Chen Y, Zhang H, Yue B, Li H
Institute of Hematology, Xiehe Hospital, Tongji Medical University, Wuhan 430030.
J Tongji Med Univ. 2000;20(3):210-1. doi: 10.1007/BF02886992.
To study the change of suppressing cancer gene P16 in acute leukemia, the P16 antigen expression of leukemia cell surfaces in 61 cases were investigated with ABC assay and gene structural defects in 51 cases of acute leukemia were examined with multiple comparative PCR method. It was found that antigen expression of P16 in leukemia was obviously lower than that innormal subjects (P < 0.001). At the same time, antigen expression in All was lower than that AML (P < 0.05). No significant difference was found between the complete remission (CR) and non-remission (NR) subjects from AML and ALL groups (P > 0.05). THe exon 2 of P16 gene showed homozygous deletion only inn 4 cases out of 30 cases in ALL. No structural defect was revealed in 21 cases of AML. It was suggested that expression defect of P16 gene was a main cause in development and progression of acute leukemia, and structural defect of exon 2 was not a primary molecular event.