Correlation of p16 hypermethylation with p16 protein loss in sporadic gastric carcinomas

Yhong Hee Shim, Gyeong Hoon Kang, Jae Y. Ro

Research output: Contribution to journalArticlepeer-review

138 Scopus citations


Hypermethylation of p16 has been detected frequently in a variety of cancer cells and is known to repress the level of p16 transcription. In human gastric carcinoma (GC) cells, p16 protein loss has often been detected, but genetic alterations of p16 are infrequent. To investigate the molecular mechanism of p16 gene inactivation in gastric carcinogenesis, we examined the methylation status of p16 in GC using methylation-specific PCR. Thirty-seven of eighty-eight (42%) GC showed p16 hypermethylation. Immunohistochemical analysis of 41 cases of GC showed a complete loss of p16 immunoreactivity in 19 of 22 (86%) methylation-positive cases, but in only 2 of 19 (11%) methylation-negative cases. Of 88 GC, 21 cases were previously identified as having microsatellite instability (MSI). Interestingly, 13 of 21 (62%) MSI- positive tumors and 24 of 67 (36%) MSI-negative tumors had hypermethylation on p16. The relatively high frequency of hypermethylation on p16 and the strong correlation between the immunoreactivity and methylation patterns suggest that methylation is an important mechanism for p 16 gene inactivation in GC.

Original languageEnglish (US)
Pages (from-to)689-695
Number of pages7
JournalLaboratory Investigation
Issue number5
StatePublished - May 2000

ASJC Scopus subject areas

  • Pathology and Forensic Medicine
  • Molecular Biology
  • Cell Biology


Dive into the research topics of 'Correlation of p16 hypermethylation with p16 protein loss in sporadic gastric carcinomas'. Together they form a unique fingerprint.

Cite this