Cs. Lee et al., IMMUNOHISTOCHEMICAL DEMONSTRATION OF THE P53 TUMOR-SUPPRESSOR GENE-PRODUCT IN CANCER OF THE PANCREAS AND CHRONIC-PANCREATITIS, Journal of gastroenterology and hepatology, 8(5), 1993, pp. 465-469
The p53 tumour suppressor gene and its protein products after point mu
tations are currently attracting wide attention in the investigation o
f human tumours. In this study we present the findings on percutaneous
pancreatic biopsies of 82 cases after routine processing and immunost
aining for the polyclonal p53 antibody CM1, an antibody directed again
st both wild and mutant forms of p53 protein. There were 51 carcinomas
, 5 islet cell tumours, 16 cases of chronic pancreatitis (including on
e with atypical ductal epithelium) and seven histologically normal pan
creatic biopsy specimens. None of the seven normal cases showed any de
finite nuclear immunostaining for p53. Thirty-two (63%) of the pancrea
tic adenocarcinomas showed moderate to intense immunoreactivity. Of th
e 16 cases of chronic pancreatitis, 11 were negative and three showed
equivocal immunostaining. The one case with ductal epithelial atypia s
howed mild to moderate immunoreactivity. All islet cell tumours were n
egative. The expression of the p53 gene, therefore, appears increased
in the majority of pancreatic adenocarcinomas while this is not observ
ed in chronic pancreatitis or normal pancreatic tissue. Nuclear immuno
reactivity for p53 protein may represent mutant forms because of the s
hort half-life of the wild-type protein. The lack of p53 expression in
some cases of pancreatic adenocarcinoma may be due to different types
of mutant proteins not detectable by the CM1 antibody. Nuclear immuno
reactivity to the p53 protein in pancreatic biopsy is more suggestive
of a malignant tumour than chronic pancreatitis.