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Hepatic stellate cell activation in dysplastic nodules: evidence for an alternate hypothesis concerning human hepatocarcinogenesi

Authors
 Young Nyun Park  ;  Chang‐Pei Yang  ;  Olcay Cubukcu  ;  Swan N. Thung  ;  Neil D. Theise 
Citation
 LIVER, Vol.17(6) : 271-274, 1997 
Journal Title
 LIVER 
ISSN
 0106-9543 
Issue Date
1997
MeSH
Actins/metabolism ; Antibodies, Monoclonal ; Carcinoma, Hepatocellular/metabolism ; Carcinoma, Hepatocellular/pathology* ; Cell Division ; Diagnosis, Differential ; Humans ; Hyperplasia ; Immunohistochemistry ; Liver Cirrhosis/metabolism ; Liver Cirrhosis/pathology* ; Liver Neoplasms/metabolism ; Liver Neoplasms/pathology* ; Precancerous Conditions/metabolism ; Precancerous Conditions/pathology*
Abstract
We have previously suggested that dysplastic nodules (also referred to as "adenomatous hyperplasia" or "macroregenerative nodules"), likely precursors of hepatocellular carcinoma (HCC), develop as an infiltrating clonal expansion, in advance of or parallel to cirrhosis. As part of this hypothesis, to explain aspects of their gross and microscopic appearance, we suggested that dysplastic nodules are resistant to the scarring process affecting the rest of the liver. We sought to test this hypothesis by examining the distribution of activated hepatic stellate cells (HSCs), the hallmark of hepatic scarring, in cirrhotic nodules, dysplastic nodules and HCC. We immunohistochemically stained 56 cirrhotic nodules, 20 low grade dysplastic nodules, 27 high grade dysplastic nodules, and 20 HCCs with monoclonal antibodies against alpha-smooth muscle actin to identify activated HSCs. Distribution and number of HSCs were graded semiquantitatively (0 to 4+). In our results, HSCs were significantly less widespread in dysplastic nodules than in cirrhotic nodules or in HCCs (both: p < 0.00001). HSCs were also more prominent in the periphery of dysplastic nodules than in the center, though still fewer in number than in cirrhotic nodules. In conclusion, the low number of activated HSCs in dysplastic nodules, compared to both cirrhotic nodules and HCC, supports our hypothesis concerning dysplastic nodule development: that they arise as clonal expansions of neoplastic hepatocytes in advance of, or parallel to, the development of cirrhosis.
Full Text
https://onlinelibrary.wiley.com/doi/abs/10.1111/j.1600-0676.1997.tb01031.x?sid=nlm%3Apubmed
DOI
10.1111/j.1600-0676.1997.tb01031.x
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Pathology (병리학교실) > 1. Journal Papers
Yonsei Authors
Park, Young Nyun(박영년) ORCID logo https://orcid.org/0000-0003-0357-7967
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/177374
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