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

研究成果: Article査読

14 被引用数 (Scopus)

抄録

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.

本文言語English
ページ(範囲)131-134
ページ数4
ジャーナルJournal of Neuro-Oncology
73
2
DOI
出版ステータスPublished - 2005 6

ASJC Scopus subject areas

  • 腫瘍学
  • 神経学
  • 臨床神経学
  • 癌研究

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