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Blood, 15 June 2001, Vol. 97, No. 12, pp. 3875-3881
NEOPLASIA
Comparative genomic hybridization analysis in adult T-cell
leukemia/lymphoma: correlation with clinical course
Kunihiro Tsukasaki,
Johannes Krebs,
Kazuhiro Nagai,
Masao Tomonaga,
H. Phillip Koeffler,
Claus R. Bartram, and
Anna Jauch
From the Division of Hematology/Oncology, Cedars-Sinai
Medical Center, UCLA School of Medicine, Los Angeles, CA; the Institute
of Human Genetics, University of Heidelberg, Heidelberg, Germany; and
the Department of Hematology, Atomic Bomb Disease Institute, Nagasaki
University School of Medicine, Nagasaki, Japan.
Sixty-four patients with adult T-cell leukemia/lymphoma (ATL; 18 patients with indolent subtype and 46 with aggressive subtype) associated with human T-lymphotropic virus type 1 (HTLV-1)
were analyzed using comparative genomic hybridization (CGH). The
most frequent observations were gains at chromosomes 14q, 7q, and 3p and losses at chromosomes 6q and 13q. Chromosome imbalances, losses, and gains were more frequently observed in aggressive ATL than in
indolent ATL, with significant differences between the 2 ATL subtypes
at gains of 1q and 4q. An increased number of chromosomal imbalances
was associated with a significantly shorter survival in all patients. A
high number of chromosomal losses was associated with a poor prognosis
in indolent ATL, whereas the presence of 7q+ was marginally associated
with a good prognosis in aggressive ATL. Paired samples (ie, samples
obtained at different sites from 4 patients) and sequential samples
from 13 patients (from 6 during both chronic disease and acute crisis
and from 7 during both acute onset and relapse) were examined by CGH
and Southern blotting for HTLV-1. All but 2 paired samples showed
differences on CGH assessment. Two chronic/crisis samples showed
distinct results regarding both CGH and HTLV-1 integration sites,
indicating clonal changes in ATL at crisis. In 11 patients, the finding
of identical HTLV-1 sites and clonally related CGH results suggested a
common origin of sequential samples. In contrast to chronic/crisis
samples, CGH results with all acute/relapse sample pairs showed the
presence of clonally related but not evolutional subclones at relapse, thereby suggesting marked chromosomal instability. In summary, clonal
diversity is common during progression of ATL, and CGH alterations are
associated with clinical course.
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