Lowp53 protein expression in salivary gland tumours compared with lung carcinomas

Abstract

Fifty-one salivary gland tumours (23 pleomorphic adenomas, 5 Warthin's tumours, 12 mucoepidermoid carcinomas, 7 adenoid cystic carcinomas, 3 undifferentiated carcinomas and 1 acinic cell tumour) and 27 lung carcinomas (18 squamous cell carcinomas) were analysed immunohistochemically for the expression of p53 nuclear phosphoprotein. Eight out of 51 (16%) salivary gland tumours were p53 positive. Three of these were benign and 5 malignant. All 3 benign salivary gland tumours were pleomorphic adenomas and expressed only occasional nuclear positivity with less than 1% of tumour cells positive. Of the 5 p53-positive malignant tumours, 3 were mucoepidermoid carcinomas and 2 undifferentiated carcinomas. The malignant salivary gland tumours expressed more than 1% of positive nuclei in every case. Seventeen lung carcinomas were p53 positive (63%). Thirteen of these were squamous cell carcinomas, 3 were adenocarcinomas and 1 small cell lung carcinoma. The results show that mutations of the p53 gene may be infrequent in salivary gland tumours when compared with lung carcinomas. The relatively indolent course of some histological types of malignant salivary gland tumours could be associated with the preservation of the non-mutated p53 gene in most of these tumours. The presence of p53 positivity in some pleomorphic adenomas might, on one hand, suggest that p53 gene alterations are also present in these tumours; on the other hand, the accumulation of the p53 protein in these tumours might also be due to some unknown mechanism, not necessarily related to p53 gene mutation.

The p53 tumor suppressor gene is regulated in vivo by nuclear factor 1-C2 in the mouse mammary gland during pregnancy

“…The cellular effects of p53 activity might become very undesirable if the protein is wrongly activated and p53 must therefore be kept under tight control, being unleashed only when a cell accumulates lesions that may otherwise drive it into a cancerous state (Oren, 1999). There are also clear evidences that regulation of the p53 gene at the transcriptional level contributes significantly for controlling cellular p53 levels (Soini et al, 1992;Balint and Reisman, 1996). Thus, detailed information about the mechanism that regulates the p53 gene is highly important for the understanding of breast tumor biology.…”

Expression of human p53 requires synergistic activation of transcription from the p53 promoter by AP-1, NF-κB and Myc/Max

“…It is, therefore, tightly controlled at the post-translational, post-transcriptional and transcriptional level (reviewed in: Hansen and Oren, 1997). The study of transcription from the human p53 promoter is of interest for tumor biology, since, in some tumors, it participates in the enhanced expression of mutant p53 (Balint and Reisman, 1996) or the reduced expression of wt p53 (Soini et al, 1992). In addition, transcriptional regulation participates in the p53-mediated control of mitogenic stimulation and induced di erentiation (Reich and Levine, 1984) as well as in the response to genotoxic stress (Sun et al, 1995).…”

“…Moreover, expression rates of mutant or wild type p53 in tumors can be altered by deregulated p53 transcription (Soini et al, 1992). To understand the mechanisms that control human p53 transcription, we have analysed the role of a putative AP-1 motif for the regulation of transcription from the human p53 promoter in context with that of the NFkB, NF-1 and Myc/Max/USF motifs in the vicinity of the transcriptional start region (TSR, see Figure 1).…”

Apoptotic activity is increased in parallel with the metaplasia–dysplasia–carcinoma sequence of the bronchial epithelium

“…A SQCLC previously shown to be p53 positive (Soini et al, 1992) was used as a positive control for p53 immunostaining. A hyperplastic lymph node was used as a control for the labelling of apoptotic DNA fragments and for bcl-2, PCNA, bax and mcl-1 immunohistochemistry.…”