Abstract
TEL-AML1 is expressed from the t(12;21) chromosomal translocation in B-precursor acute lymphocytic leukemia (ALL). Creation of the TEL-AML1 fusion disrupts one copy of the TEL and AML1 genes, and loss of TEL or AML1 is also associated with cases of acute leukemia without TEL-AML1. To determine whether TEL-AML1 can contribute to leukemogenesis, we transduced marrow from C57BL/6 mice with a retroviral vector expressing TEL-AML1 or with a control vector. Transduced cells were introduced into irradiated syngeneic recipients. Two of 9 TEL-AML1 mice developed ALL (one T-lineage ALL and one B-precursor ALL), whereas 0 of 20 control mice developed leukemia. The B-precursor ALL was retransplantable and expressed TEL-AML1. We similarly transduced marrow from C57BL/6 mice lacking the overlapping p16INK4ap19ARF genes and transplanted the cells into wild-type recipients. No control mice died, but six of eight TEL-AML1/p16p19 mice died with leukemia. Overall, these findings indicate that TEL-AML1 contributes to leukemogenesis and may cooperate with loss of p16INK4ap14ARF to transform lymphoid progenitors.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 3904-3908 |
| Number of pages | 5 |
| Journal | Cancer Research |
| Volume | 62 |
| Issue number | 14 |
| State | Published - Jul 15 2002 |
ASJC Scopus subject areas
- Oncology
- Cancer Research