Fuerst J, Fiebiger E, Jungwirth A, Mack D, Talwar P G, Frick J, Rovan E
Department of Zoology, University of Salzburg, Austria.
Prostate. 1997 Jul 1;32(2):77-84. doi: 10.1002/(sici)1097-0045(19970701)32:2<77::aid-pros1>3.0.co;2-c.
The objective of this study was to determine the effect of active immunization against LHRH on the growth characteristics and histology of subcutaneously implanted tumors of the androgen-sensitive Dunning R3327-PAP and androgen-independent R3327-AT2.1 rat prostate adenocarcinoma sublines.
We herein demonstrate that 1) active immunization with an LHRH-diphtheria toxoid-conjugate (LHRH-DT) leads to the downregulation of gonadotropins and testosterone and consequently the atrophy of testosterone-dependent organs such as the testes, prostate, and androgen-sensitive Dunning R3327-PAP tumors, 2) growth inhibition of Dunning R3327-PAP tumors is caused by suppression of cell division rather than by an increase in cell death and is associated with an increase of the tumor stroma content, and 3) volume increase of the androgen-independent Dunning R3327-AT2.1 tumor is slightly but significantly reduced, indicating a local stimulatory LHRH loop within this tumor cell line.
本研究的目的是确定针对促黄体生成素释放激素（LHRH）进行主动免疫对雄激素敏感的邓宁R3327-PAP和雄激素非依赖性R3327-AT2.1大鼠前列腺腺癌亚系皮下植入肿瘤的生长特性和组织学的影响。
我们在此证明：1）用LHRH-白喉类毒素偶联物（LHRH-DT）进行主动免疫会导致促性腺激素和睾酮下调，从而使睾丸、前列腺和雄激素敏感的邓宁R3327-PAP肿瘤等睾酮依赖器官萎缩；2）邓宁R3327-PAP肿瘤的生长抑制是由细胞分裂受抑制引起的，而非细胞死亡增加所致，并且与肿瘤基质含量增加有关；3）雄激素非依赖性邓宁R3327-AT2.1肿瘤的体积增加略有但显著减少，表明该肿瘤细胞系内存在局部刺激性LHRH环路。
