Up‐regulation of L1CAM is linked to loss of hormone receptors and E‐cadherin in aggressive subtypes of endometrial carcinomas

• DOI: 10.1002/path.2673
• Publication Date: 2009-12-11T15:00:11Z
• Authors: Monica Huszar; Marco Pfeifer; Uwe Schirmer; Helena Kiefel; Gottfried E Konecny; Alon Ben‐Arie; Lutz Edler; Maria Münch; Elisabeth Müller‐...; Susanne Jerabek‐K...; Samira Abdel‐Azim; Christian Marth; Alain G Zeimet; Peter Altevogt; Mina Fogel
• Keywords: L1

Endometrial carcinomas (ECs) are classified into type 1 (less aggressive) and 2 (aggressive) tumours that differ in genetic alterations. So far, reliable immunohistochemical markers can identify patients with high risk for recurrence rare. We have defined the expression of L1 cell adhesion molecule (L1CAM), a biomarker previously identified EC, compared its to oestrogen receptor (ER)/progesterone (PR) E-cadherin. found L1CAM was absent normal endometrium vast majority endometrioid ECs (type 1) but strongly expressed serous clear-cell ECs, considered as 2. 78/272 cases were L1CAM-positive correlated poor prognosis. Strikingly, we observed an inverse relationship between ER/PR/E-cadherin all ECs. In mixed composed (L1CAM(-) ER/PR(+) E-cadherin(+)) clear-cell/serous (L1CAM(+) ER/PR(-) E-cadherin(-)), both phenotypes co-expressed. some these up-regulated at leading edge tumour, where ER/PR E-cadherin selectively lost. EC lines treated epithelial-mesenchymal transition (EMT) inducer TGFbeta1, vimentin up-regulated, while reduced. The treatment also resulted increased EMT transcription factor Slug enhanced invasion. Depletion by siRNA knockdown prevented up-regulation According our analysis, suggest is novel marker L1CAM-typing could 2-like features recurrence.