Abstract
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‐β1 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.
Original language | English (US) |
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Pages (from-to) | 165-179 |
Number of pages | 15 |
Journal | Molecular Carcinogenesis |
Volume | 7 |
Issue number | 3 |
DOIs | |
State | Published - 1993 |
Externally published | Yes |
Keywords
- Genetic predisposition
- mesenchymal‐epithelial interaction
- prostate cancer
ASJC Scopus subject areas
- Molecular Biology
- Cancer Research