Association of clinicopathological features with E-cadherin (CDH1) gene-160 C>A promoter polymorphism in Turkish colorectal cancer patients
Anzel Bahadir1, Gokalp Eral2, Metin Budak3, Fumio Shimamoto4, Mehmet Ali Korpinar5, Sibel Erdamar6, Handan Tuncel5
1 Department of Biophysics, Faculty of Medicine, Duzce University, Duzce, Turkey
2 Department of Biostatistics, Cerrahpasa Medical Faculty, Istanbul University, Istanbul, Turkey
3 Department of Biophysics, Cerrahpasa Medical Faculty, Istanbul University, Istanbul; Department of Biophysics, Faculty of Medicine, Trakya University, Edirne, Turkey
4 Department of Human Sciences, Hiroshima Shudo University, Hiroshima, Japan
5 Department of Biophysics, Cerrahpasa Medical Faculty, Istanbul University, Istanbul, Turkey
6 Department of Pathology, Cerrahpasa Medical Faculty, Istanbul University, Istanbul, Turkey
Department of Biophysics, Cerrahpasa Medical Faculty, Istanbul University, Istanbul 34303
Source of Support: None, Conflict of Interest: None
Background and Aim of Study: The role of E-cadherin (CDH1) gene-160 C>A (rs16260) promoter polymorphism in colorectal cancer (CRC) still remains inconclusive. The aim of this study is to investigate the associations between the CDH1-160 C>A polymorphism with the susceptibility and clinicopathological development of CRC in the Turkish patients. To our knowledge, this is the first report examining the role of CDH1 polymorphism in Turkish CRC patients.
Materials and Methods: A total of 92 colorectal carcinoma cases (including 62 colon and 30 rectal cancer patients) and the corresponding adjacent normal tissues as controls were studied. The polymorphism was genotyped using polymerase chain reaction-restriction fragment length polymorphism analysis. Clinicopathological features including patient's age, gender, tumor stage, and tumor location (colon/rectum) were compared statistically with the polymorphism status.
Results: There was no significant difference in both genotype and allele frequencies of the CDH1 polymorphism between colorectal tumor cases and normal samples (P = 0.472 and 0.508, respectively). Furthermore, no significant associations were observed between the CDH1 polymorphism status and age, gender, tumor stage, and tumor location of the colorectal tumor cases (all P > 0.05).
Conclusions: These results indicate that CDH1-160 C>A polymorphism does not contribute to the genetic susceptibility of CRC and the polymorphism may not be a direct effect on the progression of the disease in Turkish CRC patients.