PCR-based methylation assay of the p15^INK4B and p16^INK4A genes. Results of various clinical subtypes are shown: no. 1, RA (patient no. 32); no. 2, RA (patient no. 2); no. 3, RARS (patient no. 31); no. 4, RAEB (patient no. 8); no. 5, OL (patient no. 3); no. 6, OL (patient no. 4); no. 7, OL (patient no. 26). (+), DNA digested by the methylation-sensitive restriction enzyme Eco52I; (−), undigested DNA. DNAs from some clinical samples digested by Eco52I were amplified by the primer set flanking the Eco52I site in the exon 1 of p15^INK4B gene, suggesting that the p15^INK4B gene is methylated; whereas none of clinical samples were amplified by the primer set for the p16^INK4A gene, suggesting that the p16^INK4A gene is not methylated. In ML1, the p16^INK4A gene was deleted homozygously.12