Home > Journals > Minerva Endocrinologica > Past Issues > Minerva Endocrinologica 2003 December;28(4) > Minerva Endocrinologica 2003 December;28(4):321-8

CURRENT ISSUE
 

JOURNAL TOOLS

eTOC
To subscribe
Submit an article
Recommend to your librarian
 

ARTICLE TOOLS

Reprints
Permissions

 

REVIEWS   

Minerva Endocrinologica 2003 December;28(4):321-8

Copyright © 2003 EDIZIONI MINERVA MEDICA

language: English

Ectopic uterine stem cell tumors in the hamster kidney. A unique model for estrogen-induced oncogenesis

Li J. J., Papa D., Li S. A.


PDF


Estrogens are intimately involved in the causation of some of the most prevalent cancers afflicting women, particularly, breast, endometrial, cervico-vaginal, and possibly ovarian. Therefore, it has become particularly pertinent to elucidate the molecular mechanisms whereby estrogens elicit their oncogenic actions so that better prevention strategies can be developed. The estrogen-induced Syrian hamster tumors of the kidney have emerged as one of the most intensively studied in vivo models in solely estrogen oncogenesis. An advantage of this model is that the tumors occur in the absence of any intervening morphologic changes, but rather they are the result of the continuous progression of some interstitial stem cells in the kidney leading to tumor formation. Evidence is presented that the origin of these tumors is deri- ved from ectopic ''uterine'' stem cells, which are responsive to estrogenic hormones. Their steroid receptor and many other gene alterations have been delineated. Importantly, a crucial early event in this solely estrogen-induced oncogenic process is the overex- pression and amplification of c-myc and its protein product. Chromosomal instability, in both early and large frank tumors, is another important characteristic of this process. This later feature has commonly been shown in solely estrogen-induced murine mammary tumors, and in ductal carcinomas in situ and in primary invasive ductal breast carcinomas. These changes are considered crucial in eliciting estrogen-induced tumorigenesis.

top of page