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. Author manuscript; available in PMC: 2015 Dec 1.
Published in final edited form as: Curr Treat Options Oncol. 2014 Dec;15(4):581–594. doi: 10.1007/s11864-014-0306-4

Figure 1. Overview of Dominant Oncogenic Pathways.

Figure 1

Panel A: WNT pathway. The extracellular ligand WNT binds to the receptor Frizzled (FRZ), leading to inhibition of the GSK3β, AXIN and APC mediated phosphorylation and degradation of betacatenin in the cytoplasm. Free beta-catenin can then translocate to the nucleus where it activates expression of pro-proliferative genes, including CYCLIN D1 and MYC.

Panel B: SHH pathway. In canonical Hedgehog signaling, SHHbinds to its receptor PTCH, relieving PTCH inhibition of SMO. This allows SMO to initiate activation of GLI2, which can then translocate to the nucleus and drive transcription of target genes, such as GLI1.

Panel C: MYC pathway. Signaling through receptor tyrosine kinases, enhanced WNT pathway activation, and gene amplification all lead to increased levels of MYC. MYC protein translocates to the nucleus, where it heterodimerizes with the E-box protein MAX.