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  • Küçük Resim Yok
    Öğe
    Association of clinicopathological features with E-cadherin (CDH1) gene-160 C>A promoter polymorphism in Turkish colorectal cancer patients
    (Wolters Kluwer Medknow Publications, 2019) Bahadir, Anzel; Eral, Gokalp; Budak, Metin; Shimamoto, Fumio; Korpinar, Mehmet Ali; Erdamar, Sibel; Tuncel, Handan
    Background and Aim of Study: The role of E-cadherin (CDH1) gene-160 C>A (rsl 6260) 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.
  • Küçük Resim Yok
    Öğe
    No mutation effect of 50 Hz sinusoidal magnetic field on beta catenin gene phosphorylation site in N-methyl-N-nitrosourea (MNU) induced colon tumor model
    (Natl Inst Science Communication-Niscair, 2023) Budak, Metin; Kilic, Mahmut Alp; Kalkan, Tunaya; Tuncel, Handan
    The dysregulation of beta-catenin, a key regulator of cadherin-mediated cell adhesion and crucial for embryonic development and adult tissue processes, has been implicated in various cancers, including colon cancer. Meanwhile, there have been longstanding concerns about the potential carcinogenic effects of magnetic fields. In this study, we investigated the possible relationship between beta-catenin dysfunction and 50 Hz sinusoidal magnetic fields (SMF) using an animal model of N-methyl-N-nitrosourea (MNU)-induced rat colon tumors. To assess beta-catenin phosphorylation, genomic DNA was extracted from 58 samples using a commercial extraction kit, and the target gene region corresponding to an important phosphorylation site of beta-catenin was amplified via polymerase chain reaction (PCR). The amplified samples were subsequently analyzed using the single-strand conformation polymorphism (SSCP) method to detect any differences between the experimental groups. Surprisingly, our results revealed no significant differences in beta-catenin gene phosphorylation sites among the groups. These findings suggest that 50 Hz SMF exposure may not directly impact beta-catenin dysfunction in the context of MNU-induced rat colon tumors. Implications of these results and avenues for further research are discussed.