Abstract: A mathematical model of in vitro cancer cell growth differentiated by cell cycle distribution and antimitotic drug interaction was presented in this paper. The model was adapted to the growth and treatment of human leukemia K562 cells with docetaxel.It described docetaxel-induced apoptosis, G2/M phase arrest as well as the relationship of drug concentration and cell response manners.The model showed that the saturation docetaxel concentrations to cause M-phase arrest and apoptosis in K562 cells were 17.96 nmol·L^-1 and 7.82 nmol·L^-1 and the effective concentrations were 2.63 nmol·L^-1 and 1.69 nmol·L^-1,respectively.Low concentration docetaxel (1.69—2.63 nmol·L^-1) induced apoptosis directly, without obvious M-phase arrest,while cells mainly reacted with concentration-dependent M-phase arrest and saturated apoptosis at high concentration docetaxel (>7.82 nmol·L^-1).The model indicated that M-phase arrest was not positively related to apoptosis, which gave a new explanation for the mechanism of docetaxel.