Clonality and allelotype analyses of focal nodular hyperplasia compared with hepatocellular adenoma and carcinoma

Figure 2 Representative data of X-chromosome inactivation (XCI) assays at PGK (A) and AR loci (B and C). Nonrandom XCI are present in HCAs (08 in A, 20 in B) and HCCs (09, 21 and 22 in A, 08 in C), revealing their monoclonality. A: The G/A single-nucleotide polymorphism at PGK exon 1 was demonstrated by BstXI-digestion and electrophoresis on an agarose gel. The intact and cleaved amplification products migrate at positions of 530 (upper band) and 433 bp (lower band), respectively. Pretreatment with HpaII (-: Before; +: After) resulted in marked reduction of the lower band in single tumor samples (T) and separate tumor areas (TA), but not in the surrounding liver parenchyma (N). M: DNA markers, with five bands at locations of 700, 600, 500, 400 and 300 bp; B and C: The length polymorphism of AR gene was resolved on a 10% polyacrylamide gel containing urea (8 mol/L) and visualized by silver staining, with one product migrating faster than the other. Pretreatment with HhaI (-: Before; +: After) resulted in loss or marked reduction of one band in tumor samples, but not in the non-neoplastic tissue. M: DNA marker at the location of 200 bp.