L1 cell adhesion molecule (L1CAM) in stage IB cervical cancer: distinct expression in squamous cell carcinomas and adenocarcinomas.

AIMS: L1 cell adhesion molecule (L1CAM) has been shown to be correlated with tumour progression, attributed to its possible association with epithelial-mesenchymal transition (EMT), characterised by the expression of vimentin and loss of e-cadherin. Herein, we investigate the associations between L1CAM and clinicopathological parameters, as well as the expression of vimentin and e-cadherin, in carcinomas restricted to the cervix.

METHODS

The study was retrospective observational and included 45 squamous cell carcinomas (63.4%) and 26 adenocarcinomas (36.6%) submitted to primary surgical treatment. Patient age, FIGO (International Federation of Gynecology and Obstetrics) stage, tumour size and follow-up were obtained from the medical records. All the slides were revised to evaluate histological differentiation, lymphovascular space invasion, depth of infiltration, disease-free cervical wall thickness, pattern of invasion front, Silva pattern (for adenocarcinomas) and the percentage of tumour-infiltrating lymphocytes. Tissue microarrays were constructed for immunohistochemical staining for L1CAM, e-cadherin and vimentin.

RESULTS

Adenocarcinomas were associated with lower disease-free and overall survival. L1CAM and vimentin expressions were more frequent among adenocarcinomas, although loss of e-cadherin expression was more common among squamous carcinomas. L1CAM expression was associated with larger tumours, vimentin expression and lower disease-free survival. No association was observed between the expression of either L1CAM or vimentin and loss of e-cadherin. High levels of tumour-infiltrating lymphocytes were more frequent in squamous cell carcinoma, high-grade tumours, destructive pattern at front of invasion and loss of e-cadherin expression.

CONCLUSIONS

Our results confirm the prognostic role of L1CAM in cervical carcinomas, but suggest a role for mechanisms other than EMT.