P53 expression in human soft tissue sarcomas. Correlation with biological aggressiveness

Abstract

The p53 gene located at chromosome 17 p13 encodes a MW 53,000 nuclear phosphoprotein which is frequently mutated in many human cancers [1]. The mutant p53 protein has a much longer half-life than the wild-type protein ; the result is a large amount of mutant proteins in transformed cells and tumours. The exact function of p53 protein expression abnormalities in tumour cells has not been completely clarified yet. Several studies have shown that reintroduction of a wild-type p53 gene into p53 deficient cells leads to suppression of the neoplastic phenotype [2]. This suppressor activity may be exerted through the transcriptional control of the proliferation-related genes [3] and/or regulation of DNA replication through wild-type p53 association with DNA replication complexes [4, 5]. It has been supposed that p53 mutations might have a predisposing effect in carcinogenesis and be a favourable event in progression of human tumours. Abnormalities of p53 have been related to the development of various cancers including bladder [6], lung [7], breast [8], colorectal [9] and brain [10] cancer. In this study we investigated p53 expression in human soft tissue sarcomas [HSTS]. The aim was to compare p53 expression with the tumour behaviour of HSTS.