EXPRESSION OF BCL-2 AND P53 PROTEINS IN NASOPHARYNGEAL CARCINOMA - ABSENCE OF CORRELATION WITH THE PRESENCE OF EBV ENCODED EBER1-2 TRANSCRIPTS AND LATENT MEMBRANE PROTEIN-1
C. Kouvidou et al., EXPRESSION OF BCL-2 AND P53 PROTEINS IN NASOPHARYNGEAL CARCINOMA - ABSENCE OF CORRELATION WITH THE PRESENCE OF EBV ENCODED EBER1-2 TRANSCRIPTS AND LATENT MEMBRANE PROTEIN-1, JCP. Clinical molecular pathology, 48(1), 1995, pp. 17-22
Aims-To investigate the immunohistochemical expression of bcl-2 and p5
3 proteins in nasopharyngeal carcinomas in relation to the expression
of the Epstein-Barr virus (EBV) encoded EBER messenger RNAs (mRNAs) an
d latent membrane protein-1 (LMP-1). Methods-Formalin fixed, paraffin
wax embedded tissue from 44 nasopharyngeal carcinomas (NPCs) was stain
ed by immunohistochemistry for p53, bcl-2 and LMP-1 proteins and by RN
A in situ hybridisation for EBER mRNAs. Results-The tumours were divid
ed histologically into 13 cases of keratinising squamous cell NPC (KNP
C), 15 cases of non-keratinising squamous cell NPC (NKNPC) and 16 case
s of undifferentiated NPC (UNPC). Bcl-2 expression was observed in fiv
e of 15 NKNPC cases and in six of 16 UNPC cases; p53 expression was ob
served in one of 13 KNPC, two of 15 NKNPC and four of 16 UNPC cases. E
BER 1-2 transcripts were detected in five of 15 NKNPC and nine of 16 U
NPC cases, while LMP-1 expression was observed in one of 16 UNPC cases
. All 13 KNPCs were EBV and bcl-2 negative. No correlation was found b
etween the presence of EBER 1-2 transcripts and the detection of bcl-2
or p53 proteins, or both, in NPC cells. Conclusions-The expression of
bcl-2 and p53 proteins may be associated with the level of the tumour
cell differentiation in NPC. In addition, in view of the important ro
le of the bcl-2 protein in the inhibition of apoptosis, the expression
of bcl-2 protein may contribute to tumour cell survival in a proporti
on of NPCs. Furthermore, in the light of previous findings that the p5
3 gene in most UNPCs is in the wild-type configuration, mechanisms oth
er than mutation may be responsible for stabilisation of the p53 prote
in in UNPCs.