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Jumping Translocations of Chromosome 1q in Multiple Myeloma:
Evidence for a Mechanism Involving Decondensation of
Pericentromeric Heterochromatin
Jeffrey R. Sawyer,
Guido Tricot,
Sandy Mattox,
Sundar Jagannath, and
Bart Barlogie
From the Departments of Pathology and Medicine, Arkansas Cancer
Reseach Center, University of Arkansas for Medical Sciences; and the
Cytogenetics Laboratory, Arkansas Children's Hospital, Little
Rock, AR.
Karyotypes in multiple myeloma (MM) are complex and exhibit numerous
structural and numerical aberrations. The largest subset of structural
chromosome anomalies in clinical specimens and cell lines involves
aberrations of chromosome 1. Unbalanced translocations and duplications
involving all or part of the whole long arm of chromosome 1 presumably
occur as secondary aberrations and are associated with tumor
progression and advanced disease. Unfortunately, cytogenetic evidence
is scarce as to how these unstable whole-arm rearrangements may take
place. We report nonrandom, unbalanced whole-arm translocations of 1q
in the cytogenetic evolution of patients with aggressive MM. Whole-arm
or "jumping translocations" of 1q were found in 36 of 158 successive patients with abnormal karyotypes. Recurring whole-arm
translocations of 1q involved chromosomes 5,8,12,14,15,16,17,19,21, and
22. A newly delineated breakpoint present in three patients involved a
whole-arm translocation of 1q to band 5q15. Three recurrent
translocations of 1q10 to the short arms of different acrocentric
chromosomes have also been identified, including three patients
with der(15)t(1;15)(q10;p10) and two patients each with
der(21)t(1;21)(q10;p13) and der(22)t(1;22) (q10;p10). Whole-arm
translocations of 1q10 to telomeric regions of nonacrocentric
chromosomes included der(12)t(1;12) (q10;q24.3) and
der(19)t(1;19)(q10;q13.4) in three and two patients, respectively. Recurrent whole-arm translocations of 1q to centromeric regions included der(16)t(1;16)(q10;q10) and der(19)t(1;19)(q10;p10). The
mechanisms involved in the 1q instability in MM may be associated with
highly decondensed pericentromeric heterochromatin, which may permit
recombination and formation of unstable translocations of chromosome
1q. The clonal evolution of cells with extra copies of 1q suggests that
this aberration directly or indirectly provides a proliferative
advantage.
Blood, Vol. 91 No. 5 (March 1), 1998:
pp. 1732-1741
© 1998 by The American Society of Hematology.
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