| Beta-catenin mutations are not observed in chronic myeloid leukemia. | |
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MedLine Citation:
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PMID: 20210255 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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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. MATERIAL AND 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. CONCLUSION: Beta-catenin amino-terminal mutations are not observed or very rare and therefore are not the underlying mechanism of activated Wnt signaling in CML. |
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Authors:
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Zeynep Sercan; Melek Pehlivan; Dilek Gokturk; Hakki Ogun Sercan |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: Tumori Volume: 95 ISSN: 0300-8916 ISO Abbreviation: Tumori Publication Date: 2009 Nov-Dec |
Date Detail:
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Created Date: 2010-03-08 Completed Date: 2010-03-19 Revised Date: 2010-04-23 |
Medline Journal Info:
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Nlm Unique ID: 0111356 Medline TA: Tumori Country: Italy |
Other Details:
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Languages: eng Pagination: 836-9 Citation Subset: IM |
Affiliation:
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Department of Medical Biology and Genetics, Dokuz Eylul University Faculty of Medicine, Izmir, Turkey. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Bone Marrow
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metabolism Gene Expression Regulation, Neoplastic Humans K562 Cells Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics*, metabolism Mutation* Phosphorylation Polymerase Chain Reaction Signal Transduction Wnt Proteins / metabolism* beta Catenin / genetics* |
| Chemical | |
Reg. No./Substance:
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0/Wnt Proteins; 0/beta Catenin |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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