Rationale for a Combination Therapy with the STAT5 Inhibitor AC-4-130 and the MCL1 Inhibitor S63845 in the Treatment of FLT3-Mutated or TET2-Mutated Acute Myeloid Leukemia

Rationale for a Combination Therapy with the STAT5 Inhibitor AC-4-130 and the MCL1 Inhibitor S63845 in the Treatment of FLT3-Mutated or TET2-Mutated Acute Myeloid Leukemia

The FMS-like tyrosine kinase 3 (<i>FLT3</i>) gene is mutated in one-third of patients with de novo acute myeloid leukemia (AML). Mutated FLT3 variants are constitutively active kinases signaling via AKT kinase, MAP kinases, and STAT5. FLT3 inhibitors have been approved for the treatment...

Full description

Bibliographic Details
Main Authors: Katja Seipel, Carolyn Graber, Laura Flückiger, Ulrike Bacher, Thomas Pabst
Format: Article
Language:English
Published: MDPI AG 2021-07-01
Series:International Journal of Molecular Sciences
Subjects:
acute myeloid leukemia (AML)
hematological malignancies
FMS-like tyrosine kinase 3 (FLT3)
signal transducer and activator of transcription 5 (STAT5)
ten-eleven translocation-2 (TET2)
tumor suppressor p53 (TP53)
Online Access:https://www.mdpi.com/1422-0067/22/15/8092

Internet

https://www.mdpi.com/1422-0067/22/15/8092

Similar Items