Cell signaling pathways as molecular targets to eliminate AML stem cells

• Published in: Critical reviews in oncology/hematology Vol. 160; p. 103277
• Main Authors: Rodrigues, Ana Carolina B. da C., Costa, Rafaela G.A., Silva, Suellen L.R., Dias, Ingrid R.S.B., Dias, Rosane B., Bezerra, Daniel P.
• Format: Journal Article
• Language: English
• Published: Netherlands Elsevier B.V 01.04.2021
• Subjects: Acute myeloid leukemia; Cell signaling; Humans; Leukemia, Myeloid, Acute - drug therapy; Leukemia, Myeloid, Acute - genetics; Leukemic stem cells; Neoplastic Stem Cells - metabolism; NF-kappa B - metabolism; Phosphatidylinositol 3-Kinases; Signal Transduction; Target therapy; LTC-IC; IRS1; RANK; IL-1R; [PtdIns (3,4,5)P3] (PIP3); AP-1; PLZF; TNF; Frz; PI3K; PPAR; GSK3; IGFR-1; PPRE; R-SMAD; CK1α; VPS34; MUC1-C; IL; TKIs; GMP; Ara-C; RUNX1; BCR; BAFFR; LPA; PDK-1; DMAPT; ERK; DNMT1; FDA; BM; LTβR; β-TRCP; SCID; Cell signaling; GPCRs; Leukemic stem cells; PDGFR; miRNA; Wnt; BMP; TNFSF13; IKK; STAT; LSCs; TBL1; RHEB; ITD; ATM; ETO; FLT3; JNK; TGFs; PTEN; MLL; NF-κB; PYGO; mTOR; RARa; VEGFR; AMH; MDS; AML; NOD; HSP; TSC; DNMT3A; IGF-1; GDFs; TYK2; I-SMADs; TCF; ROS; PCP; PI-103; Acute myeloid leukemia; [PtdIns (4,5)P2] (PIP2); TCR; Target therapy; A-PACs; XIAP; RXR; Raptor; Co-SMAD; TLR; IFNs; CEBPa; TNFR; PDX; VEGF; siRNA; LEF; TSGs; LICs; PML; NIK; APC; JAK; PH; HSCs; DVL
• ISSN: 1040-8428; 1879-0461
• DOI: 10.1016/j.critrevonc.2021.103277

•Acute myeloid leukemia remains the most lethal of leukemias.•Leukemic stem cells are associated with disease relapses.•Cell signaling pathways are targets to eliminate AML stem cells. Acute myeloid leukemia (AML) remains the most lethal of leukemias and a small population of cells called leukemic stem cells (LSCs) has been associated with disease relapses. Some cell signaling pathways play an important role in AML survival, proliferation and self-renewal properties and are abnormally activated or suppressed in LSCs. This includes the NF-κB, Wnt/β-catenin, Hedgehog, Notch, EGFR, JAK/STAT, PI3K/AKT/mTOR, TGF/SMAD and PPAR pathways. This review aimed to discuss these pathways as molecular targets for eliminating AML LSCs. Herein, inhibitors/activators of these pathways were summarized as a potential new anti-AML therapy capable of eliminating LSCs to guide future researches. The clinical use of cell signaling pathways data can be useful to enhance the anti-AML therapy.