Infrequent mutation of APC, AXIN1, and GSK3B in human pituitary adenomas with abnormal accumulation of CTNNB1

Chunlan Sun, Takashi Yamato, Emiko Kondo, Toru Furukawa, Hidetoshi Ikeda, Akira Horii

Research output: Contribution to journalArticlepeer-review

13 Citations (Scopus)

Abstract

We analyzed mutation of the APC, AXIN1, and GSK3 genes in 14 pituitary adenomas with abnormal nuclear accumulations of CTNNB1. These tumors did not harbor mutation of the CTNNB1 gene. The genes analyzed encode proteins associated with ubiquitin-mediated degradation of CTNNB1. Although the regions encoding functional domains of these protein products were analyzed, no significant genetic alterations were found. Furthermore, the antibody for the C-terminus of APC detected normal expression of the APC protein in these pituitary adenomas. Our present results imply that an unknown mechanism(s) accelerates the accumulation of CTNNB1 that plays an important role in the pathogenesis of human pituitary adenomas. However, the possibility that mutation of regions outside of our survey or epigenetic mechanism play an important role cannot be excluded.

Original languageEnglish
Pages (from-to)131-134
Number of pages4
JournalJournal of Neuro-Oncology
Volume73
Issue number2
DOIs
Publication statusPublished - 2005 Jun 1

Keywords

  • APC
  • AXIN1
  • CTNNB1
  • GSK3B
  • Pituitary adenoma
  • Wnt

ASJC Scopus subject areas

  • Oncology
  • Neurology
  • Clinical Neurology
  • Cancer Research

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