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Acute lymphoblastic leukaemia.

C J Harrison1

  • 1Leukaemia Research Fund/UK Cancer Cytogenetics Group Karyotype Database in Acute Lymphoblastic Leukaemia, Department of Haematology, Royal Free and University College School of Medicine, Rowland Hill Street, London, NW3 2PF, UK.

Best Practice & Research. Clinical Haematology
|October 20, 2001
PubMed
Summary
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Chromosomal abnormalities in acute lymphoblastic leukaemia (ALL) impact prognosis and treatment. FISH screening identifies these genetic markers, aiding risk-adjusted therapy for better patient outcomes.

Area of Science:

  • Cytogenetics
  • Molecular Biology
  • Oncology

Background:

  • Karyotype analysis in acute lymphoblastic leukaemia (ALL) provides critical prognostic information influencing treatment strategies.
  • Specific chromosomal abnormalities, including BCR/ABL fusion, MLL gene rearrangements, E2A/PBX1, ETV6/AML1 fusion, and p16(INK4A) deletions, are linked to patient outcomes.
  • Numerical chromosomal abnormalities, such as high hyperdiploidy and near haploidy, significantly correlate with prognosis in ALL.

Purpose of the Study:

  • To highlight the prognostic significance of chromosomal abnormalities in childhood ALL.
  • To describe the development of an interphase Fluorescence In Situ Hybridization (FISH) screening program for identifying prognostic markers.
  • To underscore the role of cytogenetic analysis in guiding risk-adjusted therapy protocols.

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Main Methods:

  • Utilized interphase FISH screening to detect chromosomal abnormalities in childhood ALL.
  • Reviewed known structural chromosomal changes (e.g., translocations) and their associated gene fusions (e.g., BCR/ABL, ETV6/AML1).
  • Assessed the prognostic impact of numerical chromosomal abnormalities (high hyperdiploidy, near haploidy) and gene deletions (p16(INK4A)).

Main Results:

  • Identified specific structural abnormalities (t(9;22), t(1;19), t(12;21)) and MLL/MYC rearrangements as significant prognostic indicators.
  • Demonstrated that high hyperdiploidy (51-65 chromosomes) is associated with a good prognosis, while near haploidy (23-29 chromosomes) indicates a poor prognosis.
  • Highlighted homozygous deletions of the p16(INK4A) tumor suppressor gene on chromosome 9p as a poor-risk factor.

Conclusions:

  • Interphase FISH screening is crucial for identifying prognostically significant chromosomal abnormalities in childhood ALL.
  • Cytogenetic findings are integral to implementing risk-adjusted therapy, improving treatment protocols.
  • Emerging molecular cytogenetic techniques continue to uncover novel cryptic abnormalities, promising further advancements in ALL treatment.