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Expression of Matrix Metalloproteinase-2 (MMP-2) and Tissue Inhibitor of Metalloproteinase-2 (TIMP-2) in Pancreatic Ductal Adenocarcinoma

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±¸¹ÌÁø, ¹è¿µ°æ, ÃÖÁØÇõ,
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±¸¹ÌÁø ( Gu Mi-Jin ) 
¼º»ïº´¿ø º´¸®°ú

¹è¿µ°æ ( Bae Young-Kyung ) 
¿µ³²´ëÇб³ ÀÇ°ú´ëÇÐ º´¸®Çб³½Ç
ÃÖÁØÇõ ( Choi Joon-Hyuk ) 
¿µ³²´ëÇб³ ÀÇ°ú´ëÇÐ º´¸®Çб³½Ç

Abstract


Background: Matrix metalloproteinase-2 (MMP-2) is known to be one of the key molecules for tumor invasion and metastasis. MMP-2 activity is modulated through interaction with the tissue inhibitor of metalloproteinase-2 (TIMP-2). The purpose of this study was to evaluate the expression of MMP-2 and TIMP-2 in pancreatic ductal adenocarcinoma.

Methods: Using immunohistochemical staining, we investigated the expression of MMP-2 and TIMP-2 in 30 pancreatic ductal adenocarcinomas and 10 normal pancreas.

Results: MMP-2 expression was present in tumor cells in 11 cases, and in stromal cells in 24 cases, out of 30 carcinomas. MMP-2 expression of tumor cells was significantly higher in poorly differentiated adenocarcinomas than in well/moderately differentiated adenocarcinomas, and in cases with vascular invasion than in cases without. MMP-2 expression was stronger in the marginal areas than in the central area of the tumor. TIMP-2 expression was detected in the tumor and stromal cells of all carcinomas. MMP-2 and TIMP-2 expression had no significant correlation with tumor size, lymph node metastasis, or TNM stage. MMP-2 expression was not correlated with TIMP-2 expression.

Conclusions: These results suggest that MMP-2 expression may play an important role in the invasive property of pancreatic ductal adenocarcinoma, whereas TIMP-2 expression increases as a reaction to invasion.

Å°¿öµå

Pancreas;Duct;Adenocarcinoma;MMP-2;TIMP-2

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