Enasidenib-induced differentiation promotes sensitivity to venetoclax in IDH2-mutated acute myeloid leukemia

Leukemia. 2022 Mar;36(3):869-872. doi: 10.1038/s41375-021-01468-y. Epub 2021 Nov 6.

Authors

Affiliations

¹ Princess Margaret Cancer Centre, University Health Network, Toronto, ON, Canada.
² Oncology Discovery, AbbVie Inc., North Chicago, IL, USA.
³ Oncology Development, AbbVie Inc., North Chicago, IL, USA.
⁴ Bristol Myers Squibb, Summit, NJ, USA.
⁵ Agios Pharmaceuticals, Inc., Cambridge, MA, USA.
⁶ Princess Margaret Cancer Centre, University Health Network, Toronto, ON, Canada. steven.chan@uhnresearch.ca.

PMID: 34743189
DOI: 10.1038/s41375-021-01468-y

No abstract available

Publication types

Letter

MeSH terms

Aminopyridines / pharmacology*
Aminopyridines / therapeutic use
Animals
Antineoplastic Agents / pharmacology*
Antineoplastic Agents / therapeutic use
Bridged Bicyclo Compounds, Heterocyclic / pharmacology*
Bridged Bicyclo Compounds, Heterocyclic / therapeutic use
Cell Line, Tumor
Enzyme Inhibitors / pharmacology*
Enzyme Inhibitors / therapeutic use
Humans
Isocitrate Dehydrogenase / antagonists & inhibitors
Isocitrate Dehydrogenase / genetics*
Leukemia, Myeloid, Acute / drug therapy*
Leukemia, Myeloid, Acute / genetics
Mutation / drug effects
Sulfonamides / pharmacology*
Sulfonamides / therapeutic use
Triazines / pharmacology*
Triazines / therapeutic use

Substances

Aminopyridines
Antineoplastic Agents
Bridged Bicyclo Compounds, Heterocyclic
Enzyme Inhibitors
Sulfonamides
Triazines
enasidenib
IDH2 protein, human
Isocitrate Dehydrogenase
venetoclax