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Abstract
Perineural invasion is a symbiotic relationship between cancer cells and nerves and
is most frequently seen in "neurotropic" cancers such as prostate cancer. It results
in increased perineural space cancer cell growth and decreased apoptosis and induces
nerve growth. Tissue microarrays were constructed from 640 radical prostatectomy specimens
with prostate cancer. The perineural diameter was measured as previously described.
Multiple biomarkers have been previously performed on this tissue microarray cohort,
and all data were kept in the same database. The biomarker results database was queried
for correlations between perineural invasion diameter and tissue biomarkers. Increased
perineural invasion diameter correlated with increased proliferation of prostate cancer
cells and with apoptosis. It also correlated with proteins involved in survival pathways
such as nuclear factor κB, c-Myc, phosphorylated AKT, and its downstream effector
FHKR, but not with GSK. Unlike nerve density, it did not correlate with decreased
PTEN expression. Increased perineural invasion diameter was associated with higher
levels of hormonal receptors such as androgen receptor, but not estrogen receptor.
Also associated with perineural invasion diameter were coregulators and corepressors
including SRC1 and TIF2. Perineural invasion diameter had the strongest correlation
with tumor volume (ρ = 0.579, P = .000), not identified with nerve density. These
data demonstrate that perineural invasion has the same biologic correlations as neural
density. However, we found a distinct and very strong correlation with increased tumor
volume. These data confirm that perineural invasion is the ultimate and most successful
interaction between cancer cells and nerve fibers, resulting in increased tumor growth.