Down Regulation of Bcl2 Expression in Invasive Ductal Carcinomas Is Both Estrogen- and Progesterone-Receptor Dependent and Associated with Poor Prognostic Factors

Sung-Hye PARK1, Hanseong KIM1, Byung-Joo SONG2

1Department of Anatomical Pathology, Inje University, College of Medicine, Ilsan Paik Hospital, Koyang-city, Korea
2Department of General Surgery, Inje University, College of Medicine, Ilsan Paik Hospital, Kyunggi-do, Korea


In normal breast, Bcl2 is expressed in the non-pregnant and non-involuting mammary epithelium. The exact mechanism and the effect of the down regulation of the Bcl2 expression on breast cancer cells are not clearly defined. We compared down regulation as well as the persistent expression of Bcl2 with ER, PR, p53, and c-erb-B2 overexpression and clinicopathologic variables, and tumor stage in 11 cases of ductal carcinomas in situ (DCIS) and 44 cases of invasive ductal carcinomas (IDC) of Korean women by immunohistochemical studies. Bcl2 down regulation was found in 39% of IDC and in 18% of DCIS cases. In IDC, while persistent Bcl2 expression was displayed in 95% and 78.9% of ER and PR immunoreactive ones and 71.9 % of c-erb-B2 immnonegative ones. Seventeen cases of Bcl2 down regulated IDC had a significant correlation with ER negativity (94.1%), PR negativity, (76.5%), and high nuclear (61.1% is grade III) and histological grade (76% is grade III). However, in DCIS, no significant correlation between the Bcl2 expression and various parameters were obtained, probably due to small sample size. In conclusion, the Bcl2 expression was both ER and PR dependent and down regulation of Bcl2 in IDC was significantly correlated with poor prognostic factors. Pathology & Oncology Research, Vol 8, Nr 1, 26-30, 2002

Key words: Bcl2; estrogen receptor; invasive ductal carcinoma; ductal carcinoma in situ; progesterone receptor

Received: Jan 10, 2002; accepted: Feb 10, 2002
Correspondence: Sung-Hye PARK, Department of Anatomical Pathology, Inje University, College of Medicine, Ilsan Paik Hospital, 2240 Daewha-dong, Ilsan-gu Koyang-city 411-706, Korea; Tel: +82-31-910-7141, Fax: +82-31-910-7139; E-mail:

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