Chung L W, Zhau H E, Ro J Y
Department of Urology, University of Texas M.D. Anderson Cancer Center, Houston 77030.
Prostate. 1990;17(2):165-74. doi: 10.1002/pros.2990170210.
Because fetal urogenital sinus mesenchyme (UGM) has been found to be highly inductive when recombined with normal adult prostate tissues or normal and neoplastic bladder epithelium, we investigated whether fetal UGM also interacts with established hormone-responsive and unresponsive rat Dunning and Nb prostate tumors. Our results indicate that: 1) fetal UGM acts directly on selected rat prostatic tumors by inducing histomorphologic changes (e.g., inducing acinar ductal structures and secretory activity) in the tumors toward more differentiated forms resembling that of the adult prostate gland; 2) fetal UGM either increased the growth rate of or maintained the sizes of three of the four interacting rat prostatic tumors; and 3) fetal UGM markedly reduced the lactate dehydrogenase activity of Nb-autonomous tumor toward a level comparable to that of the normal rat prostate gland. Our data suggest that fetal UGM can directly affect the growth and differentiative functions of selected rat prostatic tumors.
由于已发现胎儿泌尿生殖窦间充质（UGM）与正常成年前列腺组织或正常及肿瘤性膀胱上皮重组时具有高度诱导性，我们研究了胎儿UGM是否也与已建立的激素反应性和无反应性大鼠邓宁和Nb前列腺肿瘤相互作用。我们的结果表明：1）胎儿UGM通过诱导肿瘤中的组织形态学变化（如诱导腺泡导管结构和分泌活性），使其向更类似于成年前列腺的分化形式直接作用于选定的大鼠前列腺肿瘤；2）胎儿UGM提高了四只相互作用的大鼠前列腺肿瘤中三只的生长速率或维持了其大小；3）胎儿UGM显著降低了Nb自主性肿瘤的乳酸脱氢酶活性，使其达到与正常大鼠前列腺相当的水平。我们的数据表明，胎儿UGM可直接影响选定的大鼠前列腺肿瘤的生长和分化功能。
