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Chromosome translocations: good genes gone wrong

J D Rowley1

  • 1Department of Medicine, University of Chicago, IL 60637-1470, USA.

Pathologie-Biologie
|March 1, 1995
PubMed
Summary
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Recurring chromosome abnormalities, particularly MLL gene rearrangements at 11q23, are common in infant acute leukemia. These genetic alterations are linked to topoisomerase II inhibitor exposure and influence MLL gene function.

Area of Science:

  • * Oncology
  • * Cytogenetics
  • * Molecular Biology

Background:

  • * Recurring chromosome abnormalities, such as translocations and inversions, are hallmarks of various tumors, including leukemias, lymphomas, and sarcomas.
  • * Rearrangements involving chromosome band 11q23 are frequently observed in acute leukemias and less commonly in lymphomas.
  • * The myeloid-lymphoid leukemia (MLL) gene, also known as ALL1, Htrx, or HRX, is a central player in 11q23 rearrangements.

Purpose of the Study:

  • * To investigate the prevalence and characteristics of MLL gene rearrangements in acute leukemia.
  • * To understand the molecular mechanisms underlying 11q23 translocations and their association with topoisomerase II inhibitors.
  • * To explore the biological implications of MLL gene alterations in leukemogenesis.

Main Methods:

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  • * Cytogenetic analysis of tumor cells to identify chromosome abnormalities.
  • * Molecular cloning and characterization of translocation breakpoints within the MLL gene.
  • * Detection of MLL rearrangements using cDNA probes and analysis of deletions 3' of breakpoints.

Main Results:

  • * Approximately 70% of infants with acute leukemia exhibit MLL rearrangements.
  • * MLL is implicated in numerous translocations, insertions, and deletions, with breakpoints clustered in an 8.3 kb region.
  • * A significant proportion of patients (25%) present with deletions 3' of the breakpoint, affecting the zinc finger region.
  • * Acute leukemias associated with prior topoisomerase II inhibitor treatment show 11q23 translocations targeting the same MLL region.
  • * Translocations result in MLL fusion genes and chimeric transcripts, involving 5' MLL and a 3' partner gene.

Conclusions:

  • * 11q23 rearrangements involving the MLL gene are critical genetic events in a substantial subset of acute leukemias, particularly in infants.
  • * The molecular dissection of MLL rearrangements provides insights into leukemogenesis and the interaction between MLL and topoisomerase II inhibitors.
  • * Understanding these genetic alterations is crucial for advancing leukemia diagnosis and therapeutic strategies.