期刊
BLOOD
卷 133, 期 21, 页码 2263-2268出版社
AMER SOC HEMATOLOGY
DOI: 10.1182/blood-2019-01-852392
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资金
- Leukemia & Lymphoma Society [6531-18, 8011-18]
- National Institutes of Health, National Cancer Institute [T32-CA09503, CA206501, CA210065]
- Alex Lemonade Stand Foundation
- Hyundai Hope On Wheels Scholar Award
Mutations in the cytosolic 59 nucleotidase II (NT5C2) gene drive resistance to thiopurine chemotherapy in relapsed acute lymphoblastic leukemia (ALL). Mechanistically, NT5C2 mutant proteins have increased nucleotidase activity as a result of altered activating and autoregulatory switch-off mechanisms. Leukemias with NT5C2 mutations are chemoresistant to 6-mercaptopurine yet show impaired proliferation and self-renewal. Direct targeting of NT5C2 or inhibition of compensatory pathways active in NT5C2 mutant cells may antagonize the emergence of NT5C2 mutant clones driving resistance and relapse in ALL.
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