Expression of Bcl-2 in human breast cancer: Correlation between hormone receptor status, p53 protein accumulation and DNA strand breaks associated with apoptosis

• Published in: Pathology international Vol. 47; no. 11; pp. 757 - 762
• Main Authors: Hori, Masao, Nogami, Tatsuya, Itabashi, Masayuki, Yoshimi, Fuyo, Ono, Hisayuki, Koizumi, Sumihiko
• Format: Journal Article
• Language: English
• Published: Oxford, UK Blackwell Publishing Ltd 01.11.1997
• Subjects: Apoptosis; Bcl-2; Breast Neoplasms - genetics; Breast Neoplasms - metabolism; Breast Neoplasms - pathology; DNA Damage; Female; hormone receptors; human breast cancer; Humans; Immunohistochemistry; p53 oncoprotein; Polymerase Chain Reaction; Proto-Oncogene Proteins c-bcl-2 - metabolism; Receptors, Estrogen - metabolism; Receptors, Progesterone - metabolism; RNA, Messenger - analysis; Transcription, Genetic; Tumor Cells, Cultured; Tumor Suppressor Protein p53 - metabolism
• ISSN: 1320-5463; 1440-1827
• DOI: 10.1111/j.1440-1827.1997.tb04453.x

The expression of Bcl‐2, a suppressor of apoptotic cell death, was Investigated in 52 invaslve carcinomas of the breast using reverse transcription‐polymerase chain reaction and Immunohistochemical methods. After consideration of both sets of results, 42 tumors (80.8%) were confirmed to be positive (Bcl‐2(+)) and 10 (19.2%) were judged negative (Bcl‐2(‐)) for Bcl‐2 expression. Related factors (p53 protein accumulation, hormone receptor status and apoptotic cell index) were also examined using Immuno‐histochemical and in situ end‐labeling methods to elucidate their correlations with Bcl‐2 expression. Bcl‐2 expression correlated significantly with the hormone receptor status, whereas it showed significant inverse correlations with p53 accumulation and the apoptotic index. It was concluded that estrogen and mutant p53 are related to the regulation of Bcl‐2 expression and that the ability to prevent tumor cell death due to Bcl‐2 can be developed by breast cancers.