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Related Experiment Videos

The TEL-AML1 fusion accompanied by loss of the untranslocated TEL allele in B-precursor acute lymphoblastic leukaemia

H M Kempski1, N T Sturt

  • 1Molecular Haematology Unit, Institute of Child Health, Great Ormond Street Hospital for Sick Children, London, UK. H.Kempski@ich.ucl.ac.uk

Leukemia & Lymphoma
|June 28, 2001
PubMed
Summary

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The TEL-AML1 fusion in childhood B-precursor acute lymphoblastic leukemia (B-precursor ALL) often involves a secondary deletion on chromosome 12p. This deletion promotes the evolution of leukemia cells with the TEL-AML1 fusion.

Area of Science:

  • Genetics
  • Oncology
  • Molecular Biology

Background:

  • Childhood B-precursor acute lymphoblastic leukemia (B-precursor ALL) is frequently associated with the t(12;21) chromosomal rearrangement, leading to the TEL-AML1 fusion gene.
  • This fusion is often accompanied by the loss of the untranslocated TEL allele, suggesting a secondary genetic event.

Purpose of the Study:

  • To investigate the nature and timing of secondary genetic events, specifically del 12p, in childhood B-precursor ALL with the TEL-AML1 fusion.
  • To elucidate the sequential order of genetic alterations in the development of TEL-AML1 positive leukemia.

Main Methods:

  • Screening of 32/109 children with B-precursor ALL for TEL-AML1 fusion and associated chromosomal abnormalities.
  • Utilizing interphase fluorescence in situ hybridization (FISH) analysis to detect chromosomal deletions.

Related Experiment Videos

  • Employing reverse-transcriptase polymerase chain reaction (RT-PCR) to confirm the loss of the normal TEL allele.

    • Main Results:

    • Evidence for del 12p, including the loss of the untranslocated TEL allele, was found in leukaemic cells as a secondary event in patients positive for TEL-AML1 fusion.
    • In 61% of patients with t(12;21), substantial evolution of the primary clonal line containing the TEL-AML1 fusion was observed.
    • Loss of normal TEL was confirmed in these patients using FISH and RT-PCR.

    Conclusions:

    • The generation of the TEL-AML1 fusion appears to be the initial event in a subset of childhood B-precursor ALL.
    • A subsequent deletion on chromosome 12p (del 12p), leading to the loss of the untranslocated TEL allele, acts as a promoting event in leukemogenesis.
    • These findings highlight a two-step model for the development of TEL-AML1 positive childhood ALL.