Abstract
FLT3-internal tandem duplication (FLT3-ITD) mutations are common in acute promyelocytic leukemia (APL) and render the disease more difficult to manage or cure. In this issue of Blood, Esnault et al begin to unravel how the mutation-activated FLT3 receptor impedes the effects of all-trans retinoic acid (ATRA) and how arsenic counters this.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 1392-1393 |
| Number of pages | 2 |
| Journal | Blood |
| Volume | 133 |
| Issue number | 13 |
| DOIs | |
| State | Published - Mar 2019 |
ASJC Scopus subject areas
- Biochemistry
- Immunology
- Hematology
- Cell Biology