Early mortality in acute promyelocytic leukemia: Potential predictors (Review)
- Can Chen
- Xilian Huang
- Kaile Wang
- Kuang Chen
- Danquan Gao
- Shenxian Qian
Published online on: January 24, 2018
Copyright: © Chen et al.
This is an open access article distributed under the terms of Creative Commons Attribution License.
Acute promyelocytic leukemia (APL) is a rare leukemia characterized by the balanced reciprocal translocation between the promyelocytic leukemia gene on chromosome 15 and the retinoic acid receptor α (RARα) gene on chromosome 17, and accounts for 10‑15% of newly diagnosed acute myeloid leukemia each year. The combined use of all‑trans retinoic acid and arsenic trioxide (ATO) as primary therapy has markedly improved the survival rate of patients with APL. Mortality in the first 30 days following therapy remains a major contribution to treatment failure. In the present study, published data was reviewed with a focus on the factors associated with early mortality. When treated with ATO as a primary treatment, the fms‑like tyrosine kinase‑internal tandem deletion has no impact on early mortality. Low lymphoid enhancer binding factor‑1 expression may be a reliable marker for early mortality and the target of therapy if it could be proven by further studies. Cluster of differentiation (CD)56+ and CD34+/CD2+ may be candidates to select high‑risk patients. The risk of early mortality in APL still cannot be predicted via the cell surface makers, despite multiple studies on their prognostic significance. Typically, a complex translocation did not alter the survival rate in patients with APL; however, if an abnormal karyotype [e.g., Ide(17), ZBTB16/ RARα and STAT5B/RARα] appeared singularly or as part of a complex mutation, there is a high possibility of early mortality if clinicians are unable to identify or monitor it.