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肿瘤发生破坏了消退期邓宁R 3327 H前列腺癌中腱生蛋白表达的激素调节。

Tumorigenesis disrupts hormonal regulation of tenascin expression in regressing Dunning R 3327 H prostate carcinoma.

作者信息

Vollmer G, Michna H, Schneider M R

机构信息

Institut für Biochemische Endokrinologie, Medizinische Universität zu Lübeck, Germany.

出版信息

Cancer Lett. 1996 Mar 29;101(2):185-92. doi: 10.1016/0304-3835(96)04133-x.

DOI:10.1016/0304-3835(96)04133-x
PMID:8620468
Abstract

We recently reported that androgen ablation either by orchiectomy or antiandrogen 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 treatment affect tenascin expression. Experimentally, male rats were inoculated s.c. with pieces of Dunning tumor into the hind limb of both sides. Three months after inoculation rats were either orchiectomized or received a daily dose of 3 mg of cyproterone acetate or flutamide. Following 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 intensity of tenascin immunoreactivity appeared to be independent of the hormonal treatment and rather correlated to the content of tumor stroma. Those tumors with small, densely packed glandular ducts possessing almost no stromal tissue stained weakly for tenascin, whereas those tumors with larger ducts and significant stroma stained intensely. Staining intensity was particularly high at these sites where tumors infiltrated neighboring tissues, in proximity of infiltrating blood cells and close to necrotic areas. In summary, our results demonstrate a specific 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.

摘要

我们最近报道,通过睾丸切除术或抗雄激素治疗进行雄激素去除会导致回归中的大鼠前列腺中细胞外基质糖蛋白腱生蛋白的表达。通过本文介绍的研究,我们调查了腱生蛋白是否在邓宁R 3327 H肿瘤中表达,以及睾丸切除术和抗雄激素治疗是否会影响腱生蛋白的表达。在实验中,将雄性大鼠双侧后肢皮下接种邓宁肿瘤组织块。接种三个月后,大鼠要么接受睾丸切除术,要么每天给予3毫克醋酸环丙孕酮或氟他胺。经过13周的治疗期后,与未治疗的对照组相比,睾丸切除术使肿瘤面积减少了60%以上。醋酸环丙孕酮和氟他胺使肿瘤面积显著减少达30%。腱生蛋白免疫反应性的数量和强度似乎与激素治疗无关,而是与肿瘤基质的含量相关。那些腺管小且紧密排列、几乎没有基质组织的肿瘤,腱生蛋白染色较弱,而那些腺管较大且有大量基质的肿瘤,染色强烈。在肿瘤浸润邻近组织、浸润血细胞附近和坏死区域附近的这些部位,染色强度特别高。总之,我们的结果表明邓宁R 3327 H大鼠前列腺癌中腱生蛋白表达具有特定模式,这似乎与激素治疗无关。因此我们得出结论,肿瘤发生破坏了我们在用抗雄激素治疗正常前列腺后检测到的腱生蛋白表达的激素调节。

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Tumorigenesis disrupts hormonal regulation of tenascin expression in regressing Dunning R 3327 H prostate carcinoma.肿瘤发生破坏了消退期邓宁R 3327 H前列腺癌中腱生蛋白表达的激素调节。
Cancer Lett. 1996 Mar 29;101(2):185-92. doi: 10.1016/0304-3835(96)04133-x.
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