Abstract
p53 messenger RNA expression was examined using a cDNA probe in 76 fresh primary breast tumour specimens, 15 of which came from patients treated with toxoxifen prior to surgery. A 2.8 kb mRNA for p53 was expressed in 43 of the 76 specimens. In 19 tumours the levels were similar to those seen in non-malignant (reduction mammoplasty) breast tissue, but in 24 tumours over-expression of mRNA for p53, approaching that seen in three breast cancer cell lines, was found. The cell lines MCF-7, T-47D and MDA-MB-231 expressed three p53 mRNA species of about 2.8 kb and a forth of 1.6 kb. Increased mRNA expression for p53 correlated (P less than 0.05) with loss of genetic material from the short arm of chromosome 17 as demonstrated by allele loss with the VNTR probe YNZ 22.1. There was also statistically significant correlation between increased p53 mRNA expression and low oestrogen receptor protein content in the tumours (P less than 0.05), but not with other clinical parameters. The findings support the view that p53 is involved in breast tumour biology, and suggest that its role may be complex.
Highlights
Summary p53 messenger ribonucleic acid (RNA) expression was examined using a cDNA probe in 76 fresh primary breast tumour specimens, 15 of which came from patients treated with taxoxifen prior to surgery
A 2.8 kb p53 mRNA was detected in 43 of the 76 tumour specimens (57%), in all three breast cancer cell lines and in six of the 10 reduction mammoplasty specimens (Figure 1). Low levels of this p53 mRNA were detected in normal human tonsil, uterus and ovarian tissue
This study has examined p53 mRNA expression and loss of genetic material from the short arm of chromosome 17 in 76 patients
Summary
Summary p53 messenger RNA expression was examined using a cDNA probe in 76 fresh primary breast tumour specimens, 15 of which came from patients treated with taxoxifen prior to surgery. Despite persuasive evidence for its role as an oncogene (Eliyahu et al, 1984, 1985; Parada et al, 1984; Editorial, 1988; Oren, 1986) there is reason to believe that p53 can act as a tumour suppressor gene (Green, 1989; Wang et al, 1989) This paradox may be resolved if rearrangements of the p53 DNA alter the structure, expression (Masuda et al, 1987) or stability (Jenkins et al, 1985) of the 53 kDa protein product and if the function of a mutated p53 product differs from that of the normal gene (Green, 1989). While previous work on human breast cancer has examined p53 protein expression (Cattoretti et al, 1988) or chromosome 17p allelic loss (Mackay et al, 1988; Devilee et al, 1989), no previous study has attempted to link the two by relating expression of p53 mRNA to clinical parameters and/
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