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Epigenetic deregulation in pediatric acute lymphoblastic leukemia

Chatterton, Zac, Morenos, Leah, Mechinaud, Francoise, Ashley, David M, Craig, Jeffrey M, Sexton-Oates, Alexandra, Halemba, Minhee S, Parkinson-Bates, Mandy, Ng, Jane, Morrison, Debra, Carroll, William L, Saffery, Richard and Wong, Nicholas C 2014, Epigenetic deregulation in pediatric acute lymphoblastic leukemia, Epigenetics, vol. 9, no. 3, pp. 459-467, doi: 10.4161/epi.27585.

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Title Epigenetic deregulation in pediatric acute lymphoblastic leukemia
Author(s) Chatterton, Zac
Morenos, Leah
Mechinaud, Francoise
Ashley, David M
Craig, Jeffrey M
Sexton-Oates, Alexandra
Halemba, Minhee S
Parkinson-Bates, Mandy
Ng, Jane
Morrison, Debra
Carroll, William L
Saffery, Richard
Wong, Nicholas C
Journal name Epigenetics
Volume number 9
Issue number 3
Start page 459
End page 467
Total pages 10
Publisher Taylor & Francis
Place of publication New York, NY
Publication date 2014-03
ISSN 1559-2308
Keyword(s) ALL
DNA methylation
acute lymphoblastic leukemia
Science & Technology
Life Sciences & Biomedicine
Biochemistry & Molecular Biology
Genetics & Heredity
Case-Control Studies
Epigenesis, Genetic
Precursor B-Cell Lymphoblastic Leukemia-Lymphoma
Summary Similar to most cancers, genome-wide DNA methylation profiles are commonly altered in pediatric acute lymphoblastic leukemia (ALL); however, recent observations highlight that a large portion of malignancy-associated DNA methylation alterations are not accompanied by related gene expression changes. By analyzing and integrating the methylome and transcriptome profiles of pediatric B-cell ALL cases and primary tissue controls, we report 325 genes hypermethylated and downregulated and 45 genes hypomethylated and upregulated in pediatric B-cell ALL, irrespective of subtype. Repressed cation channel subunits and cAMP signaling activators and transducers are overrepresented, potentially indicating a reduced cellular potential to receive and propagate apoptotic signals. Furthermore, we report specific DNA methylation alterations with concurrent gene expression changes within individual ALL subtypes. The ETV6-RUNX1 translocation was associated with downregulation of ASNS and upregulation of the EPO-receptor, while Hyperdiploid patients (> 50 chr) displayed upregulation of B-cell lymphoma (BCL) members and repression of PTPRG and FHIT. In combination, these data indicate genetically distinct B-cell ALL subtypes contain cooperative epimutations and genome-wide epigenetic deregulation is common across all B-cell ALL subtypes.
Language eng
DOI 10.4161/epi.27585
Field of Research 111403 Paediatrics
110202 Haematology
111203 Cancer Genetics
Socio Economic Objective 920102 Cancer and Related Disorders
HERDC Research category C1 Refereed article in a scholarly journal
ERA Research output type C Journal article
Copyright notice ©2014, Taylor & Francis
Free to Read? Yes
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Document type: Journal Article
Collections: Faculty of Health
School of Medicine
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