Prognostic Impact of TEL-AML-1 Fusion Gene on Acute Lymphoblastic Leukemia

Abstract

AML-1 is normally expressed in all hematopoietic lineage and acts to regulate the expression of various genes such as granulocyte–colony stimulating factor, interleukin-3, T-cell receptors, and myeloperoxidase genes (1). Frequent translocation variants result in fusion between intron-5 of TEL and intron-2 of AML-1 (2). The t(12:21) results in the chimeric fusion gene TEL–AML-1. The basis of this selectivity is an important unresolved issue (3), but most likely reflects a selective impact of the chimeric protein on the proliferation and/or survival of B-cell precursor (4). Although the mechanism of leukemogenesis induced by TEL–AML-1 remains obscure, recent data have demonstrated the importance of both TEL and AML-1 for normal hematopoiesis, thus suggesting that the presence of TEL–AML-1 fusion protein leads to disordered hematopoietic development as a critical component (5). ABSTRACT