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Blood, Vol. 92 No. 5 (September 1), 1998:
pp. 1743-1748
Multicolor Spectral Karyotyping Identifies New Recurring
Breakpoints and Translocations in Multiple Myeloma
Pulivarthi H. Rao,
Juan C. Cigudosa,
Yi Ning,
María J. Calasanz,
Shinsuke Iida,
Shinichi Tagawa,
Joseph Michaeli,
Bernard Klein,
Riccardo Dalla-Favera,
Suresh C. Jhanwar,
Thomas Ried, and
R.S.K. Chaganti
From the Cell Biology and Genetics Program and the Departments of
Human Genetics and Medicine, Memorial Sloan Kettering Cancer Center,
New York; the Department of Pathology, College of Physicians and
Surgeons of Columbia University, New York, NY; the Department of
Genetics, University of Navarra, Pamplona, Spain; the Department of
Clinical Hematology, Osaka City University Medical School, Osaka,
Japan; Institute for Molecular Genetics, University of Montpellier,
Montpellier, France; and the Genome Technology Branch, Human Genome
Research Institute, Bethesda, MD.
Karyotypic information on multiple myeloma (MM) is less extensive
than that on other myeloid or lymphoid malignancies due to low mitotic
activity of plasma cells. An add(14)(q32) marker chromosome has been
reported to be the most frequent recurring abnormality in clonally
abnormal cases; in approximately one third of the latter cases, this
marker has been identified as a der(14)t(11;14)(q13;q32) chromosome. To
map chromosomal breakpoints, characterize the add(14)(q32) marker
chromosomes, and to identify other recurring translocations in MM, we
used spectral karyotyping (SKY) to analyze a panel of nine bone marrow
(BM) biopsy samples from eight patients and 10 tumor cell lines derived
from MM patients. SKY involves hybridization of 24 fluorescently
labeled chromosome painting probes to metaphase spreads in such a
manner that simultaneous visualization of each of the chromosomes in a
different color is accomplished. By this method, it was possible to
define all chromosomal rearrangements and identify all of the clonal
marker chromosomes in tumor cells. By detailed mapping of breakpoints
of rearrangement, it was also possible to identify several novel
recurring sites of breakage that map to the chromosomal bands 3q27,
17q24-25, and 20q11. The partner chromosomes in translocations that
generated the add (14)(q32) marker chromosomes were identified in all
cases in which they were detected by G-banding (one biopsy and six cell
lines). In addition, two new translocations involving band 14q32, ie,
t(12;14)(q24;q32) and t(14;20)(q32;q11) have also been identified.
These studies demonstrate the power of SKY in resolving the full
spectrum of chromosome abnormalities in tumors.
© 1998 by The American Society of Hematology.
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