Absence of ABL1 exon 2-encoded SH3 residues in BCR::ABL1 destabilizes the autoinhibited kinase conformation and confers resistance to asciminib
Author:
Funder
American Society of Hematology
U.S. Department of Health & Human Services | National Institutes of Health
Samuel Waxman Cancer Research Foundation
Publisher
Springer Science and Business Media LLC
Link
https://www.nature.com/articles/s41375-024-02353-0.pdf
Reference15 articles.
1. Hochhaus A, Wang J, Kim DW, Kim DDH, Mayer J, Goh YT, et al. Asciminib in newly diagnosed chronic myeloid leukemia. N Engl J Med. 2024. online ahead of print.
2. Wylie AA, Schoepfer J, Jahnke W, Cowan-Jacob SW, Loo A, Furet P, et al. The allosteric inhibitor ABL001 enables dual targeting of BCR-ABL1. Nature. 2017;543:733–7.
3. Hochhaus A, Rea D, Boquimpani C, Minami Y, Cortes JE, Hughes TP, et al. Asciminib vs bosutinib in chronic-phase chronic myeloid leukemia previously treated with at least two tyrosine kinase inhibitors: longer-term follow-up of ASCEMBL. Leukemia. 2023;37:617–26.
4. Eide CA, Zabriskie MS, Savage Stevens SL, Antelope O, Vellore NA, Than H, et al. Combining the Allosteric Inhibitor Asciminib with Ponatinib Suppresses Emergence of and Restores Efficacy against Highly Resistant BCR-ABL1 Mutants. Cancer Cell. 2019;36:431–43.e435. online ahead of print.
5. Leyte-Vidal A, Garrido Ruiz D, DeFilippis R, Leske IB, Rea D, Phan S, et al. BCR::ABL1 Kinase N-lobe mutants confer moderate to high degrees of resistance to asciminib. Blood. 2024.
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