Abstract: Many tumorigenesis in human are closely linked to the functional loss of P53. The tumor-suppressive functions of P53 are abrogated by mutations, but in 50% of all tumors remains wild type. In these cases, loss of P53 tumor-suppressive function mainly results from the abnormal methylation of 5' CpG islands of tumor suppressor genes such as INK4a, ARF and ASPP. Restoring to normal methylation state of these genes may provide new means for tumor therapeutics.

Key words: INK4a/ARF, ASPPs, methylation, DNMTs