Expression of Cell-Cell Adhesion Molecules in Matrical Tumors of Hairs, Nails, Teeth and Pituitary Gland - Adhesion Molecules - page 301

forms and more aggressive solid variants (Neville et al. 2002). h ey exhibit 'ghost
cells' similar to matrical tumors from the hair follicle. Ameloblastomas are tumors
originating from the odontogenic epithelium and include phenotypical variants
with follicular, plexiform, desmoplastic, granular, basaloid and acanthomatous
histological patterns (Neville et al. 2002). Less frequently, ameloblastomas can
be extraosseous, probably arising from misplaced odontogenic remmants, and
frankly malignant forms with metastatic potential (Rosai 2004). Ameloblastomas
are biphasic tumors with epithelial tissues containing peripheral cylindrical cells,
a central loose network of stellate epithelial cells, and surrounding stroma with
various degrees of maturation, resembling the developing tooth (Rosai 2004).
Matrical Pituitary Gland Tumors
h e matrical tumor of the pituitary gland is the craniopharyngioma.
Craniopharyngiomas most likely originate from odontogenic embryonic remnants
of the Rathke's pouch, which exhibits histological features similar to the enamel
tissue of the teeth. Moreover, the microscopic appearance of craniopharyngioma
is highly similar to that of calcifying odontogenic cysts and ameloblastomas
(Rosai 2004). Craniopharyngiomas are frequently cystic tumors. h ey exhibit a
biphasic architecture consisting of anastomosing epithelial strands with peripheral
cylindrical cells aligned in palisade, a center of loose stellate epithelial cells, and
a i broblastic stroma with variable degrees of cellularity (Rosai 2004). Foci of
squamous dif erentiation, calcii cation and inl ammatory reaction and clearly
discernible embryonic tooth structures are ot en seen (Rosai 2004).
CADHERIN AND CATENIN EXPRESSION AND
SIGNALING IN MATRICAL TUMORS
h e study of signaling pathways is crucial for the understanding of tumor
development, as well as for the clarii cation of the cellular progeny of the tumors.
Tumors with a phenotype of matrix cells from the hair, nails, teeth and pituitary
gland share morphological features. h ere are also immunohistochemical evidence
and mutational studies that support the role of β-catenin as a transcriptional
activator in the oncogenesis of these tumors. h ere are, however, dif erences in
expression of nuclear-cytoplasmic and mutation rates of β-catenin within tumors
of each group (Table 2) . h ese dif erences indicate that the molecular mimicry of
tumors with the tissues of origin is more complex than previously thought, and
there is still much work to do in understanding the dif erent stimuli that lead to
the formation and maintenance of these tumors.