Abstract
Mutated JAK3 has been considered a promising target for cancer therapy. Activating mutations of JAK3 are observed in 3.9%–10% of acute myeloid leukemia (AML) patients, but it is unclear whether AML cells are sensitive to JAK3 inhibitors, and no disease-related human AML cell model has been reported. We have identified U937 as the first human AML cell line expressing the JAK3M511I activated mutation and confirmed that JAK3 inhibitors sensitively suppress the proliferation of U937 AML cells.
Highlights
IntroductionJAK3 is different from the other members of the family including JAK1, JAK2, and Tyk
JAK3 belongs to the Janus non-receptor tyrosine kinase (JAK) family
We evaluated the antiproliferative activity of the JAK inhibitors against a panel of hematological malignancy cells including U937, MOLT-4, OCI-LY3, Jurkat, Daudi, HL-60, and MV4-11
Summary
JAK3 is different from the other members of the family including JAK1, JAK2, and Tyk. JAK3 is different from the other members of the family including JAK1, JAK2, and Tyk2 It is exclusively expressed in the hematopoietic compartment and interacts with the common g chain of several interleukin receptors where it mediates the development and functions of T cells, B cells, and natural killer (NK) cells. Activated mutations of JAK3 have been found in a variety of hematopoietic malignancies, including acute myeloid leukemia (AML), T-cell acute lymphoblastic leukemia (T-ALL), and T-cell prolymphocytic leukemia (T-PLL) [1–3]. JAK3 mutations account for 3.9%–10% of AML patients [4, 5]. 10%–16% of T-ALL patients carry at least one type of JAK3 mutation, and JAK3M511I is the most frequently detected mutation [6]
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