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Blood, 1 June 2001, Vol. 97, No. 11, pp. 3612-3620
NEOPLASIA
Cytogenetic analysis and clinical significance in adult
T-cell leukemia/lymphoma: a study of 50 cases from the
human T-cell leukemia virus type-1 endemic
area, Nagasaki
Takahiro Itoyama,
R. S. K. Chaganti,
Yasuaki Yamada,
Kunihiro Tsukasaki,
Sunao Atogami,
Hideo Nakamura,
Masao Tomonaga,
Koichi Ohshima,
Masahiro Kikuchi, and
Naoki Sadamori
From the Laboratory of Cancer Genetics, Cell Biology
Program, Memorial Sloan-Kettering Cancer Center, New York, NY; the
Department of Laboratory Medicine, Nagasaki University School of
Medicine, Japan; the Department of Hematology, Atomic
Disease Institute, Nagasaki University School of Medicine,
Japan; the First Department of Pathology, Fukuoka
University School of Medicine, Japan; and the Department of Nursing,
Siebold University of Nagasaki, Japan
Identification of cytogenetic abnormalities is an important clue
for the elucidation of carcinogenesis. However, the cytogenetic and
clinical significance of adult T-cell leukemia/lymphoma (ATLL) is still
unclear. To address this point, cytogenetic findings in 50 cases of
ATLL were correlated with clinical characteristics. Karyotypes showed a
high degree of diversity and complexity. Aneuploidy and multiple breaks
(at least 6) were observed frequently in acute and lymphoma subtypes of
ATLL. Breakpoints tended to cluster at specific chromosomal
regions, although characteristic cytogenetic subgroups of abnormalities
were not found. Of these, aberrations of chromosomes 1p, 1q, 1q10-21,
10p, 10p13, 12q, 14q, and 14q32 correlated with one or more of the
following clinical features: hepatosplenomegaly, elevated lactate
dehydrogenase, hypercalcemia, and unusual immunophenotype, all
indicators of clinical severity of ATLL. Multiple breaks (at least 6);
abnormalities of chromosomes 1p, 1p22, 1q, 1q10-21, 2q, 3q, 3q10-12,
3q21, 14q, 14q32, and 17q; and partial loss of chromosomes 2q, 9p, 14p,
14q, and 17q regions correlated with shorter survival. These
cytogenetic findings are relevant in predicting clinical outcome and
provide useful information to identify chromosomal regions responsible
for leukemogenesis. This study also indicates that one model of an
oncogenic mechanism, activation of a proto-oncogene by translocation of
a T-cell-receptor gene, may not be applicable to the main pathway of
development of ATLL and that a multistep process of leukemogenesis is
required for the development of ATLL.
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