We examined eye lesions in five lines of transgenic mice carrying the human rasT24 oncogene driven by the type I γ glutamyl transferase (γGT) promoter. In three lines, hyperplasia developed as early as 11.5 days postconception in the outer neuroectodermal layer, which gives rise to ciliary body and retinal pigment epithelium. At birth, the eyes from many animals contained adenomas, and by day 27, mice developed invasive adenocarcinomas originating in the region of the ciliary body. Microphthalmia, cataracts, and chronic nongranulomatous inflammation involving the anterior and/or posterior segments of the eye were also found. γGT is detectable histochemically as early as 11.5 gestational days in the outer neuroectodermal layer and after birth is more abundant in the ciliary body than in the retinal pigment epithelium. Using a reverse transcriptase- polymerase chain reaction, we found that type I (but not types II or III) γGT RNA is made by the mouse eye: the γGT(I)rasT24 transgene transcription product was detected in the eyes of all five transgenic lines. The sequential progression of hyperplasia to invasive neoplasms in the ciliary body in response to γGT(I)rasT24 expression differs from the process in the kidney of these animals in which tubular hyperplasia and microadenomas with little evidence of progression are the major lesions.
|Original language||English (US)|
|Number of pages||9|
|Journal||American Journal of Pathology|
|State||Published - 1993|
ASJC Scopus subject areas
- Pathology and Forensic Medicine