Cancer of the Prostate: Molecular Genetics
gene. E-cadherin, located at chromosome
16q22.1, has been studied thoroughly. The
protein is a calcium-dependent, epithe-
lial cell–cell adhesion molecule and plays
a vital role in the invasive potential of
cancer cells (Fig. 3). Decreased E-cadherin
expression is found in prostate cancer
and is associated with higher grade and
worse clinical outcome. In addition, metas-
tases express less E-cadherin than primary
tumors. Blocking E-cadherin function us-
ing antibodies or antisense transcripts
increases invasive behavior. Conversely,
reexpression of E-cadherin in epithelial
cells can induce a reversion to a noninva-
sive phenotype (Fig. 4). Newer techniques
in immunohistochemistry may reduce the
inconsistencies from formalin ±xation and
autolytic artifacts that characterized prior
studies. An alterative approach has been
described for ±xing prostatectomy spec-
imens that yields samples amenable to
E-cadherin immunohistochemistry as well
as extraction of longer DNA fragments.
Fig. 3
Illustration depicting the role of
E-cadherin. The surface molecule
interacts with other E-cadherin
molecules, contributing to epithelial cell
adhesion. The cytoplasmic domain, not
shown, normally interacts with
intracellular catenin proteins.
Fig. 4
Immunocytochemistry after staining using an antibody to
E-cadherin. The immortalized, but nontumorigenic, prostate
epithelial cells demonstrate strong staining for E-cadherin in the
areas of cell–cell adhesion.
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