多唾液酸化N-细胞黏附分子、嗜铬粒蛋白A和B以及分泌粒蛋白II在肺神经内分泌肿瘤中的表达

Polysialylated N-CAM, chromogranin A and B, and secretogranin II in neuroendocrine tumours of the lung.

作者信息

Patriarca C, Pruneri G, Alfano R M, Carboni N, Ermellino L, Guddo F, Buffa R, Siccardi A G, Coggi G

机构信息

II Department of Pathology, Ospedale S. Paolo, University of Milan School of Medicine, Italy.

出版信息

Virchows Arch. 1997 Jun;430(6):455-60. doi: 10.1007/s004280050055.

DOI:10.1007/s004280050055

PMID:9230910

Abstract

Highly alpha 2-8-sialylated N-CAM (neural cell adhesion molecule) impairs N-CAM-mediated cell adhesion. We investigated polysiaN-CAM immunoreactivity in a range of neuroendocrine lung tumours: 15 typical carcinoids, 21 atypical carcinoids, 2 large cell neuroendocrine carcinomas and 12 small cell lung carcinomas were selected on a morphological basis and by their immunoreactivity for chromogranin A and B and secretogranin II. A progressive loss of chromogranin expression, particularly of chromogranin B, was paralleled by the up-regulation of polysiaN-CAM in histologically more aggressive tumours (P = 0.001). These data support the hypothesis that loss of cell-cell adhesion properties might be a relevant factor in the origin of the aggressivity of lung neuroendocrine tumours.

摘要

高度α2-8-唾液酸化的神经细胞黏附分子（N-CAM）会损害N-CAM介导的细胞黏附。我们研究了一系列神经内分泌性肺肿瘤中的多唾液酸N-CAM免疫反应性：根据形态学以及它们对嗜铬粒蛋白A、B和分泌粒蛋白II的免疫反应性，选取了15例典型类癌、21例非典型类癌、2例大细胞神经内分泌癌和12例小细胞肺癌。在组织学上更具侵袭性的肿瘤中，嗜铬粒蛋白表达逐渐丧失，尤其是嗜铬粒蛋白B，同时多唾液酸N-CAM上调（P = 0.001）。这些数据支持这样的假说，即细胞间黏附特性的丧失可能是肺神经内分泌肿瘤侵袭性起源中的一个相关因素。