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. 2009 Oct 7;15(37):4695–4708. doi: 10.3748/wjg.15.4695

Table 1.

Clinicopathological features of 12 FNH lesions and data of immunohistochemistry, clonality and LOH assays

Case numbers Age (yr)/gender Lesion codes Lesion sizes (cm) Ki-67-LI (%) p53-LI (%) Clonality by XCIA No. of LOH
01 40/F 011 5.0 1.6 0 PC2 0
02 30/F 02 2.5 0.5 0 PC2 0
03 7.0 0.8 0 PC2 0
03 22/M 043 5.2 0.7 0 NT 0
04 44/M 051 1.2 0.5 0 NT 0
05 31/F 061 4.7 0.3 0 PC2 0
06 43/F 07 3.2 1.0 0 PC2 NT
07 44/F 081 2.0 0.8 0 PC4 NT
08 53/F 095 4.8 1.0 0 PC2 NT
09 23/F 101,5 4.5 1.2 0 PC4 NT
10 46/F 111,5 5.3 0.8 0 PC3 NT
121 1.5 0.9 0 PC4 NT
1

Some small preneoplastic foci, composed of clear cells, identified in surrounding liver parenchyma;

2

Tested on phosphoglycerate kinase (PGK) locus;

3

Nodules of altered hepatocytes (NAH) isolated from FNH by microdissection for LOH detection;

4

Noninformative at PGK locus and the data obtained by the assay on androgen receptor (AR) locus;

5

NAH isolated from FNH by microdissection for clonality assessment by XCIA. FNH: Focal nodular hyperplasia; Ki-67-LI: Ki-67 antigen-labeling indices; p53-LI: p53 protein-labeling indices by DO-7; XCIA: X-chromosomal inactivation assay; LOH: Loss of heterozygosity; F: Female; M: male; PC: Polyclonality; NT: Not tested for its origin from a male patient.