PMID- 20107422
OWN - NLM
STAT- MEDLINE
DCOM- 20100527
LR  - 20220311
IS  - 1556-1380 (Electronic)
IS  - 1556-0864 (Linking)
VI  - 5
IP  - 3
DP  - 2010 Mar
TI  - High MET gene copy number leads to shorter survival in patients with non-small 
      cell lung cancer.
PG  - 305-13
LID - 10.1097/JTO.0b013e3181ce3d1d [doi]
AB  - INTRODUCTION: Activation of MET, either by increased gene copy number (GCN) or 
      mutation, has been detected in various cancers. We investigate the 
      clinicopathologic features of MET gene copy in nonsmall cell lung cancer (NSCLC). 
      METHODS: Tumor tissues were obtained from 180 resected NSCLCs, including 97 
      squamous cell carcinomas (SCCs) and 72 adenocarcinomas. No patient received 
      epidermal growth factor receptor (EGFR)-targeted therapy. EGFR and MET GCNs were 
      studied using fluorescence in situ hybridization (FISH) and were estimated 
      according to the University of Colorado Cancer Center (UCCC) criteria. For MET, 
      we also assessed GCNs using the Cappuzzo system. RESULTS: FISH-positive MET was 
      observed in 16.7% using the UCCC criteria; specifically, amplification was seen 
      in 3.9% and high polysomy in 12.8%. FISH-positive MET status was significantly 
      correlated with FISH-positive EGFR (p = 0.003). In the Cappuzzo system, high MET 
      GCN (mean, >/=5 copies/cell) was found in 6.7% and also associated with 
      FISH-positive EGFR (p = 0.031). MET gene copy status was not associated with 
      gender, smoking history, histology, or stage. However, true MET amplification was 
      more frequent in patients with SCC than in those with adenocarcinoma. 
      FISH-positive MET status predicted worse survival in patients with NSCLC at 
      advanced stages (p = 0.034) and in patients with SCC (p = 0.028). In multivariate 
      analyses, increased MET GCN was significantly associated with shorter survival in 
      patients with SCC, as analyzed using both the UCCC and Cappuzzo criteria (p = 
      0.019 and 0.008). CONCLUSIONS: Our results suggest that increased MET GCN would 
      be an independent poor prognostic factor in SCC of the lung.
FAU - Go, Heounjeong
AU  - Go H
AD  - Department of Pathology, Seoul National University College of Medicine, Seoul, 
      Republic of Korea.
FAU - Jeon, Yoon Kyung
AU  - Jeon YK
FAU - Park, Hyo Jin
AU  - Park HJ
FAU - Sung, Sook-Whan
AU  - Sung SW
FAU - Seo, Jeong-Wook
AU  - Seo JW
FAU - Chung, Doo Hyun
AU  - Chung DH
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Thorac Oncol
JT  - Journal of thoracic oncology : official publication of the International 
      Association for the Study of Lung Cancer
JID - 101274235
RN  - 0 (Receptors, Growth Factor)
RN  - EC 2.7.10.1 (MET protein, human)
RN  - EC 2.7.10.1 (Proto-Oncogene Proteins c-met)
SB  - IM
MH  - Adenocarcinoma/genetics/*mortality/pathology
MH  - Adult
MH  - Aged
MH  - Aged, 80 and over
MH  - Carcinoma, Non-Small-Cell Lung/genetics/*mortality/pathology
MH  - Carcinoma, Squamous Cell/genetics/*mortality/pathology
MH  - Female
MH  - *Gene Dosage
MH  - Genotype
MH  - Humans
MH  - In Situ Hybridization, Fluorescence
MH  - Lung Neoplasms/genetics/*mortality/pathology
MH  - Male
MH  - Middle Aged
MH  - Prognosis
MH  - Proto-Oncogene Proteins c-met/*genetics
MH  - Receptors, Growth Factor/*genetics
MH  - Risk Factors
MH  - Survival Rate
EDAT- 2010/01/29 06:00
MHDA- 2010/05/28 06:00
CRDT- 2010/01/29 06:00
PHST- 2010/01/29 06:00 [entrez]
PHST- 2010/01/29 06:00 [pubmed]
PHST- 2010/05/28 06:00 [medline]
AID - S1556-0864(15)32301-7 [pii]
AID - 10.1097/JTO.0b013e3181ce3d1d [doi]
PST - ppublish
SO  - J Thorac Oncol. 2010 Mar;5(3):305-13. doi: 10.1097/JTO.0b013e3181ce3d1d.