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. Author manuscript; available in PMC: 2020 Aug 1.
Published in final edited form as: Br J Haematol. 2019 Jun 24;186(4):524–537. doi: 10.1111/bjh.16074

Figure 2. Pathways commonly associated with survival of LSCs from AML, CML, and MDS patients.

Figure 2.

The illustration summarizes some of the major pathways commonly activated in LSCs, including WNT/β-catenin, NF-κB, Sonic hedgehog (SHH), Notch, and oxidative phosphorylation (OXPHOS), which is facilitated by upregulation of the anti-apoptotic protein, BCL-2. All of these pathways can be activated through various mechanisms. To date, the leading commonality among stem cells from each disease is a reliance on OXPHOS. AML, acute myeloid leukaemia; APC, adenomatous polyposis; β-Cat, beta-catenin; BAK, BCL2 homologous antagonist killer; BAX, BCL2-associated X protein; BCL2, B-cell lymphoma 2; CBF1, core binding factor 1;CML, chronic myeloid leukaemia; Cyt C, cytochrome c; DVL, dishevelled; FZD, frizzled; GLI1, glioma-associated oncogene homolog 1; GSK3β, Glycogen Synthase Kinase 3 Beta; IκBα, nuclear factor-kappa B inhibitor alpha; LEF, lymphoid enhancer-binding factor; LRP5/6, low density lipoprotein receptor-related protein 5/6; LSC, leukaemic stem cell;MDS, myelodysplastic syndrome; SMO, smoothened; NF-κB, nuclear factor kappa B; NICD, notch intracellular domain, OXPHOS, oxidative phosphorylation; PTCH, patched; SHH, sonic hedgehog; STCF, T-cell factor; TNFR, tumour necrosis factor receptor; Ub, ubiquitin.