2). E-cadherin expression levels with the G-allele and GA-allele were compared between CRC patients and normal controls, as well as between Vandetanib poorly differentiated and well differentiated CRC patients (Figure (Figure3).3). E-cadherin expression was significantly higher in normal controls, well differentiated CRC patients and the G-allele CRC patients than in CRC patients (t-test, P < 0.001), poorly differentiated CRC patients (t-test, P = 0.001) and the GA-allele CRC patients (t-test, P = 0.018), however, there was no significant difference in E-cadherin expression between the G-allele and GA-allele in normal controls (t-test, P = 0.292). Figure 2 Immunohistochemical staining for E-cadherin. A,B: E-cadherin expression in normal colorectal tissue with the G-allele (A) and GA-allele (B) (each, �� 200); C,D: E-cadherin expression in well differentiated CRC with the GA-allele (C) and G-allele .

.. Figure 3 E-cadherin expression in colon tissues of different types. A: E-cadherin expression is significantly higher in normal controls than in CRC patients (t-test, P < 0.001); B: E-cadherin expression is significantly higher in well differentiated CRC ... DISCUSSION Several molecular epidemiological studies have confirmed an association between the CDH1 -347G��GA polymorphism and the risk of cancers, including gastric, colorectal and esophageal cancers[14,15]. The authors of these studies proposed that the CDH1 -347G��GA polymorphism may be functional, and that the GA-allele could lead to transcriptional downregulation of CDH1 and low expression of E-cadherin compared with the G-allele, thereby increasing the risk of cancer.

However, recent studies have indicated that some functional polymorphisms may play more important roles in the prognosis of cancer than in its formation[16,17]. To further investigate the association between the functional CDH1 -347G��GA polymorphism and sporadic CRC, we conducted the present case-control study in a Chinese population. We found that the GA-allele did not increase the risk of CRC compared with the G-allele in this Chinese population. This finding is not consistent with the study by Shin et al[18], who reported that the GA-allele was associated with a significantly increased risk of CRC in Korea. Furthermore, their GA-allele frequency in normal controls (41/147, 27.9%) was obviously lower than the frequency observed in the present study (141/335, 42.

1%). These discrepancies may be caused by racial differences. At the same time, we found that there was no significant difference in E-cadherin expression between the G-allele and GA-allele in normal controls, as evaluated by immunohistochemical staining. In other words, the GA-allele did not increase the risk of CRC Brefeldin_A or influence the expression of E-cadherin in normal controls.