Subset of Esophageal Adenocarcinoma Expresses Adhesion Molecule L1 in Contrast to Squamous Cell Carcinoma
Background: Esophageal adenocarcinoma is currently the most rapidly increasing cancer in Western populations. L1 (CD171), a neural cell adhesion molecule, has an essential function in tumor progression and has been shown to be expressed in the proliferating cells of the intestinal crypts in mice. Th...
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Published in | Anticancer research Vol. 29; no. 4; pp. 1195 - 1199 |
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Main Authors | , , , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
Attiki
International Institute of Anticancer Research
01.04.2009
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Subjects | |
Online Access | Get full text |
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Summary: | Background: Esophageal adenocarcinoma is currently the most rapidly increasing cancer in Western populations. L1 (CD171),
a neural cell adhesion molecule, has an essential function in tumor progression and has been shown to be expressed in the
proliferating cells of the intestinal crypts in mice. The aim of the current study was to determine L1 expression in esophageal
cancer and to evaluate whether L1 could serve as a potential marker and therapeutic target for this tumor type. Materials
and Methods: L1 expression was assessed on a tissue microarray with 257 surgically resected esophageal cancer samples by immunohistochemistry
with a monoclonal antibody (Clone UJ127). L1 expression was correlated with clinicopathological data. Results: L1 was detected
in 22 (9%) of 257 esophageal cases, whereas 235 (91%) were L1 negative. Nineteen (86%) of the 22 L1-positive cases were adenocarcinoma.
Cross table analysis showed a significant association between L1 expression and adenocarcinoma subtype (p<0.001), but not
squamous cell carcinoma. Conclusion: L1 expression in a subgroup of esophageal cancer is specifically prevalent in adenocarcinoma.
Data suggest L1 as a potential target for biological therapy in L1-positive esophageal adenocarcinoma patients. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0250-7005 1791-7530 |