Beta-catenin mutations are not observed in chronic myeloid leukemia.

Sercan Z., Pehlivan M., Gokturk D., Sercan H. O.

Tumori, vol.95, no.6, pp.836-9, 2009 (SCI-Expanded) identifier identifier identifier

  • Publication Type: Article / Article
  • Volume: 95 Issue: 6
  • Publication Date: 2009
  • Doi Number: 10.1177/030089160909500633
  • Journal Name: Tumori
  • Journal Indexes: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Page Numbers: pp.836-9
  • Keywords: beta-catenin, chronic myeloid leukemia, Wnt signaling, BCR-ABL, STEM-CELLS, WNT, PATHWAYS, RENEWAL, CML, BCR
  • Dokuz Eylül University Affiliated: Yes

Abstract

Aims and background. 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