JAK/STAT pathway mutations in T-ALL, including the STAT5B N642H mutation, are sensitive to JAK1/JAK3 inhibitors
I Govaerts, K Jacobs, R Vandepoel, J Cools - HemaSphere, 2019 - journals.lww.com
T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive malignancy of the lymphocytes
that is driven by the cooperation of various mutations. Constitutive activation of JAK-STAT
signaling is observed in one-third of T-ALL patients and is caused by activating mutations in
the interleukin 7 receptor alpha chain (IL7R), in the Janus kinases JAK1 or JAK3, or in the
Signal transducer and activator of transcription 5B (STAT5B). 1–3 STAT5B mutations are
most frequently the N642H variant and are associated with an unfavorable prognosis and …
that is driven by the cooperation of various mutations. Constitutive activation of JAK-STAT
signaling is observed in one-third of T-ALL patients and is caused by activating mutations in
the interleukin 7 receptor alpha chain (IL7R), in the Janus kinases JAK1 or JAK3, or in the
Signal transducer and activator of transcription 5B (STAT5B). 1–3 STAT5B mutations are
most frequently the N642H variant and are associated with an unfavorable prognosis and …
