Burkitt lymphoma (BL) is an aggressive B-cell tumor characterized by high growth rate with a large fraction of cycling cells. All Burkitt lymphomas (BLs) carry reciprocal chromosomal translocations that activate the c-myc oncogene through juxtaposition to one of the immunoglobulin (Ig) loci, providing a constitutive proliferative signal. This genetic anomaly is the critical event in BL development, but subsequent tumor progression involves the selection of additional genetic and epigenetic changes. It has been reported that both pRb and P53 pathways play a pivotal rule in this process. The alteration of these pathway is well know in endemic Burkitt lymphomas BLe but no data as reported for sporadic ones. Here we showed that p16 and p21 expression are altered in Gal-01, a new sporadic BL cell line. Western blotting and immunocytochemistry assay have revealed the lack of p16/INK4a protein in the Gal1. Methylation-Specific (PCR) MSP revealed that loss of p16/INK4a is due to improper methylation of the promoter region. 5-Aza-2 deoxycytidine (5-Aza-CdR) treatment reactivates p16/INK4a expression and specifically inhibited tumor cell growth, suggesting that aberrant promoter methylation is a common mechanism in sporadic burkitt lymphoma. At the same time, we analyzed the expression changes of some cell cycle regulating genes after demethylating tratment. 5-Aza-CdR treatment significantly increased the level of p21WAFI/CIPI without changing the amount of its direct activator p53. It suggests that also p21WAF1/CIP1 may be silenced by aberrant promoter methylation in Gal1 cell line. These data demonstred at the first that loss of expression of p21 and p16 by promoter methylation may be a common mechanism in addition with c-myc overexpression in sporadic Burkitt lymphoma progression.