| Autor: |
Heiden, Thomas, Nickel, Janette, Preissner, Robert, Seeger, Karl |
| Zdroj: |
Blood; December 2015, Vol. 126 Issue: 23 p4812-4812, 1p |
| Abstrakt: |
Acute lymphoblastic leukemia (ALL), a clinically and biologically heterogeneous disease, is the most common type of childhood cancer. Approximately 25% of B-cell precursor ALL (BCP-ALL) carry the cryptic chromosomal translocation t(12;21)(p13;q22), the most frequent genetic aberration in pediatric ALL. This translocation combines two transcription factors and essential regulators of normal hematopoiesis, ETV6and RUNX1, generating the fusion oncogene ETV6/RUNX1(synonym TEL/AML1). Recent studies in various animal models have strengthened the view that ETV6/RUNX1positive cells give rise to preleukemic clones with a differentiation block in the pro/pre-B stage of B cell development that, after acquisition of additional mutations, may transform into full malignancy. However, the effects triggered by the expression of ETV6/RUNX1and the associated additional mutated genes are not well understood. |
| Databáze: |
Supplemental Index |
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