Transient and etiology-related transcription regulation in cirrhosis prior to hepatocellular carcinoma occurrence

Figure 3 Changes in transcript levels in cirrhosis. The transcripts are those listed in Table 3, footnote 2F. Their levels were determined by real-time qRT-PCR in training and testing samples (18 CLs, 34 HCC-free cirrhosis and 35 peritumoral cirrhosis). Every transcript name is noted on top and its level per cirrhosis type is expressed on the ordinate as a log2 [level in type/median level in CLs]. The mean value of transcripts is shown as an horizontal bar. A : CL: control; CIR: HCC-free cirrhosis (regardless of etiology); PCIR: perinodular cirrhosis (regardless of etiology). Significant difference between CIR and CL (^aP < 0.05, ^bP < 0.01, Mann-Whitney U test), between CIR and PCIR (^cP < 0.05, ^dP < 0.01) and between PCIR and CL (^eP < 0.05, ^fP < 0.01). B: Transcripts separated per etiology : alcoholism (blue), HCV (red); A or V: alcoholic or viral, HCC-free cirrhosis; PA or PV: perinodular, alcoholic or viral cirrhosis. Significant difference between A and PA (^gP < 0.05, ^hP < 0.01), between V and PV (ⁱP < 0.05, ^jP < 0.01), between A and V (^kP < 0.05, ^lP < 0.01) and between PA and PV (^mP < 0.05, ⁿP < 0.01).