MET amplification, protein expression, and mutations in XXXX .

@entity1 @entity11968 @entity5 @entity420 @entity2220
OBJECTIVES: MET amplification, protein expression, and splice mutations at exon 14 are known to cause dysregulation of the MET/ @entity11968 pathway. Our study aimed to confirm the relationship among MET amplification, protein expression, and mutations in @entity420 . MATERIALS AND METHODS: MET protein expression by immunohistochemistry (IHC) and MET amplification by fluorescence in situ hybridization (FISH) were evaluated in 316 surgically resected @entity2220 . @entity1 were divided into 4 groups (IHC-negative/FISH-negative, IHC-negative/FISH-positive, IHC-positive/FISH-negative, and IHC-positive/FISH-positive), and 15-20 @entity5 in each group were randomly selected for mutation analyses to find splice mutations at exon 14. RESULTS: An IHC score of 0-3 was found in 168 (53.2%), 71 (22.5%), 59 (18.7%), and 18 (5.7%) @entity5 , respectively. The mean gene copy number (GCN) was 3.56; MET FISH positivity was detected in 123 (38.9%) samples, and 26 (8.2%) of them were gene amplifications. MET amplification were significantly associated with the IHC score (P<0.001,   (2) test). Splice mutations were identified in only 2 (2.9%) of 70 cases. One had a MET IHC score of 2 and negative FISH without amplification; The other had a MET IHC score of 0 and positive FISH without amplification. MET IHC or FISH results were not prognostic indicators of overall survival in multivariate analysis. CONCLUSION: There is a significant relationship between MET amplification and protein expression, and selection of @entity5 with amplification using IHC was effective. However, because of its rarity, a selection strategy for mutated @entity5 is implausible using IHC or FISH.
