H19 OVEREXPRESSION IN BREAST ADENOCARCINOMA STROMAL CELLS IS ASSOCIATED WITH TUMOR VALUES AND STEROID-RECEPTOR STATUS BUT INDEPENDENT OF P53 AND KI-67 EXPRESSION

Citation
E. Adriaenssens et al., H19 OVEREXPRESSION IN BREAST ADENOCARCINOMA STROMAL CELLS IS ASSOCIATED WITH TUMOR VALUES AND STEROID-RECEPTOR STATUS BUT INDEPENDENT OF P53 AND KI-67 EXPRESSION, The American journal of pathology, 153(5), 1998, pp. 1597-1607
Citations number
111
Categorie Soggetti
Pathology
ISSN journal
00029440
Volume
153
Issue
5
Year of publication
1998
Pages
1597 - 1607
Database
ISI
SICI code
0002-9440(1998)153:5<1597:HOIBAS>2.0.ZU;2-D
Abstract
In a previous study we described the expression of the H19 gene by in situ hybridization (ISH) in normal breast and in benign or malignant b reast tumors (Dugimont T, Curgy JJ, Wernert N, Delobelle A, Raes MB, J oubel A, Stehelin D, Coll J: Biol Cell 1995, 85:117-124), in the prese nt work, 1) we extend the previous one to a statistically useful numbe r of adenocarcinomas, including 10 subclasses, 2) we provide informati on on the precise ISH localization of the H19 RNA by using, on serial tissue sections, antibodies delineating specifically the stromal or th e epithelial component of the breast, and 3) we consider relationships between the H19 gene expression and various clinicopathological infor mation as tumor values (T0 to T4), grades, steroid receptors, lymph no de status, and molecular features as the p53 gene product and the Ki-6 7/MIB-1 protein, which is specific to proliferating cells. Data indica te that 1) in 72.5% of studied breast adenocarcinomas an overall H19 g ene expression is increased when compared with healthy tissues, 2) the H19 gene is generally overexpressed in stromal cells (92.2%) and rare ly in epithelial cells (2.9% only), 3) an up-regulation of the H19 gen e is significantly correlated with the tumor values and the presence o f both estrogen and progesterone receptors, and 4) at the cellular lev el, the H19 gene demonstrates an independent expression versus accumul ation of both the p53 protein and the Ki-67/MIB-1 cell-cycle marker.