AIM To investigate the relationship between the expression of p16 gene and
the gastric carcinogenesis, depth of invasion and lymph node metastases, an
d to evaluate the deletion and mutation of exon 2 in p16 gene in gastric ca
rcinoma.
METHODS The expression of P16 protein was examined by streptavidin-peroxida
se conjugated method (S-P); the deletion and mutation of p16 gene were resp
ectively examined by polymerase chain reaction ( PCR ) and polymerase chain
reaction single-strand conformation polymorphism analysis (PCR-SSCP) in ga
stric carcinoma.
RESULTS Expression of P16 protein was detected in 96.25% (77/80) of the nor
mal gastric mucosa, in 92.00% (45/ 50) of the dysplastic gastric mucosa and
in 47.54% (58/ 122) of the gastric carcinoma, The positive rate of P16 pro
tein expression in gastric carcinoma was significantly lower than that in n
ormal gastric mucosa and dysplastic gastric mucosa (P <0.05). The positive
rate of P16 protein expression in mucoid carcinoma 10.00% (1/ 10) was signi
ficantly lower than that in poorly differentiated carcinoma 51.22% ( 21/ 41
), undifferentiated carcinoma 57.69% ( 15/ 26) and signet ring cell carcino
ma 62.50% (10/ 16) (P <0.05). The positive rate of p16 protein in 30 cases
paired primary and lymph node metastatic gastric carcinoma: There was 46.67
% ( 14/ 30) in primary gastric carcinoma, 16.67% (5/ 30) in lymph node meta
static gastric carcinoma. The positive rate of lymph node metastatic carcin
oma was significantly lower than that of primary carcinoma (P <0.05). There
was of p16 gene mutation in exon 2, but 5 cases displayed deletion of p16
gene in exon 2 in the 25 primary gastric carcinomas.
CONCLUSIONS The expression loss of P16 protein related to the gastric carci
nogenesis, gastric carcinoma histopathological subtypes and lymph merastasi
s. The mutation of p16 gene in exon 2 may not be involved in gastric carcin
ogenesis. But the deletion of p16 gene in exon 2 may be involved in gastric
carcinogenesis.