was no significant difference between ALK GCN gain/amplification and histologic subtypes. Univariate survival analysis revealed that patients with ALK GCN gain/amplification showed shorter progression-free survival durations and decreased overall survival rates (p＜0.001). However, multivariate analysis proved that ALK GCN gain/amplification is not an independent prognostic factor for progression-free survival or overall survival.
Conclusion: ALK GCN gain is frequently identified in NSCLCs and the incidence is similar among histologic subtypes. Although ALK GCN gain/amplification is not an independent prognostic marker, it is associated with tumor progression in NSCLC.
|
|
|
KEYWORD
|
|
|
ALK, Copy number gain, Gene amplification, Non-small cell lung carcinoma
|
|
|
FullTexts / Linksout information
|
|
|
|
|
|
Listed journal information
|
|
|
|