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Association between rb ‐1 gene alterations and factors of favourable prognosis in human breast cancer, without effect on survival
Author(s) -
Berns Els M. J. J.,
De Klein Annelies,
Van Putten Wim L. J.,
Van Staveren Iris L.,
Bootsma Aart,
Klijn Jan G. M.,
Foekens John A.
Publication year - 1995
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/ijc.2910640212
Subject(s) - retinoblastoma , oncogene , tumor suppressor gene , cancer research , breast cancer , biology , retinoblastoma protein , gene duplication , cancer , lung cancer , estrogen receptor , carcinoma , mammary gland , gene , medicine , pathology , oncology , carcinogenesis , cell cycle , genetics
The retinoblastoma (RB) tumour suppressor gene has been associated not only with retinoblastoma but also with several other tumours like osteosarcoma, small cell lung carcinoma and prostate and breast cancer. We have studied the incidence of RB gene alterations in 96 primary breast tumours using Southern blotting techniques. The outcome has been related with patient and tumour characteristics, oncogene amplifications, p53 mutations and prognosis. RB gene alterations were found to occur more frequently in estrogen receptor (ER)‐positive than in ER‐negative tumours and less frequently in tumours with oncogene amplification than in tumours without oncogene amplification of HHR2/ neu , c‐ myc or 11q13. RB gene alteration was observed in tumours both with and without a p53 gene mutation. Data on 87 patients (mean age, 59.6 years; median follow‐up, 108 months) and RB gene alterations revealed a significant association between the frequency of RB gene alterations and node‐negative patients ( p < 0.01) or smaller (<2 cm) tumours ( p < 0.01), but no relation with age, differentiation grade or (relapse‐free) survival. Patients with and without RB gene alterations showed the same relapse‐free and overall survival. © 1995 Wiley‐Liss, Inc.