Abstract
Background: Activated leukocyte cell adhesion molecule (ALCAM/CD166) is a member of the immunoglobulin superfamily that contributes to cell migration. The present study investigated the potential role of ALCAM in the transition from normal endometrium to endometrioid adenocarcinoma (EEC). Methods: To clarify the role of ALCAM in endometrial tumorigenesis, we determined the levels of protein and messenger RNA expression of ALCAM in human endometrial tissue (proliferative phase [n = 20], secretory phase [n = 20], simple hyperplasia [n = 15], complex hyperplasia [n = 12], atypical hyperplasia [AH, n = 14], EEC [n = 42]) using immunohistochemistry, Western blot, and semiquantitative reverse transcriptionYpolymerase chain reaction, respectively. Results: Expression of ALCAM detected by immunohistochemistry showed a gradual increase from normal endometrium to atypical hyperplasia in a membranous pattern; in addition, cytoplasmic staining emerged in a few cases of simple hyperplasia and complex hyperplasia, which also showed an increasing tendency. Most cases of EEC showed a homogenously strong staining in all parts of the tumor; other cases showed either membranous or cytoplasmic strong staining; heterogeneous loss of membranous staining was also found in some cases. Similar results of ALCAM expression were detected by reverse transcription-polymerase chain reaction and Western blot. In EEC, ALCAM expression was significantly increased in high-grade tumors and cases with myometrial invasion; however, no correlation was found between ALCAM expression and surgical pathological stages. Conclusions: The up-regulation of ALCAM expression during endometrial carcinogenesis and the correlations of ALCAM expression with grade and myometrial invasion suggest its potential role as a diagnostic and prognostic biomarker. Copyright © 2011 by IGCS and ESGO.
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Liang, S., Huang, C., Jia, S., & Wang, B. (2011). Activated leukocyte cell adhesion molecule expression is up-regulated in the development of endometrioid carcinoma. International Journal of Gynecological Cancer, 21(3), 523–528. https://doi.org/10.1097/IGC.0b013e31820e135a
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