Abstract
The epithelial cell adhesion molecule (EpCAM) is a type I glycoprotein located on the surface of epithelial cells. It is strongly expressed in many neoplasms and already used in the diagnosis and distinction of various tumour subtypes. Comparative studies about EpCAM expression in cystic sellar lesions are lacking. Therefore, we analysed its distribution pattern in adamantinomatous (aCP) and papillary (pCP) craniopharyngiomas (CP) and Rathke’s Cleft Cysts (RCC) using immunohistochemistry and gene expression profiling. Whereas the protein was not detectable in pCP (n = 10), all aCP (n = 64) showed distinct staining patterns. The vast majority of RCC (n = 10) also appeared positive, but these displayed notably lower labeling scores. Additionally, significantly higher mRNA levels were detectable in aCP (n = 19) when compared to pCP (n = 10) (p = 9.985−8). Furthermore, pediatric aCP cases, in general, exhibited stronger EpCAM staining levels compared to adult ones (p = 0.015). However, we were not able to verify this result on mRNA level. In summary, our findings demonstrate that EpCAM can be used as an additional distinction-marker for cystic lesions of the sellar region. Its unknown function in aCP and the presence of an approved monoclonal bispecific trifunctional antibody for cancer therapy are interesting starting points for further studies.
Highlights
EpCAM staining was detectable in all adamantinomatous CP (aCP) tumour samples (Fig. 1a,b), no specific immunoreaction was visible in the group of papillary CP (pCP) (Fig. 1c,d)
Monoclonal antibodies against epithelial cell adhesion molecules (EpCAM, CD326) were introduced in the late 1970’s33, representing the first molecular markers for colorectal cancer
EpCAM turned out to be a well-established and widely used diagnostic tool for human carcinomas[34,35,36,37]. Today it is frequently utilised as a differentiation marker for non-epithelial and epithelial derived neoplasms and it has been identified as a potential targed for cancer therapies since appropriate anti-EpCAM-antibodies (e.g. Adecatumumab and Catumaxomab) are available[32,42]
Summary
Activated Wnt signaling[23,24,25,26], as well as SHH and EGFR pathways have been suggested to play pivotal roles in aCP8,27, whereas the activation of the MAPK pathway seems to be essential for pCP28 These findings serve for pathological differentiation, but they represent potential targets for future therapy[29,30]. EpCAM mediates cell-cell contacts and weakens E-cadherin adhesions via the PI3 kinase pathway[39,42,43] It further acts as a signaling molecule by regulated intramembrane cleavage and nuclear translocation, initiating the transcription of Wnt target genes like c-myc or cyclin-D144–46, and influences renewal of epithelial cells by inhibition of TGF-β41. As it is known to be a helpful marker in the distinction of various tumour entities[42,47], we aimed to precisely describe EpCAM expression in a representative number of aCP, pCP and RCC specimens
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