A number of studies on the putative relation between Polycomb-Group (PcG) proteins overexpression and carcinogenesis have been published recently. BMI1, the prototype PcG gene, is critically involved in cell cycle control and differentiation, and despite the regulatory role demonstrated in central nervous system (CNS) development, its implication in brain tumorigenesis is scarcely known. Moreover, to the best of our knowledge, large studies on human brain tumors tissue are lacking. To gain a new insight, we tested 80 primary brain astrocytomas for BMI1 expression using immunohistochemistry and established a correlation with the expression of p16, a negatively regulated target of BMI1 function. Fifty-four cases (72.5%) were BMI1 + /p16-, and 22 cases (27.5%) were BMI1 + /p16+. Slight non-significant differences were noted in the expression profile between grades II, III, and IV astrocytomas. However, when the 22 BMI1 + /p16+ tumors were examined cytologically, a substantial proportion contained a significant gemistocytic component, which is thought to be an adverse prognostic factor or to display a high degree of anaplasia, suggesting a common molecular mechanism of BMI1/p16 pathway disruption, which may have prognostic implications.