Nuclear accumulation of [beta]-catenin in human endocrine tumors: Association with Ki-67 (MIB-1) proliferative activity

• Published in: Endocrine pathology 2000-09, Vol.11 (3), p.243
• Main Authors: Semba, Shuho, Kusumi, Ryoko, Moriya, Takuya, Sasano, Hironobu
• Format: Article
• Language: English
• Subjects: Adrenal glands; Cells; Proteins; Tumors
• ISSN: 1046-3976; 1559-0097
• DOI: 10.1385/EP:11:3:243

β-Catenin is closely associated with carcinoma invasion/metastasis and poor survival. Recent studies have demonstrated that abnormal expression of β-catenin, especially its nuclear accumulation, also plays an important role in wingless/Wnt signaling pathway. In this study, we evaluated immunohistochemically the nuclear localization of β-catenin in a total of 93 human-endocrine-related tumors including 1 medullary carcinoma (thyroid gland), 12 parathyroid tumors, 22 carcinoid tumors (digestive tract and liver), 7 islet cell tumors, 26 adrenocortical tumors, 13 neuroblastoma (adrenal gland), and 12 pheochromocytoma (adrenal gland), and also studied genetic alterations of the β-catenin gene. Nuclear accumulation of β-catenin was frequently detected in 8 of 22 (36%) carcinoid tumors and 2 of 7 (29%) islet cell tumors. No genetic alteration in exon 3 of the β-catenin gene encoding serine/threonine rich domain, which was phosphorylated by GSK-3β, was detected in any groups of the endocrine tumors. However, nuclear accumulation of β-catenin in carcinoid tumors was significantly correlated with the proliferative marker Ki-67 (MIB-1) labeling index (p