***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
    ***DOCUMENTATION*** 
    ***EXAMPLES*** 
    Input: PURPOSE Amplification of the MET proto-oncogene in gastroesophageal cancer ( GEC ) may constitute a molecular marker for targeted therapy . We examined a GEC cohort with follow-up and reported the clinical response of four additional patients with MET-amplified tumors to the small molecule inhibitor crizotinib  as part of an exp and ed phase I cohort study . PATIENTS AND METHODS From 2007 to 2009 , patients with GEC were genetically screened as a consecutive series of 489 tumors ( stages 0 , I , and II , 39 % ; III , 25 % ; IV , 36 % ; n = 222 esophageal , including n = 21 squamous carcinomas ) .  MET , EGFR , and HER2 amplification status was assessed by using fluorescence in situ hybridization . RESULTS Ten ( 2 % ) of 489 patients screened harbored MET amplification ; 23 ( 4.7 % ) harbored EGFR amplification ; 45 ( 8.9 % ) harbored HER2 amplification ; and 411 ( 84 % ) were wild type for all three genes ( ie , negative ) . MET-amplified tumors were typically high- grade adenocarcinomas that presented at advanced stages ( 5 % ; n = 4 of 80 ) . EGFR-amplified tumors showed the highest fraction of squamous cell carcinoma ( 17 % ; n = 4 of 23 ) . HER2 , MET , and EGFR amplification were , with one exception ( MET and EGFR positive ) , mutually exclusive events . Survival analysis in patients with stages III and IV disease showed substantially shorter median survival in MET/EGFR-amplified groups , with a rank order for all groups by median survival ( from most to least aggressive ) : MET ( 7.1 months ; P < .001 ) less than EGFR ( 11.2 months ; P = .16 ) less than HER2 ( 16.9 months ; P = .89 ) when compared with the negative group ( 16.2 months ) . Two of four patients with MET-amplified tumors treated with crizotinib experienced tumor shrinkage ( -30 % and -16 % ) and experienced progression after 3.7 and 3.5 months . CONCLUSION MET amplification defines a small and aggressive subset of GEC with indications of transient sensitivity to the targeted MET inhibitor crizotinib ( PF-02341066 ) PURPOSE To investigate whether prognosis of patients with high-risk gastric cancer may depend on MET copy number gain ( CNG ) or an activating truncation within a deoxyadenosine tract element ( DATE ) in the promoter region of the MET lig and HGF . PATIENTS AND METHODS A single-institution cohort of 230 patients with stage II/III gastric cancer was studied .  Formalin-fixed paraffin-embedded tumor specimens were used for DNA extraction . Quantitative polymerase chain reaction ( qPCR ) for MET CNG and sequencing for HGF DATE truncation ( < 25 deoxyadenosines instead of 30 ) were used . Results were analyzed for association with disease-free survival ( DFS ) and overall survival ( OS ) . To assess the reliability of the qPCR measurement , a r and om sample of cases was reanalyzed using an alternative assay ( fluorescent in situ hybridization [ FISH ] ) with calculation of the intracorrelation coefficient ( ICC ) . RESULTS In 216 assessable patients , MET CNG five or more copies and homozygous HGF-truncated DATE occurred in 21 patients ( 10 % ) and 30 patients ( 13 % ) , respectively . Patients with MET CNG five or more copies ( MET-positive ) showed significantly worse prognosis with multivariate hazard ratio ( HR ) of 3.02 ( 95 % CI , 1.71 to 5.33 ; P < .001 ) for DFS and multivariate HR of 2.91 ( 95 % CI , 1.65 to 5.11 ; P < .001 ) for OS . The agreement between qPCR and FISH was high , with ICC = 0.9 % ( 95 % CI , 0.81 % to 0.95 % ; the closer the ICC is to 1 , the greater is the agreement ) . HGF-truncated DATE did not show relevant prognostic effect . CONCLUSION In this study , qPCR revealed approximately 10 % of white patients with gastric cancer harboring MET CNG of five or more copies . This marker was significantly associated with unfavorable prognosis . This information is relevant to the current clinical development of anti-MET compounds 
    Output:
    
Subgroup analysis showed the prognostic effect of c-Met was identical in protein-level and gene-level based methodology .
The same effect was also seen in Asian and Western ethnicity subgroup analysis .
Meta-regression showed HR was not associated with disease stage .
Patients with tumors that harbor high c-Met expression are more likely to have a worse Os , with this prognostic effect independent of disease stage .