APL is a model for oncogene-targeted therapies: <i>all-trans</i> retinoic acid (ATRA) and arsenic both target and degrade its ProMyelocytic Leukemia/Retinoic Acid Receptor α (PML/RARA) driver.
Autophagy and Ubiquitin-Mediated Proteolytic Degradation of PML/Rarα Fusion Protein in Matrine-Induced Differentiation Sensitivity Recovery of ATRA-Resistant APL (NB4-LR1) Cells: in Vitro and in Vivo Studies.
The t(15;17) translocation generates a PML-RARα fusion protein causative for acute promyelocytic leukemia (APL).Li et al. now identify the pseudokinase stress protein TRIB3 as an important factor in APL disease progression and therapy resistance.
The t(15;17) translocation generates a PML-RARα fusion protein causative for acute promyelocytic leukemia (APL).Li et al. now identify the pseudokinase stress protein TRIB3 as an important factor in APL disease progression and therapy resistance.
APL is characterized by a balanced reciprocal chromosomal translocation fusing the promyelocytic leukaemia (PML) gene on chromosome 15 with the retinoic acid receptor α (RARα) gene on chromosome 17.
APL is characterized by a balanced reciprocal chromosomal translocation fusing the promyelocytic leukaemia (PML) gene on chromosome 15 with the retinoic acid receptor α (RARα) gene on chromosome 17.
APL is most commonly caused by a translocation (15:17) and expression of the promyelocytic leukemia and the retinoic receptor α (PML-RARA) fusion product; however, the events that cooperate with PML-RARA in APL pathogenesis are not well understood.
APL cell treatment with all-trans-retinoic acid (RA) degrades the chimeric, dominant-negative-acting transcription factor promyelocytic leukemia gene (PML)/RARα, which is generated in APL by chromosomal translocation.