[Expressions and clinical significances of c-met, c-erbB-2, COX-2, and IL-6 in the biliary tract cancers]

Authors: Joo, HH  Song, EY  Jin, SH  Oh, SH  Choi, YK 
Citation: Joo HH, etal., Korean J Gastroenterol. 2007 Dec;50(6):370-8.
Pubmed: (View Article at PubMed) PMID:18159174

BACKGROUND/AIMS: c-met, c-erbB-2, interleukin (IL)-6, and cyclooxygenase (COX)-2 expressions are considered to be implicated in the carcinogenesis and progression of cholangiocarcinoma, but the molecular pathogenesis of cholangiocarcinoma is still poorly understood. We aimed to analyze the expressions of each marker and their relationships with clinicopathologic factors. METHODS: One hundred and fourteen tissue samples were obtained from surgically resected specimens from patients with biliary tract cancer. The expressions of c-met, c-erbB-2, COX-2, and IL-6 were examined by immunohistochemically. The expression of each marker and correlations between these markers and clinicopathologic factors were analyzed. RESULTS: The expression rates of each maker were as follows: c-met 34/112 (30.4%), c-erbB-2 5/112 (4.5%), COX-2 53/113 (46.9%), and IL-6 68/113 (60.2%), respectively. c-met expression was more frequently observed in cases with invasion through the adjacent connective tissues (p=0.0263). IL-6 overexpression was more frequently observed in cases with absent lymph node metastasis (p=0.0325). Either c-erbB-2 expression or COX-2 expression was significantly associated with lymph node metastasis (p=0.0442). CONCLUSIONS: The expression of c-met was closely related to the invasiveness of cholangiocarcinoma. Co-expression of c-met, COX-2 and, IL-6 showed a significant correlation with invasiveness and lymph node metastasis and these could be useful marker to guide clinical outcome in patients with cholangiocarcinoma.


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CRRD Object Information
CRRD ID: 2317165
Created: 2010-03-17
Species: All species
Last Modified: 2010-03-17
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.