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p16 protein expression and promoter methylation of p16 gene in gastric cancer

Zhao Guo-ha

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Abstract

Objective To investigate the mechanism of p16 gene inactivation in gastric cancer. Methods The expression of p16 protein in the tissues from 40 gastric cancers and 43 normal gastric mucosas were detected by immunohistochemical method, so were the promoter region methylation of p16 gene in the specimens from 40 gastric cancers and 35 normal gastric mucosas by methylation-specific PCR (MSP). Results The promoter region of p16 gene was methylated in 23 specimens of carcinoma, with a methylation frequency of 58%, while no methylation was detectable in the normal gastric mucosas, revealing a significant difference between cancerous tissue and normal mucosa (P0.01). There were significant differences in the occurrence of loss of p16 protein expression between the cancerous tissue and the normal mucosa (31 vs 6,P 0.01). The outcomes of detecting the cancerous tissue did not differ significantly between immunohistochemistry and MSP(P 0.05). Conclusions Gastric carcinogenesis is closely associated with p16 gene inactivation. Promoter methylation may inhibit the level of protein expression which can be an important mechanism of p16 gene inactivated in gastric cancer.

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Objective To investigate the mechanism of p16 gene inactivation in gastric cancer. Methods The expression of p16 protein in the tissues from 40 gastric cancers and 43 normal gastric mucosas were detected by immunohistochemical method, so were the promoter region methylation of p16 gene in the specimens from 40 gastric cancers and 35 normal gastric mucosas by methylation-specific PCR (MSP). Results The promoter region of p16 gene was methylated in 23 specimens of carcinoma, with a methylation frequency of 58%, while no methylation was detectable in the normal gastric mucosas, revealing a significant difference between cancerous tissue and normal mucosa (P0.01). There were significant differences in the occurrence of loss of p16 protein expression between the cancerous tissue and the normal mucosa (31 vs 6,P 0.01). The outcomes of detecting the cancerous tissue did not differ significantly between immunohistochemistry and MSP(P 0.05). Conclusions Gastric carcinogenesis is closely associated with p16 gene inactivation. Promoter methylation may inhibit the level of protein expression which can be an important mechanism of p16 gene inactivated in gastric cancer.

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Available abstract

Objective To investigate the mechanism of p16 gene inactivation in gastric cancer. Methods The expression of p16 protein in the tissues from 40 gastric cancers and 43 normal gastric mucosas were detected by immunohistochemical method, so were the promoter region methylation of p16 gene in the specimens from 40 gastric cancers and 35 normal gastric mucosas by methylation-specific PCR (MSP). Results The promoter region of p16 gene was methylated in 23 specimens of carcinoma, with a methylation frequency of 58%, while no methylation was detectable in the normal gastric mucosas, revealing a significant difference between cancerous tissue and normal mucosa (P0.01). There were significant differences in the occurrence of loss of p16 protein expression between the cancerous tissue and the normal mucosa (31 vs 6,P 0.01). The outcomes of detecting the cancerous tissue did not differ significantly between immunohistochemistry and MSP(P 0.05). Conclusions Gastric carcinogenesis is closely associated with p16 gene inactivation. Promoter methylation may inhibit the level of protein expression which can be an important mechanism of p16 gene inactivated in gastric cancer.

Key concepts: Methylation, Immunohistochemistry, Carcinogenesis, Cancer, Biology, Gene, DNA methylation, Cancer research

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