P16 hypermethylation contributes to the characterization of gene inactivation profiles in primary gastric cancer

Corrado Ficorella, Katia Cannita, Enrico Ricevuto, Elena Toniato, Carlo Fusco, Nuntia Teresa Sinopoli, Federica De Galitiis, Zorika Christiana Di Rocco, G. Porzio, Luigi Frati, Alberto Gulino, Stefano Martinotti, Paolo Marchetti

Research output: Contribution to journalArticlepeer-review


The objective of this study was to investigate the contribution of p16 inactivation in gastric cancer and to compare it with p53. A cohort of 34 primary GCs were analyzed for p16 mutations and transcriptional silencing of the gene due to hypermethylation of the promoter. SSCP analysis and direct sequencing of exons 1 and 2 of the p16 gene were performed to detect any structural alterations. The methylation specific PCR (MSP) assay was applied to reveal hypermethylation of the 'CpG' island in the regulatory region using specific primer pairs for methylated and unmethylated nucleotides after a chemical reaction converting cytosines into uracile when unmethylated. SSCP and direct sequencing analysis did not detect any p16 mutations. The MSP assay showed 4 MSP+ variants (11.8%). Three MSP+ were stage III-IV disease and 1 MSP+ was detected in an early stage disease (IB). All MSP+ were diffuse type adenocarcinomas. The MSP+ samples were different from previously reported samples harboring p53 mutations in the same cohort. These data increase the number of gastric cancers showing alterations of either p53 or p16 to 29.4% (10/34). Functional inactivation by hypermethylation of the p16 locus and p53 mutations could play a significant, complementary role in the pathogenesis of sporadic gastric cancer.

Original languageEnglish
Pages (from-to)169-173
Number of pages5
JournalOncology Reports
Issue number1
Publication statusPublished - Jan 2003


  • CpG islands
  • Gastric cancer
  • p16 methylation
  • p53

ASJC Scopus subject areas

  • Cancer Research
  • Oncology


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