Current concepts in the immunohistochemical evaluation of liver tumors

Figure 1 Focal nodular hyperplasia. A: On low-power, focal nodular hyperplasia (FNH) is characterized by nodular hepatocellular proliferation with central scar (hematoxilin and eosin stain, × 1); B: FNH showing typical map-like pattern on glutamine synthetase immunohistochemistry (anti-glutamine synthetase/diaminobenzidine chromogen, × 2).

Figure 2 Hepatocellular adenoma. A and B: HNF1α-inactivated hepatocellular adenoma (HCA) with marked steatosis [A, hematoxylin and eosin (HE) stain, × 20] and loss of liver fatty acid binding protein (LFABP) expression by immunohistochemistry (left) in comparison to non-neoplastic liver (right) [B, anti-LFABP/3,3’-diaminobenzidine (DAB), × 1]; C and D: Inflammatory HCA with dilated sinusoids (telangiectasia, black arrowheads) and patchy inflammation (blue arrowheads) (C, HE stain, × 5) and diffuse serum amyloid A staining by immunohistochemistry (D, anti-serum amyloid A/DAB, × 5); E and F: β-catenin-activated HCA with strong diffuse staining for glutamine synthetase (upper left), in comparison to centrilobular staining of normal liver (lower right) (E, HE stain, × 20; F, anti-glutamine synthetase/DAB, × 1).

Figure 3 Scirrhous hepatocellular carcinoma. A: Cords and thin trabeculae of neoplastic hepatocytes are embedded in dense, abundant fibrous stroma (hematoxylin and eosin stain, × 20); B: By immunohistochemistry, strong glypican-3 positivity is present in tumor cells (anti-glypican-3/3,3’-diaminobenzidine, × 20).