Aim:To examine the differentiation induction and growth inhibition of HL-60 cellsby diallyl disulfide(DADS),and its relationship with the alterations of histoneacetylation and p21~(WAF1)expression in vitro and in vivo.Methods:Differentiationwas studied by nitroblue tetrazolium(NBT)reduction of HL-60 cell in vitro.HL-60cells 5×10~6 were injected into the right side of the peritoneal cavity of severecombined immunodeficiency(SCID)mice.When the peritoneal neoplasms weredetected,the SCID mice were randomly divided into 3 groups and received an ipinjection of vehicle alone(NS),DADS or sodium butyrate(SB).The growthinhibition of peritoneal neoplasms induced by DADS was observed by a growthcurve.The cycle distribution of HL-60 cells in SCID mice was monitored by flowcytometry.The expression of acetylated histone H3,H4 and p21~(WAF1)were mea-sured by Western blot.Results:After treatment with DADS for 0-72 h,the NBTreduction ability of HL-60 cells increased in a time-dependent manner,comparedwith no treatment of HL-60 cells.In the HL-60 cells treated with DADS for 24 h,theexpression of acetylated histone H3,H4,and p21~(WAF1)increased obviously.Aftertreatment with DADS,tumor growth was markedly suppressed.HL-60 cells frommice treated with DADS were blocked in the G_1 phase,from 25.4% to 63.4%.Thetumors from the mice treated with DADS showed an increase of acetylated his-tone H3,H4,and p21~(WAF1).Conclusion:DADS could induce differentiation andinhibit the growth of HL-60 cells through increasing the expression of acetylatedhistone H3,I44,and p21~(WAF1)in vitro and in vivo. Aim: To examine the differentiation induction and growth inhibition of HL-60 cells by diallyl disulfide (DADS), and its relationship with the alterations of histoneacetylation and p21 ~ (WAF1) expression in vitro and in vivo. Methods: Differentiationwas studied by nitroblue tetrazolium NBT) reduction of HL-60 cell in vitro. HL-60 cells 5 × 10 ~ 6 were injected into the right side of the peritoneal cavity of severecombined immunodeficiency (SCID) mice.When the peritoneal neoplasms weredetected, the SCID mice were randomly divided into 3 groups and received an ipjection of vehicle alone (NS), DADS or sodium butyrate (SB). The growth inhibition by peritoneal neoplasms induced by DADS was observed by a growthcurve. The cycle distribution of HL-60 cells in SCID mice was monitored by flowcytometry Results: After treatment with DADS for 0-72 h, the NBT depression ability of HL-60 cells increased in a time-dependent manner , comparedw ith no treatment of HL-60 cells. The HL-60 cells treated with DADS for 24 h, the expression of acetylated histone H3, H4, and p21 ~ (WAF1) were significantly altered. A treatment with DADS, tumor growth was markedly suppressed -60 cells frommice treated with DADS were blocked in the G_1 phase from 25.4% to 63.4%. The tumors from the mice treated with DADS showed an increase of acetylated his-tone H3, H4, and p21 ~ (WAF1) .Conclusion: DADS could induce differentiation and inhibition of the growth of HL-60 cells through increasing the expression of acetylated histone H3, I44, and p21 ~ (WAF1) in vitro and in vivo.