Park Hee-Ug, Kim Jong-Woo, Kim Grace E, Bae Han-Ik, Crawley Suzanne C, Yang Stacey C, Gum James R, Batra Surinder K, Rousseau Karine, Swallow Dallas M, Sleisenger Marvin H, Kim Young S
Gastrointestinal Research Laboratory, Veterans Affairs Medical Center, San Francisco, California 94121, USA.
Pancreas. 2003 Apr;26(3):e48-54. doi: 10.1097/00006676-200304000-00022.
Ductal adenocarcinoma of the pancreas has recently been suggested to arise from histologically identifiable ductal lesions known as pancreatic intraepithelial neoplasia (PanINs). Altered levels and patterns of mucin gene expression have been reported to occur in epithelial cancers.
To examine the pattern of expression of membrane-associated mucins, MUC3 and MUC4, and a mucin-associated carbohydrate tumor antigen, sialyl Le(x), in these precursor lesions and ductal adenocarcinoma of the pancreas.
A total of 144 PanIN lesions and 85 cases of ductal adenocarcinoma of the pancreas were examined by using immunohistochemistry and in situ hybridization methods.
MUC3 showed a progressive increase in expression in PanINs of increasing dysplasia and was also highly expressed in ductal adenocarcinoma. In contrast, neoexpression of MUC4 and sialyl Le(x) antigen was observed, mainly in PanIN-3 and ductal adenocarcinoma. In addition, a decrease in the expression of MUC3 and MUC4 was correlated with the degree of de-differentiation of the tumor.
Aberrant expression of membrane mucins MUC3 and MUC4 and of a mucin-associated carbohydrate tumor antigen Sialyl Le(x) in PanINs and adenocarcinoma further supports the progression model for pancreatic adenocarcinoma.
最近有人提出胰腺导管腺癌起源于组织学上可识别的导管病变,即胰腺上皮内瘤变(PanINs)。据报道,上皮癌中粘蛋白基因表达水平和模式发生改变。
研究膜相关粘蛋白MUC3和MUC4以及粘蛋白相关碳水化合物肿瘤抗原唾液酸化刘易斯x(sialyl Le(x))在这些胰腺前体病变和导管腺癌中的表达模式。
采用免疫组织化学和原位杂交方法,共检测了144个PanIN病变和85例胰腺导管腺癌。
MUC3在发育异常程度增加的PanINs中表达逐渐增加,在导管腺癌中也高表达。相比之下,主要在PanIN-3和导管腺癌中观察到MUC4和唾液酸化刘易斯x抗原的新表达。此外,MUC3和MUC4表达的降低与肿瘤的去分化程度相关。
膜粘蛋白MUC3和MUC4以及粘蛋白相关碳水化合物肿瘤抗原唾液酸化刘易斯x在PanINs和腺癌中的异常表达进一步支持了胰腺腺癌的进展模型。