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A distinct DNA methylation signature defines pediatric pre-B cell acute lymphoblastic leukemia

Wong, Nicholas C., Ashley, David, Chatterton, Zac, Parkinson-Bates, Mandy, Ng, Hong Kiat, Halemba, Minhee S., Kowalczyk, Adam, Bedo, Justin, Wang, Qiao, Bell, Katrina, Algar, Elizabeth, Craig, Jeffrey M. and Saffery, Richard 2012, A distinct DNA methylation signature defines pediatric pre-B cell acute lymphoblastic leukemia, Epigenetics, vol. 7, no. 6, pp. 535-541, doi: 10.4161/epi.20193.

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Title A distinct DNA methylation signature defines pediatric pre-B cell acute lymphoblastic leukemia
Author(s) Wong, Nicholas C.
Ashley, David
Chatterton, Zac
Parkinson-Bates, Mandy
Ng, Hong Kiat
Halemba, Minhee S.
Kowalczyk, Adam
Bedo, Justin
Wang, Qiao
Bell, Katrina
Algar, Elizabeth
Craig, Jeffrey M.
Saffery, Richard
Journal name Epigenetics
Volume number 7
Issue number 6
Start page 535
End page 541
Total pages 7
Publisher Landes Bioscience
Place of publication Georgetown, Tex.
Publication date 2012
ISSN 1559-2308
1559-2294
Keyword(s) DNA Methylation
childhood acute lymphoblastic leukemia
pre B cell acute lymphoblastic leukemia
Summary Pre-B cell acute lymphoblastic leukemia (ALL) is the most prevalent childhood malignancy and remains one of the highest causes of childhood mortality. Despite this, the mechanisms leading to disease remain poorly understood. We asked if recurrent aberrant DNA methylation plays a role in childhood ALL and have defined a genome-scale DNA methylation profile associated with the ETV6-RUNX1 subtype of pediatric ALL. Archival bone marrow smears from 19 children collected at diagnosis and remission were used to derive a disease specific DNA methylation profile. The gene signature was confirmed in an independent cohort of 86 patients. A further 163 patients were analyzed for DNA methylation of a three gene signature. We found that the DNA methylation signature at diagnosis was unique from remission. Fifteen loci were sufficient to discriminate leukemia from disease-free samples and purified CD34+ cells. DNA methylation of these loci was recurrent irrespective of cytogenetic subtype of pre-B cell ALL. We show that recurrent aberrant genomic methylation is a common feature of pre-B ALL, suggesting a shared pathway for disease development. By revealing new DNA methylation markers associated with disease, this study has identified putative targets for development of novel epigenetic-based therapies.
Language eng
DOI 10.4161/epi.20193
Field of Research 119999 Medical and Health Sciences not elsewhere classified
Socio Economic Objective 970111 Expanding Knowledge in the Medical and Health Sciences
HERDC Research category C1.1 Refereed article in a scholarly journal
Free to Read? Yes
Persistent URL http://hdl.handle.net/10536/DRO/DU:30052150

Document type: Journal Article
Collections: School of Medicine
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Every reasonable effort has been made to ensure that permission has been obtained for items included in DRO. If you believe that your rights have been infringed by this repository, please contact drosupport@deakin.edu.au.