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β-Catenin Is Expressed Aberrantly in Tumors Expressing Shadow Cells
Pilomatricoma, Craniopharyngioma, and Calcifying Odontogenic Cyst

Ashraf M. Hassanein MD, PhD, Steven M. Glanz MD, Harvey P. Kessler DDS, Thomas A. Eskin MD, Chen Liu MD, PhD
DOI: http://dx.doi.org/10.1309/EALEG7LD6W7167PX 732-736 First published online: 1 November 2003


We studied the β-catenin immunohistochemical profile in tumors expressing shadow cells: pilomatricoma, 10 cases; calcifying odontogenic cyst, 6 cases; and craniopharyngioma, 9 cases. There was strong membranous, cytoplasmic, and nuclear staining of the immature basaloid cells in all of these tumors. Shadow cells were negative in all tumors. It has been documented that rising levels of free β-catenin drive the formation of complexes with T-cell factor/lymphoid enhancer factor (TCF-Lef) and up-regulate the wingless-Wnt cell-cell signals. The end result is an abnormality of β-catenin degradation and, thus, a buildup of free β-catenin in the cytoplasm and/or nucleus, resulting in the stimulation of cellular proliferation and/or inhibition of cell death. β-Catenin seems to have an important role in the oncogenesis of these tumors. The similar pattern of keratinization in these tumors and the similar pattern of β-catenin immunoreactivity in the cytoplasm and the nucleus are important findings. It seems that the activation of a common cellular pathway, namely Wnt–β-catenin–TCF-Lef, has a role in the pathogenesis of these tumors. The latter could be related to their shared method of keratinization or shared dysfunction of the cellular adhesion complex leading to tumorigenesis.

Key Words:
  • β-Catenin
  • Pilomatricoma
  • Craniopharyngioma
  • Odontogenic cyst