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AIM To investigate the relationship between theexpression of p16 gene and the gastric carcinogenesis,depth of invasion and lymph node metastases,and toevaluate the deletion and mutation of exon 2 in p16 genein gastric carcinoma.METHODS The expression of P16 protein was examinedby streptavidin-peroxidase conjugated method(S-P);thedeletion and mutation of p16 gone were respectivelyexamined by polymerase chain reaction(PCR)andpolymerase chain reaction single-strand conformationpolymorphism analysis(PCFI-SSCP)in gastric carcinoma.RESULTS Expression of P16 protein was detected in96.25%(77/80)of the normal 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 ofP16 protein expression in gastric carcinoma wassignificantly lower than that in normal gastric mucose anddysplastic gastric mucose (P<0.05).The positive rate ofP16 protein expression in mucoid carcinoma 10.00%(1/10)was significantly lower than that in poorlydifferentiated carcinoma 51.22%(21/41),undifferentiated carcinoma 57.69%(15/26)and signetring cell carcinoma 62.50%(10/16)(P<0.05).Thepositive rate of p16 protein in 30 cases paired primary andlymph node metastatic gastric carcinoma:There was46.67%(14/30)in primary gastric carcinoma,16.67%(5/30)in lymph node metastatic gastric carcinoma.Thepositive rate of lymph node metastatic carcinoma wassignificantly lower than that of primary carcinoma(P<0.05).There was of p16 gene mutation in exon 2,but5 cases displayed deletion of p16 gene in exon 2 in the 25primary gastric carcinomas.CONCLUSIONS The expression loss of P16 protein relatedto the gastric carcinogenesis,gastric carcinomahistopathological subtypes and lymph merastasis.Themutation of p16 gene in exon 2 may not be involved ingastric carcinogenesis.But the deletion of p16 gane in exon 2 may be involved in gastric carcinogenesis.
AIM To investigate the relationship between the expression of p16 gene and the gastric carcinogenesis, depth of invasion and lymph node metastases, and toevaluate the deletion and mutation of exon 2 in p16 genein gastric carcinoma.METHODS The expression of P16 protein was examinedby streptavidin-peroxidase conjugated Method(SP);thedeletion and mutation of p16 gone was respectively criticalexamined by polymerase chain reaction(PCR)and polymerase chain reaction single-strand conformity polymorphism analysis(PCFI-SSCP) in gastric carcinoma.RESULTS Expression of P16 protein was detected in 96.25%(77%) /80)of the normal 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 ofP16 protein expression in gastric carcinoma was significantly lower than that in Normal gastric mucose and dysplastic gastric mucosal (P<0.05). The positive rate of P16 protein expression in mucoid carcinoma 10.00%(1/10) was significantly lower than that in poorlydiff The positive rate of p16 protein in 30 cases paired primary and lymph node metastatic gastric was 51.22% (21/41), undifferentiated carcinoma 57.69% (15/26) and signetring cell carcinoma 62.50% (10/16) (P<0.05). Carcinoma:There was 46.67%(14/30)in primary gastric carcinoma,16.67%(5/30)in lymph node metastatic gastric carcinoma.The positive rate of lymph node metastatic carcinoma was significantly lower than that of primary carcinoma(P<0.05) .There was of p16 gene mutation in exon 2,but5 cases showed deletion of p16 gene in exon 2 in the 25 primary warehouse carcinomas.CONCLUSIONS The expression loss of P16 protein relatedto the gastric carcinogenesis,gastric carcinomahistopathological subtypes and lymph merastasis.Themutation of p16 gene In exon 2 may not be involved in gastrictric carcinogenesis.But the deletion of p16 gane in exon 2 may be involved in gastric carcinogenesis.