American Society of Hematology

$Mutations in As2O3-refractory APL support clinical relevance of experimental model of As2O3 action. (A) B2-Box missense mutation sites from Figure 1D in the article by Goto et al that begins on page 1600. (B-C) Relationship of As2O3 resistance-associated mutations (A216V and L218P) to preclinical model for As2O3-mediated PML-RARα degradation: all steps blocked by experimental site-specific mutation of the critical arsenic-binding/cross-linking dicysteine motif (C212A or C213A; Jeanne et al7); matrix association and sumoylation demonstrated to be blocked by A216V and L218P. Adapted from Jeanne et al7 with copyright permission from Elsevier. Professional illustration by Alice Y. Chen.$

Mutations in As₂O₃-refractory APL support clinical relevance of experimental model of As₂O₃ action. (A) B2-Box missense mutation sites from Figure 1D in the article by Goto et al that begins on page 1600. (B-C) Relationship of As₂O₃ resistance-associated mutations (A216V and L218P) to preclinical model for As₂O₃-mediated PML-RARα degradation: all steps blocked by experimental site-specific mutation of the critical arsenic-binding/cross-linking dicysteine motif (C212A or C213A; Jeanne et al⁷); matrix association and sumoylation demonstrated to be blocked by A216V and L218P. Adapted from Jeanne et al⁷ with copyright permission from Elsevier. Professional illustration by Alice Y. Chen.

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