Document Detail


Factors influencing a second myeloid malignancy in patients with Philadelphia-negative -7 or del(7q) clones during tyrosine kinase inhibitor therapy for chronic myeloid leukemia.
MedLine Citation:
PMID:  21356190     Owner:  NLM     Status:  In-Data-Review    
Abstract/OtherAbstract:
The detection of Philadelphia-negative (Ph(neg)) cells with non-random karyotypic abnormalities after tyrosine kinase inhibitor (TKI) therapy of chronic myeloid leukaemia (CML) can be associated with myelodysplastic syndrome (MDS) or acute myeloid leukemia (AML). To our knowledge, however, there have been no studies on variables influencing the risk of MDS/AML in patients with specific Ph(neg) karyotypes. We systematically examined studies reporting -7 or del(7q) within Ph(neg) cells in TKI-treated CML patients, and abstracted clinical and cytogenetic data from individual reports into a standardized format for further analysis. Of 53 patients, 43 had Ph(neg) -7 clones [as the sole abnormality (-7(sole)) in 29, or with other clones (-7(dual)) in 14], and del(7q) was present in 10. A total of 16/51 evaluable patients, all with -7, transformed to MDS/AML. Transformation was more frequent (15/16 patients) within 6 months of Ph(neg) -7 detection rather than subsequently (P < 0.0001). At first detection after TKI therapy, Ph(neg) abnormal clones comprised ≥50% of Ph(neg) cells in a greater proportion of patients with -7 than del(7q) (P = 0.035). Upon comparing -7(sole) and -7(dual), the latter was likely to be transient (P = 0.004), and AML was frequently observed with persistent -7 clones (P = 0.03). By logistic regression analysis (n = 36), clone size (P = 0.017), time-to-detection longer than 15 months (P = 0.02), and CML response (P = 0.085) were associated with MDS/AML. Validation of these novel associations in registry-based studies will help develop predictive criteria that define the MDS/AML risk in individual patients.
Authors:
Michael J Groves; Mark Sales; Lee Baker; Michael Griffiths; Norman Pratt; Sudhir Tauro
Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Cancer genetics     Volume:  204     ISSN:  2210-7762     ISO Abbreviation:  Cancer Genet     Publication Date:  2011 Jan 
Date Detail:
Created Date:  2011-03-01     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  101539150     Medline TA:  Cancer Genet     Country:  United States    
Other Details:
Languages:  eng     Pagination:  39-44     Citation Subset:  IM    
Copyright Information:
Copyright © 2011 Elsevier Inc. All rights reserved.
Affiliation:
Centre for Oncology & Molecular Medicine, Division of Medical Sciences, University of Dundee, Ninewells Hospital & Medical School, Dundee, United Kingdom.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


Previous Document:  Implementation of high resolution single nucleotide polymorphism array analysis as a clinical test...
Next Document:  Exon scanning by reverse transcriptase-polymerase chain reaction for detection of known and novel EM...