Beta-catenin mutations are not observed in chronic myeloid leukemia.
OBJECTIVE
Studies reporting activated Wnt signaling in all stages of chronic myeloid leukemia (CML) have demonstrated that deregulation of the pathway plays a role in the pathogenesis of this disease. Several reports have suggested mechanisms for the deregulated Wnt signaling and beta-catenin stabilization observed in CML. One possible mechanism for beta-catenin stabilization could be the acquisition of mutations at its N-terminal domain, especially in the third exon where it is marked via phosphorylation for degradation. We sought to determine whether mutations in the third exon of the beta-catenin gene are responsible for the observed Wnt activation in CML.


METHODS
We screened bone marrow specimens from 33 patients with CML in the chronic phase and also examined the K562 cell line for beta-catenin mutations.


RESULTS
None of the patients nor the K562 cell line were found to carry mutations.


CONCLUSIONS
Beta-catenin amino-terminal mutations are not observed or very rare and therefore are not the underlying mechanism of activated Wnt signaling in CML.
Sercan
Zeynep
Z
Department of Medical Biology and Genetics, Dokuz Eylul University Faculty of Medicine, Izmir, Turkey.
Pehlivan
Melek
M
Gokturk
Dilek
D
Sercan
Hakki Ogun
HO
D001853:Bone Marrow / Q000378:metabolism; D015972:Gene Expression Regulation, Neoplastic; D006801:Humans; D020014:K562 Cells; D015464:Leukemia, Myelogenous, Chronic, BCR-ABL Positive / Q000235:genetics* / Q000378:metabolism; D009154:Mutation; D010766:Phosphorylation; D016133:Polymerase Chain Reaction; D015398:Signal Transduction; D051153:Wnt Proteins / Q000378:metabolism*; D051176:beta Catenin / Q000235:genetics*
D051153:Wnt Proteins; D051176:beta Catenin