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FLT3 mutations in a 10 year consecutive series of 177 childhood acute leukemias and their impact on global gene expression patterns

Andersson, A. (author)
Department of Clinical Genetics, University Hospital, Lund, Sweden, Department of Clinical Genetics, University Hospital, SE-221 85 Lund, Sweden
Paulsson, K. (author)
Department of Clinical Genetics, University Hospital, Lund, Sweden, Cancer Research UK Medical Oncology Centre, Barts and The Royal London School of Medicine, Queen Mary College, London, United Kingdom
Lilljebjorn, H. (author)
Lilljebjörn, H., Department of Clinical Genetics, University Hospital, Lund, Sweden
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Lassen, C. (author)
Department of Clinical Genetics, University Hospital, Lund, Sweden
Strombeck, B. (author)
Strömbeck, B., Department of Clinical Genetics, University Hospital, Lund, Sweden
Heldrup, J. (author)
Department of Pediatrics, University Hospital, Lund, Sweden
Behrendtz, Mikael (author)
Östergötlands Läns Landsting,Barn- och ungdomskliniken i Linköping
Johansson, B. (author)
Department of Clinical Genetics, University Hospital, Lund, Sweden
Fioretos, T. (author)
Department of Clinical Genetics, University Hospital, Lund, Sweden
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 (creator_code:org_t)
Wiley, 2008
2008
English.
In: Genes, Chromosomes and Cancer. - : Wiley. - 1045-2257 .- 1098-2264. ; 47:1, s. 64-70
  • Journal article (peer-reviewed)
Abstract Subject headings
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  • During 1995-2004, 209 children/adolescents were diagnosed with acute lymphoblastic or myeloid leukemia (ALL, AML) in Southern Sweden, of which 177 (85%), comprising 128 B-lineage ALL, 34 AML, and 15 T-cell ALL, could be analyzed for internal tandem duplications (ITD) and activating point mutations in the second tyrosine kinase domain (ATKD) of FLT3. Seventeen (10%) FLT3 mutations (6 ITD, 11 ATKD, mutually exclusive) were detected. None of the T-cell ALL harbored any mutations. ITD and ATKD were found in 2% and 6% of the B-lineage ALL and in 12% and 9% of the AML, being particularly common in high hyperdiploid ALL (14%), ALL (20%), and AML (23%) with 11q23/MLL rearrangements, and in AML with a normal karyotype (60%). All ATKD-positive AML with MLL rearrangements harbored the t(9,11)(p21,q23). Global gene expression data were available for 76 of the B-lineage ALL and 19 of the AML, of which 6 (8%) and 3 (16%) had FLT3 mutations, respectively. No distinct expression pattern associated with FLT3 mutations was identified. © 2007 Wiley-Liss, Inc.

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