Sai-Juan Chen

TL;DR: As2O3 treatment is an effective and relatively safe drug in APL patients refractory to ATRA and conventional chemotherapy, and Pharmacokinetic studies showed that after a peak level of 5.54 micromol/L, plasma arsenic was rapidly eliminated, and the continuous administration of As2O2 did not alter its pharmacokinetic behaviors.

TL;DR: The results encouraged us to hypothesize that As2O3 induces APL cell differentiation through direct or indirect activation of retinoic acid receptor-related signaling pathway(s), while ΔΨm collapse is the common mechanism of As 2O3-induced apoptosis.

TL;DR: Molecular studies showed rearrangements of the retinoic acid receptor alpha (RAR alpha) gene but no rearrangement of the promyelocytic leukemia gene consistent with the cytogenetic data.

TL;DR: Interestingly, As2O3 over a wide range of concentration induces degradation of a key leukemogenic protein, PML–RARα, as well as the wild-type PML, thus setting up a good example of targeting therapy for human cancers.

TL;DR: It is demonstrated that low-dose As2O3 had the same effect as the conventional dosage and the mechanism of low- dose arsenic seemed to primarily induce differentiation of APL cells.