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ORIGINAL ARTICLE
Year : 2020  |  Volume : 45  |  Issue : 2  |  Page : 105-110

β-catenin mutations in acute myeloid leukemia


1 Vocational School of Health Services; Department of Medical Biology, Faculty of Medicine, Ankara University, Ankara, Turkey
2 Department of Medical Biology, Faculty of Medicine, Ankara University, Ankara, Turkey
3 Department of Medical Biology, Faculty of Medicine, Ankara University, Ankara; Departmentof Medical Biology, Faculty of Medicine, Usak University, Usak, Turkey, Turkey
4 Department of Hematology, Faculty of Medicine, Ankara University, Ankara, Turkey

Correspondence Address:
Buket A Gunes
Department of Medical Biology, Faculty of Medicine, Vocational School of Health Services, Ankara University, Ankara 06290
Turkey
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/ejh.ejh_54_19

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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/β-catenin are disrupted in AML. Stabilization of β-catenin, the key point of activated Wnt/β-catenin pathway, has been shown in AML in various studies. One of the mechanisms that may lead to the β-catenin stabilization is the mutations in exon 3 at its N-terminal domain, where β-catenin is phosphorylated particularly during the degradation process, and these mutations have been investigated in chronic myeloid leukemia and many other cancer types. Aim β-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 β-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 β-catenin gene exon 3 mutations were detected in patients with AML and the cell line. Conclusion β-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 β-catenin stabilization in AML.


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