## Abstract The extravasation of cancer cells is a key step of the metastatic cascade. Polymorphisms in genes encoding adhesion molecules can facilitate metastasis by increasing the strength of interaction between tumor and endothelial cells as well as impacting other properties of cancer cells. We
Analysis of E-Selectin S128R gene polymorphism in pancreatic cancer
✍ Scribed by George S. Panoussopoulos; George Theodoropoulos; Nikolaos V. Michalopoulos; Maria Gazouli; John Flessas; Stela Taka; Paraskevas Stamopoulos; Andreas Manouras; George C. Zografos
- Publisher
- John Wiley and Sons
- Year
- 2010
- Tongue
- English
- Weight
- 69 KB
- Volume
- 102
- Category
- Article
- ISSN
- 0022-4790
No coin nor oath required. For personal study only.
✦ Synopsis
Abstract
Background
E‐selectin, an intercellular adhesion molecule that plays important roles in metastasis of tumor cells, has a polymorphism in exon 4 that results in the substitution of a serine by an arginine within the extracellular domain of the receptor, which increases its affinity for ligands. No evidence exist on the role of E‐selectin polymorphism in pancreatic cancer.
Methods
Eighty pancreatic cancer patients and 160 cases of normal healthy control subjects were investigated for genotype and allelic frequencies of S128R polymorphism of E‐selectin gene by PCR–RFLPs.
Results
The frequencies for “AA,” “CA,” and “CC” genotypes were 46.25%, 50%, and 3.75% in patients, and 63.75%, 26.9%, and 9.4% in healthy subjects, respectively. The “C” carriers group of patients (“CA + CC” genotype) and the “C” allele were over‐represented among the pancreatic cancer cases (P = 0.012 and 0.096, respectively). Advanced T stage, the presence of lymph node and other adverse pathologic characteristics were not significantly correlated with either the “CA + CC” genotype group of patients or the presence of “C” allele.
Conclusions
E‐selectin S128R “C” allele may confer an increased susceptibility to pancreatic cancer development, while its carriage status does not appear to be related to the aggressive features of this malignancy. J. Surg. Oncol. 2010;102:604–607. © 2010 Wiley‐Liss, Inc.
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