Combined analysis identifies six genes correlated with XXXX from non-small cell to small cell lung cancer.

@entity39556 @entity1 @entity4153 @entity16262 @entity21248 @entity5 @entity957 @entity2 @entity29146 @entity1149 @entity71236 @entity152 @entity420 @entity14097
UNASSIGNED: With @entity5 , @entity2 can be classified into @entity420 ( @entity420 ), @entity957 ( @entity957 ), @entity152 ( @entity152 ), and the small cell subtype ( @entity4153 ); yet, elucidations to this @entity5 has not been addressed. In this study, we elucidated the molecular diversity among these subtypes by investigating large-scale sequencing datasets. Among genes upregulated from normal, @entity420 , @entity957 , @entity152 to @entity4153 , six hub genes were found closely correlated with adverse clinical outcome and were testified on cellular or tissue level with quantitative RT-PCR. Cox regression model was then built to generate a risk signature. The possible linkages among these genes were also explored. Transcript levels of @entity29146 , @entity16262 , @entity21248 , @entity39556 , @entity14097 , and @entity71236 were found significantly elevated from normal, @entity420 , @entity957 , @entity152 to @entity4153 . Overexpression of one or multiple of these genes was correlated with adverse overall survival (OS) and relapse-free survival (RFS) in the whole @entity1 cohort or groups stratified according to clinical variables, while most of all six genes were independent prognostic factors. When used as a six-gene risk signature, @entity1 with high signature score displayed more unfavorable clinical variables and poorer outcome. Tight regulative relationships were found within these genes, while @entity29146 and @entity16262 were likely to be the drivers. We considered the @entity5 from @entity1149 ( @entity1149 ) to @entity4153 might be due to the elevation of these six genes. We believe these genes were powerful cancer prognostic markers and potential therapeutic targets in @entity2 ; moreover, changes of their level might be correlated with @entity2 phenotype plasticity.
