p14 ARF , generated through an alternative splicing process that replaces the first exon, 1โฃ, of p16 INK4a with exon 1โค, located >15 kb upstream of exon 1โฃ, has been shown to function as a growth suppressor. We examined 11 gastric cancer cell lines for mRNA expression, homozygous deletion, mutation, and promoter methylation of the p14 ARF gene. No mRNA expression was detected in 5 of the 7 diffuse-type cell lines. All intestinal cell lines displayed normal levels of expression except for one with a low level of expression. Of the 5 cell lines without expression, 3 (MKN45, NUGC-2, and NUGC-4) and 1 (KATO III) displayed homozygous deletion and methylation of the p14 ARF gene, respectively. No mutation was found in the whole coding region of the p14 ARF gene in 8 cell lines without homozygous deletion. Our results indicate that the p14 ARF gene is more frequently inactivated by homozygous deletion or methylation in diffuse-type gastric cancer cell lines (5/7, 71.4%) than in intestinal ones (0/4, P โซุโฌ 0.022). When we also analyzed 62 primary gastric cancers for the methylation status of the p14 ARF promoter region, the methylation frequency tended to be higher in diffuse-type gastric cancers (15/33, 45.5%) than in intestinal ones (7/28, 25%). Thus, p14 ARF alterations might be involved in diffuse-type gastric carcinogenesis.