Changes in Expression of Bile Canalicular CD10 and Sinusoidal CD105 (Endoglin) in Peritumoral Hepatic Tissue

2009 ◽  
Vol 95 (4) ◽  
pp. 495-500 ◽  
Author(s):  
Toshitsugu Nakamura

Aims and background Hepatic tissues, including bile canaliculi and sinusoids, around primary or metastatic tumors are destructed and regenerate associated with tumor growth, and may show some phenotypic changes. The present study was undertaken to examine the expression of CD10 in bile canaliculi [CD10(BC)] and CD105 (endoglin) along hepatic sinusoids [CD105(HS)] in peritumoral hepatic tissue (PTH). Methods Fifty samples of resected liver bearing hepatocellular carcinoma (HCC) or metastatic carcinoma were immunostained for CD10 and CD105. The immunoreactivity for CD10(BC) and CD105(HS) in the background hepatic tissue of tumors and PTH was scored separately. Results CD10(BC) was moderately or markedly expressed in the background hepatic tissue without chronic hepatitis or cirrhosis in most of the cases, and was significantly downregulated in chronic hepatitis and cirrhosis. CD105(HS) was negative or minimally positive in most of the cases of hepatic tissue bearing metastatic carcinoma, and showed a significant increase in chronic hepatitis and cirrhosis. Compared with the background, PTH revealed significantly decreased CD10(BC) staining irrespective of HCC or metastatic carcinoma, and showed belt-like CD105(HS) expression in 66.7% of the cases of metastatic carcinoma and in 88.6% of those with HCC. Conclusions These data indicate that the expression patterns of CD10(BC) and CD105(HS) in PTH are similar to those in chronic hepatitis and cirrhosis, which may be caused by persistent injury and resultant regeneration of hepatic tissue.

2001 ◽  
Vol 16 (10) ◽  
pp. 1131-1137 ◽  
Author(s):  
Hidenori Toyoda ◽  
Takashi Kumada ◽  
Takashi Honda ◽  
Kazuhiko Hayashi ◽  
Yoshiaki Katano ◽  
...  

2012 ◽  
Vol 153 (25) ◽  
pp. 978-989 ◽  
Author(s):  
Gábor Lendvai ◽  
András Kiss ◽  
Ilona Kovalszky ◽  
Zsuzsa Schaff

The details of molecular alterations occurring during hepatocarcinogenesis have not been revealed yet. Nevertheless, it is known that microRNAs (miRNA), these short RNA molecules regulating gene expression mainly in a negative way, are also involved in this process. Altered miRNA expression levels are present in liver diseases when compared with normal liver tissue, and the observed alterations depend mainly on which is more advantegous for the disease: activation or inhibition of the genes (e.g. oncogenes or tumor suppressor genes) regulated by the altered miRNAs. The miRNA expression pattern described in hepatocellular carcinoma seems to differ the most from that found in the normal liver; however, remarkable alterations at miRNA levels have been published in early stages of hepatic tumor progression such as fibrosis and chronic hepatitis. For example, the expression of miR-21, miR-221, miR-222 and miR-199a showing characteristic alterations in hepatocellular carcinoma also displayed deregulated expressions in these two early stages. The liver characteristic miRNA, miR-122, usually exhibits a decreased expression level upon liver injury as well as miR-122 expression tends to decrease as hepatic carcinogenesis progresses. Besides, miR-122 enhances the replication of hepatitis C virus and the initial low or high level of miR-122 seems to influence the efficiency of interferon therapy. Recently, statistically significant differences have been detected in the expression of several miRNAs being present in the serum of patients with chronic hepatitis, chirrhosis and hepatocellular carcinoma when compared with normal controls. It suggests that serum miRNAs could be potential biomarkers. In this article, the major and recent alterations of microRNA expression patterns in stages of hepatocarcinogenesis such as fibrosis, viral infections (hepatitis), cirrhosis and hepatocellular carcinoma are summarized. Orv. Hetil., 2012, 153, 978–989.


Sign in / Sign up

Export Citation Format

Share Document