Expression of Liver Fatty Acid Binding Protein (LFABP) in Hepatocellular Carcinomas
Soo-Jin Cho, Linda D Ferrell, Ryan M Gill. University of California San Francisco, San Francisco, CA
Background: Recently, loss of expression of liver fatty acid binding protein (LFABP) by immunohistochemistry has been shown to be characteristic of a subset of hepatocellular adenomas (HCAs) in which the HNF-1α gene is inactivated. Transformation to hepatocellular carcinoma (HCC) is thought to be a very rare phenomenon in the HNF-1α inactivated variant of HCA. However, we recently observed two cases at our institution, one definite HCC and one possible HCC, in which loss of LFABP staining was seen, raising the possibility that LFABP downregulation may be associated with hepatocellular carcinogenesis. Our aim is to evaluate HCCs arising in various backgrounds and with varying degrees of differentiation for LFABP loss.
Design: 17 total cases of HCC were examined. 13/17 HCCs arose in a background of cirrhosis due to hepatitis C (HCV; 8) or steatohepatitis (SH; 5). 4/17 HCCs arose in a noncirrhotic background, with one arising within an inflammatory HCA. Differentiation of HCC ranged from well-differentiated (WD; 6) to well to moderately differentiated (WD-MD; 2) to moderately differentiated (MD; 5) to moderately to poorly differentiated (MD-PD; 1) to poorly differentiated (PD; 3). Immunohistochemical staining for LFABP was performed in all cases.
Results: Expression of LFABP varied from intact/positive (++; 7) to diffusely but weakly positive (+; 2) to focal loss (+/-; 2) to complete loss/negative (-; 6) (summarized in table).
|Case||Cirrhosis||Degree of HCC differentiation||LFABP expression|
|6||No (inflammatory HCA)||WD||++|
|7||No (mild steatosis)||WD-MD||++|