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Nat. Rev. Endocrinol. doi:10.1038/nrendo.2016.217 Figure 1 Molecular pathways involved in human adamantinomatous craniopharyngioma Figure 1 | Molecular pathways involved in human adamantinomatous craniopharyngioma. A schematic representation of the major genes and deregulated pathways in adamantinomatous craniopharyngioma that result from activating mutations in β-catenin (which is encoded by CTNNB1) is shown. Most, if not all, adamantinomatous craniopharyngioma tumours harbour mutations in CTNNB1, which directly result in overactivation of the WNT–β-catenin pathway. Overactivation of this pathway is evidenced by the expression of target genes such as AXIN2 and lymphoid enhancer-binding factor 1 (LEF1). As a result of this initial oncogenic hit (defined as the driver mutation), several further genes and pathways become deregulated, which probably affect multiple biological processes such as cell proliferation, survival, differentiation, inflammation, angiogenesis, adhesion and tumour infiltration, among others. The colour code indicates the potential involvement of the deregulated pathways in these biological processes, as deduced from other cellular and/or tumoural contexts. This assessment is not exclusive, as many pathways might be involved either directly or indirectly in several, or all, processes that are indicated. Knowing whether inhibition or stimulation of some of these pathways might be of therapeutic use requires robust preclinical data to confirm their pathogenic effects. AREG, amphiregulin; BMP, bone morphogenetic protein; CXCL12, C-X-C motif chemokine ligand 12; CXCR4, C-X-C chemokine receptor type 4; EGF, epidermal growth factor; EGFR, EGF receptor; FGF, fibroblast growth factor; IL-2Rβ, interleukin-2 receptor, beta chain; MMP9, matrix metalloproteinase 9; PTCH1, protein patched homologue 1; PTGS2, prostaglandin- endoperoxide synthase 2; SHH, sonic hedgehog. Müller, H. L. et al. (2017) New outlook on the diagnosis, treatment and follow‑up of childhood-onset craniopharyngioma Nat. Rev. Endocrinol. doi:10.1038/nrendo.2016.217