G. Vollmer et al., TUMORIGENESIS DISRUPTS HORMONAL-REGULATION OF TENASCIN EXPRESSION IN REGRESSING DUNNING R-3327-H PROSTATE CARCINOMA, Cancer letters, 101(2), 1996, pp. 185-192
We recently reported that androgen ablation either by orchiectomy or a
ntiandrogen treatment resulted in the expression of the extracellular
matrix glycoprotein tenascin in the regressing rat prostate. With the
study presented here we investigated whether tenascin is expressed in
the Dunning R 3327 H tumor and if orchiectomy and antiandrogen treatme
nt affect tenascin expression. Experimentally, male rats were inoculat
ed s.c. with pieces of Dunning tumor into the hind limb of both sides.
Three months after inoculation rats were either orchiectomized or rec
eived a daily dose of 3 mg of cyproterone acetate or flutamide. Follow
ing a treatment period of 13 weeks, orchiectomy reduced tumor area by
more than 60% compared to untreated controls. Cyproterone acetate and
flutamide reduced tumor area significantly up to 30%. The amount and i
ntensity of tenascin immunoreactivity appeared to be independent of th
e hormonal treatment and rather correlated to the content of tumor str
oma. Those tumors with small, densely packed glandular ducts possessin
g almost no stromal tissue stained weakly for tenascin, whereas those
tumors with larger ducts and significant stroma stained intensely, Sta
ining intensity was particularly high at these sites where tumors infi
ltrated neighboring tissues, in proximity of infiltrating blood cells
and close to necrotic areas. In summary, our results demonstrate a spe
cific pattern of tenascin expression in Dunning R 3327 H rat prostate
carcinomas, which appear to be independent of the hormonal treatment.
We therefore conclude that tumorigenesis disrupts hormonal regulation
of tenascin expression which we detected in the normal prostate gland
after treatment with antiandrogens.