摘要
p73基因与经典的抑瘤基因 p5 3高度同源。p73基因的过表达可诱导肿瘤细胞的生长阻滞并诱导其调亡。约 1/3的急性淋巴细胞白血病和Burkitt淋巴瘤病人的 p73基因由于高甲基化而表达缺失 ,但急性髓系白血病病人的 p73表达水平高于正常白细胞。
p73 has high homology with the classical tumor suppressor gene p53. When overexpressed, p73 can lead to tumor cells growth arrest and induce apoptosis. Lost of p73 gene expression due to hypermethylation has been found in about one third patients with acute lymphoblastic leukemia and Burkitt′s lymphoma, but the expression level of p73 is higher in patients with acute myelogenous leukemia than that in normal white blood cells. Further research will be necessary to find out the role of p73 in leukemogensis.
出处
《中国实验血液学杂志》
CAS
CSCD
2001年第3期273-276,共4页
Journal of Experimental Hematology