PMID: 9553810Apr 29, 1998Paper

Random nuclear p53 overexpression pattern in tamoxifen-mediated endometrial carcinoma

International Journal of Gynecological Pathology : Official Journal of the International Society of Gynecological Pathologists
Y KuwashimaK Kishi

Abstract

In a previous paper, we suggested that tamoxifen (TAM)-mediated endometrial carcinogenesis may not involve estrogenic pathways because of random estrogen receptor positivity among endometrial carcinomas with and without TAM treatment for breast cancer. DNA adduct formation (reported in rat liver and human endometrium) was considered to be a more plausible mechanism for TAM-mediated carcinogenesis. To examine the reported correlation between DNA adduct formation and p53, the present study examined p53 expression in the endometrial carcinomas reported in the previous study. Seven endometrial adenocarcinomas associated with long-term TAM treatment for breast carcinoma and 4 carcinomas without TAM treatment but with history of breast carcinoma were immunohistochemically investigated for nuclear p53 expression. The bcl-2 product was also examined. Diffuse and intense nuclear reactivity for p53 protein was present in only one TAM-related case. Essentially, no differences were observed in the bcl-2 staining patterns of TAM-treated and -untreated patients with cancer. Thus, p53 overexpression in endometrial carcinomas occurring in patients with breast cancer seems to be not specific for TAM-treated patients, and, if DNA adduct formatio...Continue Reading

Citations

May 7, 2011·Human Cell·Akira YasueYasuhiro Udagawa
Aug 9, 2003·Expert Opinion on Drug Safety·Karen Brown
Nov 18, 2005·The Breast : Official Journal of the European Society of Mastology·Harold A HarveyAlajos Hajba
May 10, 2002·The American Journal of Pathology·Robert H PierceNelson Fausto
Oct 31, 2000·Critical Reviews in Toxicology·L L SmithI N White
Oct 5, 2001·Expert Opinion on Pharmacotherapy·G H Eltabbakh, S L Mount

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