Abstract
Background: The receptor tyrosine kinase c-kit is known to play an important role in the progression of gastrointestinal stromal tumors, but its biological significance in other solid malignancies is unclear. Recent publications have suggested a regulatory role for TGF-β1 in c-kit-mediated cell growth. The present study assessed the clinicopathological significance of c-kit protein (KIT) and TGF-β1 expression in resectable invasive ductal carcinomas (IDCs) of the pancreas. Patients and Methods: This study included 91 pancreatic IDC patients who received a pancreatectomy between 1982 and 2003. The expression of KIT and TGF-β1 was analyzed by immunohistochemistry. Results: KIT and TGF-β1 were expressed in 77% (70/91) and 59% (54/91) of the IDC, respectively. The expression of KIT was not correlated with that of TGF-β1. TGF-β1 expression correlated inversely with nodal involvement, but KIT expression did not correlate with any clinicopathological factors. KIT expression had no significant influence on the survival of the patients, whereas the survival rate of TGF-β1 (+) IDC patients was significantly higher than that of TGF-β1 (-) IDC patients. Co-expression analysis of KIT and TGF-β1 indicated that, in patients with KIT (+) IDC, the TGF-β1 (+) group showed a significantly better survival rate than the TGF-β1 (-) group. Neither KIT expression nor TGF-β1 expression had a significant effect on the efficacy of adjuvant chemotherapy (ACT). In multivariate analysis, TGF-β1 expression was one of the significant variables for survival in IDC patients overall, but KIT expression was not. Conclusion: TGF-β1 expression is suggested to have a significant influence on c-kit-mediated cell proliferation in human pancreatic IDCs.
Footnotes
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Abbreviations: Ab, antibody; ACT, adjuvant chemotherapy; Cdk, cyclin-dependent kinase; CPA, cyclophosphamide; 5-FU, 5-fluorouracil; GIST, gastrointestinal stromal tumor; IDC, invasive ductal carcinoma; KIT, c-kit protein; pAb, polyclonal Ab; PBS, phosphate-buffered saline; Rcp, receptor; RT, radiotherapy; SA, surgery alone; SCF, stem cell factor; TGF-β1, transforming growth factor-beta 1
- Received April 15, 2005.
- Accepted July 15, 2005.
- Copyright© 2005 International Institute of Anticancer Research (Dr. John G. Delinassios), All rights reserved