Thompson T C, Timme T L, Kadmon D, Park S H, Egawa S, Yoshida K
Scott Department of Urology, Baylor College of Medicine, Houston, Texas 77030.
Mol Carcinog. 1993;7(3):165-79. doi: 10.1002/mc.2940070307.
Using a mouse prostate reconstitution (MPR) model system, strain-specific responses to the ras and myc oncogenes were investigated. When ras + myc were introduced into both the mesenchymal and epithelial compartments of the urogenital sinus, poorly differentiated prostate cancer was produced at a high frequency (> 90%) in inbred C57BL/6 mice. In contrast, under similar conditions, inbred BALB/c MPRs formed benign prostatic hyperplasia that converted to cancer at a low frequency (< 10%). Restricting the oncogenes to the mesenchymal or epithelial compartments revealed that oncogene activities were more pronounced in the mesenchyme of C57BL/6 mice and resulted in elevated transforming growth factor-beta 1 expression along with a severe desmoplastic reaction. Heterologous MPRs composed of BALB/c mesenchyme and C57BL/6 epithelium or vice versa demonstrated that intrinsic properties of BALB/c mesenchyme can arrest the progression of ras + myc-initiated C57BL/6 epithelium from benign hyperplasia to malignant carcinoma.
利用小鼠前列腺重建（MPR）模型系统，研究了不同品系对ras和myc癌基因的反应。当将ras + myc导入泌尿生殖窦的间充质和上皮区室时，近交系C57BL/6小鼠中高频率（> 90%）产生低分化前列腺癌。相比之下，在类似条件下，近交系BALB/c MPR形成良性前列腺增生，且低频（< 10%）转化为癌症。将癌基因限制在间充质或上皮区室显示，癌基因活性在C57BL/6小鼠的间充质中更明显，并导致转化生长因子-β1表达升高以及严重的促结缔组织增生反应。由BALB/c间充质和C57BL/6上皮组成的异种MPR，反之亦然，表明BALB/c间充质的内在特性可阻止ras + myc启动的C57BL/6上皮从良性增生发展为恶性癌。
