Akademik Veri Yönetim Sistemi
EGYPTIAN JOURNAL OF HAEMATOLOGY, cilt.45, sa.2, ss.105-110, 2020 (ESCI)
Background Acute myeloid leukemia (AML) is a hematopoietic stem cell disorder characterized by uncontrolled proliferation and impaired differentiation of normal hematopoietic stem or progenitor cells. Various pathways like RAF/MEK/ERK, PI3K/AKT, receptor tyrosine kinases, members of RAS family, and Wnt/beta-catenin are disrupted in AML. Stabilization of beta-catenin, the key point of activated Wnt/beta-catenin pathway, has been shown in AML in various studies. One of the mechanisms that may lead to the beta-catenin stabilization is the mutations in exon 3 at its N-terminal domain, where beta-catenin is phosphorylated particularly during the degradation process, and these mutations have been investigated in chronic myeloid leukemia and many other cancer types. Aim beta-Catenin gene exon 3 mutations were analyzed in this study with the aim of determining the relationship between mutations and molecular biology of AML. Patients and methods In this study, we examined beta-catenin gene mutations in AML cell line U937 and 31 untreated patients with AML by using the DNA sequence analysis for the first time in a Turkish population. Results No beta-catenin gene exon 3 mutations were detected in patients with AML and the cell line. Conclusion beta-catenin mutations have been detected in various types of cancer; however, the authors did not find any mutation in this gene, which may be responsible for the activation of Wnt signaling in AML. Further research is required to understand the mechanisms apart from mutations that may induce beta-catenin stabilization in AML.