Expression of sonic hedgehog (SHH) pathway components is enriched in adamantinomatous craniopharyngiomas (ACPs) arising in Hesx1Cre/+;Ctnnb1lox(ex3)/+ mice compared to control pituitaries. An MRI-embedded trial of smoothened inhibitor vismodegib in this genetically-engineered mouse model was undertaken to assess SHH pathway inhibition in ACP. Longitudinal MRI identified accelerated solid tumour growth in response to 28 days vismodegib treatment, which was associated with increased tumour cell proliferation, and resulted in shorter survival. 7 days of treatment induced early tumoural lesions in Hesx1Cre/+;Ctnnb1lox(ex3)/+ pituitaries, resulted in a more undifferentiated and proliferative phenotype, and was associated with an elevated number of cells with clonogenic potential.
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