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Chromosomal and Gene Amplification in Diffuse Large B-Cell Lymphoma
Pulivarthi H. Rao,
Jane Houldsworth,
Katerina Dyomina,
Nasser Z. Parsa,
Juan C. Cigudosa,
Diane C. Louie,
Leslie Popplewell,
Kenneth Offit,
Suresh C. Jhanwar, and
R.S.K. Chaganti
From the Cell Biology Program and the Departments of Pathology and
Human Genetics, Memorial Sloan-Kettering Cancer Center, New York, NY.
Chromosomal translocations leading to deregulation of specific
oncogenes characterize approximately 50% of cases of diffuse large
B-cell lymphomas (DLBL). To characterize additional genetic features
that may be of value in delineating the clinical characteristics of
DLBL, we studied a panel of 96 cases at diagnosis consecutively ascertained at the Memorial Sloan-Kettering Cancer Center (MSKCC) for
incidence of gene amplification, a genetic abnormality previously shown
to be associated with tumor progression and clinical outcome. A subset
of 20 cases was subjected to comparative genomic hybridization (CGH)
analysis, which identified nine sites of chromosomal amplification (1q21-23, 2p12-16, 8q24, 9q34, 12q12-14, 13q32, 16p12, 18q21-22, and
22q12). Candidate amplified genes mapped to these sites were selected
for further analysis based on their known roles in lymphoid cell and
lymphoma development, and/or history of amplification in
tumors. Probes for six genes, which fulfilled these criteria, REL (2p12-16), MYC (8q24), BCL2 (18q21),
GLI, CDK4, and MDM2 (12q13-14), were used in a
quantitative Southern blotting analysis of the 96 DLBL DNAs. Each of
these genes was amplified (four or more copies) with incidence ranging
from 11% to 23%. This analysis is consistent with our
previous finding that REL amplification is associated with
extranodal presentation. In addition, BCL2 rearrangement
and/or REL, MYC, BCL2, GLI,
CDK4, and MDM2 amplification was associated with
advanced stage disease. These data show, for the first time, that
amplification of chromosomal regions and genes is a frequent phenomenon
in DLBL and demonstrates their potential significance in
lymphomagenesis.
Blood, Vol. 92 No. 1 (July 1), 1998:
pp. 234-240
© 1998 by The American Society of Hematology.
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