PMID- 15356655
OWN - NLM
STAT- MEDLINE
DCOM- 20041101
LR  - 20130304
IS  - 0887-6924 (Print)
IS  - 0887-6924 (Linking)
VI  - 18
IP  - 10
DP  - 2004 Oct
TI  - Incidence and relevance of secondary chromosome abnormalities in childhood 
      TEL/AML1+ acute lymphoblastic leukemia: an interphase FISH analysis.
PG  - 1611-6
AB  - The aim of the present study was to determine the frequency and clinical 
      relevance of the most common secondary karyotype abnormalities in TEL/AML1+ 
      B-cell precursor acute lymphoblastic leukemia (ALL) as assessed with fluorescence 
      in situ hybridization (FISH) analyses. Screening of 372 patients who were 
      enrolled in two consecutive Austrian childhood ALL multicenter trials identified 
      94 (25%) TEL/AML1+ cases. TEL deletions, trisomy 21 and an additional 
      der(21)t(12;21) were detected in 52 (55%), 13 (14%) and 14 (15%) TEL/AML1+ 
      patients, respectively. The 12p aberrations (P=0.001) and near tetraploidy 
      (P=0.045) were more common in TEL/AML1+ patients, whereas the incidence of 
      diploidy, pseudodiploidy, hypodiploidy, low hyperdiploidy, near triploidy, 
      del(6q), chromosome 9 and 11q23 abnormalities was similar among TEL/AML1+ and 
      TEL/AML1- patients. None of the TEL/AML1+ patients had a high hyperdiploid 
      karyotype. Univariate analysis indicated that among TEL/AML1+ patients those with 
      a deletion of the nontranslocated TEL allele had a worse prognosis than those 
      without this abnormality (P=0.034). We concluded that the type and incidence of 
      the most common secondary aberrations in TEL/AML1+ ALL can be conveniently 
      identified with little additional effort during interphase screening with 
      appropriate TEL and AML1 FISH probes. We also provided preliminary evidence that 
      the deletion of the nontranslocated TEL allele may adversely influence the 
      clinical course of TEL/AML1+ ALL.
FAU - Attarbaschi, A
AU  - Attarbaschi A
AD  - 1St Anna Children's Hospital, Vienna, Austria.
FAU - Mann, G
AU  - Mann G
FAU - Konig, M
AU  - Konig M
FAU - Dworzak, M N
AU  - Dworzak MN
FAU - Trebo, M M
AU  - Trebo MM
FAU - Muhlegger, N
AU  - Muhlegger N
FAU - Gadner, H
AU  - Gadner H
FAU - Haas, O A
AU  - Haas OA
CN  - Austrian Berlin-Frankfurt-Munster cooperative study group
LA  - eng
PT  - Journal Article
PT  - Multicenter Study
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Leukemia
JT  - Leukemia
JID - 8704895
RN  - 0 (Core Binding Factor Alpha 2 Subunit)
RN  - 0 (Oncogene Proteins, Fusion)
RN  - 0 (TEL-AML1 fusion protein)
SB  - IM
MH  - Child
MH  - Child, Preschool
MH  - *Chromosome Aberrations
MH  - Chromosomes, Human, Pair 12/genetics
MH  - Chromosomes, Human, Pair 21/genetics
MH  - Core Binding Factor Alpha 2 Subunit
MH  - Down Syndrome
MH  - Female
MH  - Gene Deletion
MH  - Humans
MH  - In Situ Hybridization, Fluorescence
MH  - Incidence
MH  - Infant
MH  - Interphase/*genetics
MH  - Karyotyping
MH  - Male
MH  - Oncogene Proteins, Fusion/genetics/*metabolism
MH  - Ploidies
MH  - Precursor Cell Lymphoblastic Leukemia-Lymphoma/*genetics
MH  - Retrospective Studies
MH  - Translocation, Genetic
EDAT- 2004/09/10 05:00
MHDA- 2004/11/02 09:00
CRDT- 2004/09/10 05:00
PHST- 2004/09/10 05:00 [pubmed]
PHST- 2004/11/02 09:00 [medline]
PHST- 2004/09/10 05:00 [entrez]
AID - 2403471 [pii]
AID - 10.1038/sj.leu.2403471 [doi]
PST - ppublish
SO  - Leukemia. 2004 Oct;18(10):1611-6. doi: 10.1038/sj.leu.2403471.