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STAT5 is the messenger that carries growth signals from FLT3, JAK2 and BCR::ABL1 into the nucleus and switches on survival genes in leukaemia cells. No drug hits STAT5 directly yet; the FLT3 and ABL inhibitors work by cutting off the signal above it.
STAT5A and STAT5B (both on chromosome 17q21.2) are transcription factors with a dual role in signal transduction and transcription: they bind GAS elements and activate prolactin-induced transcription; STAT5A mediates responses to KIT ligand, other growth factors, ERBB4 and possibly activated FGFRs, and STAT5B mediates responses to cytokines, hormones and growth factors including oncostatin M and positively regulates haematopoietic and erythroid differentiation (UniProt P42229, P51692). In OnCo, STAT5 is the downstream node that collapses when gilteritinib, midostaurin and quizartinib block FLT3-ITD and TKD signalling in AML and when ponatinib blocks BCR::ABL1 in Ph-positive leukaemia; the MPL record places it among the proteins docked by the activated thrombopoietin receptor.
In plain words · STAT5 is the messenger that carries growth signals from FLT3, JAK2 and BCR::ABL1 into the nucleus and switches on survival genes in leukaemia cells. No drug hits STAT5 directly yet; the FLT3 and ABL inhibitors work by cutting off the signal above it.
STAT5 is the messenger that carries growth signals from FLT3, JAK2 and BCR::ABL1 into the nucleus and switches on survival genes in leukaemia cells. No drug hits STAT5 directly yet; the FLT3 and ABL inhibitors work by cutting off the signal above it.
The JAK-STAT pathway record lists STAT5 as the STAT of leukaemias, alongside STAT3 as the hub of IL-6-driven survival.
No product in this corpus aims at STAT5 (STAT5A, STAT5B) yet. Transcription factors have no pocket to plug, so drugs either degrade them or block the partner protein they need to dock on DNA.
The JAK-STAT pathway record lists STAT5 as the STAT of leukaemias, alongside STAT3 as the hub of IL-6-driven survival. Constitutive STAT5 signalling is the readout of FLT3, JAK2, MPL and BCR::ABL1 activity in the corpus mechanism steps, and no direct STAT5 inhibitor is recorded.
Query for this target: (TITLE:"STAT5" OR ABSTRACT:"STAT5" OR TITLE:"STAT5A, STAT5B" OR ABSTRACT:"STAT5A, STAT5B" OR TITLE:"STAT5A" OR ABSTRACT:"STAT5A" OR TITLE:"STAT5B" OR ABSTRACT:"STAT5B" OR TITLE:"signal transducer and activator of transcription 5" OR ABSTRACT:"signal transducer and activator of transcription 5") AND (cancer OR tumor OR tumour OR oncology OR carcinoma OR lymphoma OR leukemia OR leukaemia OR myeloma OR sarcoma OR melanoma OR glioma). Results are unfiltered search hits about STAT5 (STAT5A, STAT5B), not a curated reading list.
Shares BCR::ABL1 (Philadelphia chromosome), Ponatinib, Chronic myeloid leukaemia (KEGG map), Chronic myeloid leukaemia, accelerated and blast phase and the tag wave5-target.
Shares JAK-STAT signalling, JAK2, Sezary syndrome, Peripheral T-cell lymphomas (including cutaneous T-cell lymphoma) and the tag wave5-target.
Shares Acute myeloid leukaemia (KEGG map), Acute lymphoblastic leukaemia, Acute myeloid leukaemia and the tag wave5-target.
Shares JAK-STAT signalling, JAK2 and the tag wave5-target.
Shares Acute myeloid leukaemia (KEGG map), Acute lymphoblastic leukaemia, Acute myeloid leukaemia and the tag wave5-target.
Shares Peripheral T-cell lymphomas (including cutaneous T-cell lymphoma), Acute myeloid leukaemia, Non-Hodgkin lymphoma (all types) and the tag wave5-target.
Shares Acute myeloid leukaemia, Non-Hodgkin lymphoma (all types) and the tag wave5-target.
Shares Peripheral T-cell lymphomas (including cutaneous T-cell lymphoma), Non-Hodgkin lymphoma (all types) and the tag wave5-target.