Supplementary Material for: Differential Expression of Stem Cell Markers in Human Adamantinomatous Craniopharyngioma and Pituitary Adenoma C.V.Chang R.V.Araujo C.S.Cirqueira C.M.G.Cani H.Matushita V.A.S.Cescato M.C.B.V.Fragoso M.D.Bronstein M.C.N.Zerbini B.B.Mendonca 2016 <b><i>Background/Aims:</i></b> Although craniopharyngioma (CP) is histologically benign, it is a pituitary tumour that grows rapidly and often recurs. Adamantinomatous CP (ACP) was associated with an activating mutation in β-catenin, and it has been postulated that pituitary stem cells might play a role in oncogenesis in human ACP. Stem cells have also been identified in pituitary adenoma. Our aim was to characterize the expression pattern of <i>ABCG2</i>, <i>CD44, DLL4, NANOG, NOTCH2, POU5F1/OCT4, SOX2, </i>and <i>SOX9</i> stem cell markers in human ACP and pituitary adenoma. <b><i>Methods and Results:</i></b> We studied 33 patients (9 ACP and 24 adenoma) using real-time quantitative PCR (RT-qPCR) and immunohistochemistry. <i>SOX9 </i>was up-regulated in ACP, exhibiting positive immunostaining in the epithelium and stroma, with the highest expression in patients with recurrence. <i>CD44</i> was overexpressed in ACP as confirmed by immunohistochemistry. <i>SOX2</i> did not significantly differ among the tumour types. The RT-qPCR array showed an increased expression of <i>MKI67,</i><i>OCT4</i>/<i>POU5F1,</i> and <i>DLL4 </i>in all tumours. <i>NANOG </i>was decreased in ACP. <i>ABCG2</i> was down-regulated in most of the tumours. <i>NOTCH2 </i>was significantly decreased in the adenomas. <b><i>Conclusion:</i></b> Our results confirm the presence of stem cell markers in human pituitary tumours as well as the different expression patterns of ACP and adenoma. These findings suggest that ACP may originate from a more undifferentiated cell cluster. Additionally, <i>SOX9</i> immunodetection in the stroma and the highest expression levels related to the relapse of patients suggest a contribution to the aggressive behaviour and high recurrence of this tumour type.