Transcriptional dysregulation of the multifunctional zinc finger factor 423 in acute lymphoblastic leukemia of childhood.
Differentiation arrest is a hallmark of acute lymphoblastic leukemia (ALL). Among a variety of structural and chromosomal alterations, especially mutations in genes encoding for regulators of B cell differentiation are common. The objective of this study was a comprehensive assessment of transcriptional dysregulation and high-resolution genomic profiling of B cell differentiation factors. Here we provide extended materials and methods regarding transcriptome and genome-wide copy number variation analyses published by Harder et al. [1]. Our data provide a resource for the identification of yet undefined factors that play a putative functional role in leukemogenesis such as ZNF423, whose aberrant expression interferes with B-cell differentiation.
Research Institute Children's Cancer Center and Clinic of Pediatric Hematology and Oncology, University Medical Center Hamburg-Eppendorf, 20246 Hamburg, Germany.
Lena
L
Harder
Institute of Clinical Chemistry, University Medical Center Hamburg-Eppendorf, 20246 Hamburg, Germany.
Benjamin
B
Otto
Research Institute Children's Cancer Center and Clinic of Pediatric Hematology and Oncology, University Medical Center Hamburg-Eppendorf, 20246 Hamburg, Germany.
Martin A
MA
Horstmann
Acute lymphoblastic leukemia; Genome-wide copy number variation; Transcriptome profiling; ZNF423