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Blood, 15 January 2008, Vol. 111, No. 2, pp. 776-784.
Prepublished online as a Blood First Edition Paper on September 21, 2007; DOI 10.1182/blood-2007-05-088310.
 Previous Article | Table of Contents | Next Article 
NEOPLASIA
Molecular allelokaryotyping of pediatric acute lymphoblastic leukemias by high-resolution single nucleotide polymorphism oligonucleotide genomic microarray
Norihiko Kawamata1,
Seishi Ogawa2,
Martin Zimmermann3,
Motohiro Kato2,
Masashi Sanada2,
Kari Hemminki4,
Go Yamatomo2,
Yasuhito Nannya2,
Rolf Koehler5,
Thomas Flohr5,
Carl W. Miller1,
Jochen Harbott6,
Wolf-Dieter Ludwig7,
Martin Stanulla3,
Martin Schrappe8,
Claus R. Bartram5, and
H. Phillip Koeffler1
1 Department of Hematology, Oncology, Cedars-Sinai Medical Center/University of California at Los Angeles School of Medicine;
2 Regeneration Medicine of Hematopoiesis, University of Tokyo, School of Medicine, Tokyo, Japan;
3 Department of Pediatric Hematology and Oncology, Children's Hospital, Hannover Medical School (MHH), Hannover, Germany;
4 Division of Molecular Genetic Epidemiology, German Cancer Research Center (DKFZ), Heidelberg, Germany;
5 Institute of Human Genetics, University of Heidelberg, Heidelberg, Germany;
6 Department of Pediatric Hematology and Oncology, Justus Liebig University, Gieβen, Germany;
7 Department of Hematology, Oncology and Tumor Immunology, Robert-Rössle-Clinic at the HELIOS-Clinic Berlin-Buch, Charité, Berlin, Germany; and
8 Department of Pediatrics, University of Kiel, Kiel, Germany
Pediatric acute lymphoblastic leukemia (ALL) is a malignant disease resulting from accumulation of genetic alterations. A robust technology, single nucleotide polymorphism oligonucleotide genomic microarray (SNP-chip) in concert with bioinformatics offers the opportunity to discover the genetic lesions associated with ALL. We examined 399 pediatric ALL samples and their matched remission marrows at 50 000/250 000 SNP sites using an SNP-chip platform. Correlations between genetic abnormalities and clinical features were examined. Three common genetic alterations were found: deletion of ETV6, deletion of p16INK4A, and hyperdiploidy, as well as a number of novel recurrent genetic alterations. Uniparental disomy (UPD) was a frequent event, especially affecting chromosome 9. A cohort of children with hyperdiploid ALL without gain of chromosomes 17 and 18 had a poor prognosis. Molecular allelokaryotyping is a robust tool to define small genetic abnormalities including UPD, which is usually overlooked by standard methods. This technique was able to detect subgroups with a poor prognosis based on their genetic status.
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