Document Detail


Increasing expression of gastrointestinal phenotypes and p53 along with histologic progression of intraductal papillary neoplasia of the liver.
MedLine Citation:
PMID:  12094375     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Intraductal papillary neoplasia of the liver (IPN-L) was recently proposed as the name for intraductal papillary proliferation of neoplastic biliary epithelium with a fine fibrovascular stalk resembling intraductal papillary mucinous neoplasm of the pancreas. We histochemically and immunohistochemically examined IPN-L alone or associated with hepatolithiasis, with an emphasis on the gastrointestinal metaplasia, nuclear p53 expression, and histologic progression. A total of 66 cases of IPN-L were divided into 4 groups: group 1, IPN-L with low-grade dysplasia (13 cases); group 2, IPN-L with high-grade dysplasia (20 cases); group 3, IPN-L lined with carcinoma in situ and no or microinvasion (19 cases); and group 4, group 3 with distinct invasive carcinoma (14 cases). It is suggested that IPN-L progresses from group 1 to group 4. As controls, 20 cases of nonneoplastic intrahepatic large bile ducts and 17 cases of nonpapillary invasive intrahepatic cholangiocarcinoma (ICC) were used. Biliary epithelial hypersecretion of sialomucin rather than sulfomucin was prevalent in IPN-L, and this was associated with the progression of INP-L. Immunohistochemically, cytokeratin (CK) 20 and MUC2, a gastrointestinal marker, were expressed more frequently in IPN-L than in nonneoplastic bile ducts and nonpapillary ICC (P <0.01), and their incidence were significantly increased in parallel with the progression of IPN-L (P < 0.01). In contrast, expression of CK 7, a biliary marker, was decreased in IPN-L compared with nonpapillary ICC. Nuclear p53 immunostaining was detected in 30% of IPN-L as a whole and increased in tandem with the progression of IPN-L (P < 0.01). It is suggested that IPN-L forms a spectrum of biliary epithelial neoplasia with frequent gastrointestinal metaplasia, different from the usual nonpapillary ICC, and shows stepwise progression from the perspective of mucin profile, gastrointestinal metaplasia, and p53 nuclear expression.
Authors:
Tomonori Shimonishi; Yoh Zen; Tse-Ching Chen; Miin-Fu Chen; Yi-Yin Jan; Ta-Sen Yeh; Yuji Nimura; Yasuni Nakanuma
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Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Human pathology     Volume:  33     ISSN:  0046-8177     ISO Abbreviation:  Hum. Pathol.     Publication Date:  2002 May 
Date Detail:
Created Date:  2002-07-02     Completed Date:  2002-07-24     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  9421547     Medline TA:  Hum Pathol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  503-11     Citation Subset:  IM    
Copyright Information:
Copyright 2002, Elsevier Science (USA). All rights reserved.
Affiliation:
Department of Pathology (II), Kanazawa University School of Medicine, Japan.
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MeSH Terms
Descriptor/Qualifier:
Adult
Aged
Bile Duct Neoplasms / complications,  metabolism*,  pathology*
Bile Ducts, Intrahepatic / metabolism*,  pathology*
Cell Nucleus / metabolism,  pathology
Cholangiocarcinoma / complications,  metabolism*,  pathology*
Disease Progression
Female
Humans
Immunoenzyme Techniques
Keratin-7
Keratins / metabolism
Lithiasis / complications,  pathology
Liver Diseases / complications,  pathology
Male
Metaplasia
Middle Aged
Mucins / metabolism
Phenotype
Precancerous Conditions / metabolism,  pathology
Tumor Suppressor Protein p53 / metabolism*
Chemical
Reg. No./Substance:
0/KRT7 protein, human; 0/Keratin-7; 0/Mucins; 0/Tumor Suppressor Protein p53; 68238-35-7/Keratins

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