Background: MicroRNA?506(miR?506) has been reported to function in several tumors as a tumor suppressor gene or oncogene. However, the expression and role of miR?506 in pancreatic ductal adenocarcinoma(PDAC) remains unclear. In this study, we aimed to evaluate the phenotype of miR?506 in PDAC.Methods: Using mi RNA in situ hybridization, we examined the expression of miR?506 in 113 PDACs and 87 paired normal pancreatic tissues. We evaluated mi R?506 expression in PDAC cells, normal pancreatic ducts, and acinus/islands, and we analyzed the associations between miR?506 expression and the clinicopathologic characteristics of PDAC patients.Results: miR?506 expression was higher in PDAC than in matched normal pancreatic ductal cells(P < 0.001). On the other hand, the combined group of well and moderately diferentiated PDACs showed higher levels of mi R?506 than the poorly diferentiated ones(P = 0.023). Moreover, mi R?506 expression was negatively associated with pathologic T category(P = 0.004) and lymph node metastasis(P = 0.033), suggesting that mi R?506 might inhibit the progression of PDAC.Conclusions: Our results suggest that mi R?506 either plays a role as an oncogene in the tumorigenesis and a tumor suppressor in the progression or serves as a house?keeping, tumor?suppressing mi RNA, whose expression can be activated by oncogenic signals in early development to hinder the progression of PDAC. Background: MicroRNA® 506 (miR® 506) has been reported to function in several tumors as a tumor suppressor gene or oncogene. However, the expression and role of miR® 506 in pancreatic ductal adenocarcinoma (PDAC) remains unclear. In this study, We aimed to evaluate the phenotype of miR? 506 in PDAC. Methods: Using mi RNA in situ hybridization, we examined the expression of miR? 506 in 113 PDACs and 87 paired normal pancreatic tissues. , normal pancreatic ducts, and acinus / islands, and we analyzed the associations between miR? 506 expression and the clinicopathologic characteristics of PDAC patients. Results: miR? 506 expression was higher in PDAC than in matched normal pancreatic ductal cells (P & lt; 0.001) . On the other hand, the combined group of well and moderately diferentiated PDACs showed higher levels of mi R? 506 than the poorly diferentiated ones (P = 0.023). Moreover, mi R? 506 expression was negatively associated with pathologic T category (P = 0.0 04) and lymph node metastasis (P = 0.033), suggesting that mi R? 506 might inhibit the progression of PDAC.Conclusions: Our results suggest that mi R? 506 either plays a role as an oncogene in the tumorigenesis and a tumor suppressor in the progression or serves as a house? keeping, tumor? suppressing mi RNA, whose expression can be activated by oncogenic signals in early development to hinder the progression of PDAC.