BACKGROUND. beta -catenin (CTNNB1) is known to be a member of the cadherin-
catenin superfamily and to function in cell-cell adhesion. However, it also
has been reported that CTNNB1 plays an important role in carcinogenesis. I
n the current study, the authors observed expression of the CTNNB1 protein
in primary pituitary adenomas to investigate the role of CTNNB1 in the deve
lopment of pituitary adenomas.
METHODS. A total of 37 pituitary adenomas were analyzed. Expression of CTNN
B1 and the cell proliferation marker Ki-67 were observed immunohistochemica
lly. In addition, the authors performed direct sequencing to detect somatic
mutations of exon 3 of the CTNNB1 gene.
RESULTS. Twenty-one of 37 pituitary adenomas (57%) demonstrated abnormal nu
clear accumulation of CTNNB1. It is interesting to note that tumors with an
accumulation of CTNNB1 in the nucleus showed a statistical tendency toward
an association with increased immunoreactivity of Ki-67 (P < 0.05) whereas
no significant correlation was detected between the status of CTNNB1 and o
ther clinicopathologic features. Missense mutations in exon 3 of the CTNNB1
gene also were detected in the cases with abnormal nuclear accumulation of
the CTNNB1 protein.
CONCLUSIONS. The results of the current study suggest that up-regulation of
the Wnt signaling pathway, including accumulation of mutant CTNNB1 in the
nuclei, plays an important role in the tumorigenesis and development of ade
noma in the pituitary gland. Cancer 2001;91:42-8. (C) 2001 American Cancer
Society.