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Interaction between bcl‐2 and p21 (WAF1/CIP1) in breast carcinomas with wild‐type p53
Author(s) -
Bukholm Ida K.,
Nesland Jahn M.,
Kåresen Rolf,
Jacobsen Ulf,
BørresenDale AnneLise
Publication year - 1997
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/(sici)1097-0215(19970926)73:1<38::aid-ijc7>3.0.co;2-2
Subject(s) - cancer research , apoptosis , p53 protein , biology , immunohistochemistry , breast cancer , mammary gland , protein expression , cancer , gene , immunology , genetics
The bcl‐2 protein is found to be over‐expressed in many types of human tumours and is a potent inhibitor of apoptosis. The exact mechanism by which bcl‐2 prevents apoptosis and exercises its oncogenic effect is still unclear. Other studies on cell lines have reported that bcl‐2 over‐expression is related to suppression of p21 (WAF1/CIP). We have investigated the relationship between bcl‐2 protein over‐expression and expression of the p21 protein in a series of human breast carcinomas. Selected tumour samples from 100 breast‐cancer patients (38 with abnormal p53 status, scored as protein accumulation and/or mutation, and 62 without detectable p53 alterations), were immunostained for bcl‐2 protein, the p21 protein and the oestrogen‐receptor (ER) protein. A highly significant association was found between reduced p21‐protein expression and over‐expression of bcl‐2 in tumours with no detectable p53 alterations ( p < 0.001). A significant association was seen between ER immunoreactivity and expression of the bcl‐2 protein, as well as between bcl‐2 protein expression and tumours of the higher differentiation grade (grade‐2 tumours). No association was seen between bcl‐2 over‐expression and the presence of metastases. Our findings indicate that down‐regulation of p21 may be a result of up‐regulation of bcl‐2 independent of p53. Int. J. Cancer 73:38–41, 1997. © 1997 Wiley‐Liss, Inc.