Gene amplification and enhanced expression of the epidermal growth facor receptor (EGFR) represent the major moiecular genetic alteration in glioblastomas and it may play an essential role in cell growth and in the carcinogenic process, On the other hand, the nuclear suppressor proteins PML and p53 are also known to play critical roles in cancer edveiopment and in suppressing cell growth. Here we report that, in glioblastoma cells with cefectivw EGFR function, the expressions of both promyetocytic leukaernia (PML) and p53 were altered. Cells that were transfected with the antisense-cDNA of EGFR were found to have more cells in G1 and fewer cells in Sphase, In Addition, the transfceted cells were found to be non-responsive to EGF-induced cell growth, Inteerestingly, the expression of the suppressors p53 and PML were found to be signillcantly increased by immunohistochemical assay in the antisense-EGFR cells. Moreover, the PML expression in many of the cells was converted from the nucleal dot pattern imto fine-granulated staining pattern, In contrast, the expressions of other cell cycle regulated geries and proto-oncogene, including the cycli-dependent kinase 4(cocik4), retinblastoma, p16 think and p21bjone, were not altered. These data indicate that there are specific inductions of PML and p53 proteins which may account for the increase in G1 and growth arrest in antisense-EGFR treated cells, It also indicates that the EGF, p53 and PML transduction pathways were liked and they may constifulte arrest in an ntegral part of an alterred growth reguiaory programme .The interactions and cross-talks of these critical molecules may be very importtant in regulating cell growth, differentiation and cellular resporise to treatment in glioblastomas.