|
|
 Previous Article | Table of Contents | Next Article 
Cytogenetic studies in untreated Hodgkin's disease
H Tilly, C Bastard, T Delastre, C Duval, M Bizet, B Lenormand, JP Dauce, M Monconduit and H Piguet
Department of Clinical Hematology, Centre Henri Becquerel, Rouen, France.
Very little data have been published on cytogenetic abnormalities in
Hodgkin's disease (HD) and their correlation with clinicopathologic
features are scanty. We have performed chromosomal analysis of lymph nodes
from 60 previously untreated HD patients and obtained analyzable metaphases
in 49 patients (82%). Chromosomal abnormalities were found in 33 patients
(55%) but only 31 karyotypes could be, at least partially, described.
Twenty-nine cases showed numerical abnormalities that involved all
chromosomes with the exception of chromosomes 13 and Y, which were gained
less frequently and lost more frequently than other chromosomes. Structural
abnormalities were found in 30 cases, involving all chromosomes except Y.
Chromosomal regions 12p11-13, 13p11- 13, 3q26-28, 6q15-16, and 7q31-35 were
rearranged in more than 20% of the analyzable cases. No correlation was
found between cytogenetic findings and initial characteristics. When
compared with diffuse B-cell lymphomas, defects in regions 2p25 (P less
than .01), 12p11-13 (P less than .01), 13p11-13 (P less than .01), 14p11 (P
less than .01), 15p11- 13 (P less than .02), and 20q12-13 (P less than .05)
were more frequent in HD. When compared with T-cell lymphomas, only defects
in regions 12p12-13 (P less than .01) and 13p11-13 (P less than .01) were
more frequent in HD. Failure to obtain analyzable metaphases was correlated
with stage IV of the disease (P less than .05) and with a poor survival (P
less than .01), but cytogenetic results showed no other correlation with
clinical outcome. We conclude that molecular studies in HD should be
focused on the short arms of chromosomes 12 and 13. Determination of the
clinical significance of cytogenetic findings will require a larger number
of patients and a longer follow-up period.
Volume 77,
Issue 6,
pp. 1298-1304,
03/15/1991
Copyright © 1991 by The American Society of Hematology
 CiteULike  Connotea  Del.icio.us  Digg  Reddit  Technorati What's this?
This article has been cited by other articles:
|
|
|
|
 
S. Hartmann, J. I. Martin-Subero, S. Gesk, J. Husken, M. Giefing, I. Nagel, J. Riemke, A. Chott, W. Klapper, M. Parrens, et al.
Detection of genomic imbalances in microdissected Hodgkin and Reed-Sternberg cells of classical Hodgkin's lymphoma by array-based comparative genomic hybridization
Haematologica,
September 1, 2008;
93(9):
1318 - 1326.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
J. I. Martin-Subero, W. Klapper, A. Sotnikova, E. Callet-Bauchu, L. Harder, C. Bastard, R. Schmitz, S. Grohmann, J. Hoppner, J. Riemke, et al.
Chromosomal Breakpoints Affecting Immunoglobulin Loci Are Recurrent in Hodgkin and Reed-Sternberg Cells of Classical Hodgkin Lymphoma
Cancer Res.,
November 1, 2006;
66(21):
10332 - 10338.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
T. Starnes, H. E. Broxmeyer, M. J. Robertson, and R. Hromas
Cutting Edge: IL-17D, a Novel Member of the IL-17 Family, Stimulates Cytokine Production and Inhibits Hemopoiesis
J. Immunol.,
July 15, 2002;
169(2):
642 - 646.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
S. Joos, C. K. Menz, G. Wrobel, R. Siebert, S. Gesk, S. Ohl, G. Mechtersheimer, L. Trumper, P. Moller, P. Lichter, et al.
Classical Hodgkin lymphoma is characterized by recurrent copy number gains of the short arm of chromosome 2
Blood,
February 15, 2002;
99(4):
1381 - 1387.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
D. Kube, U. Holtick, M. Vockerodt, T. Ahmadi, B. Haier, I. Behrmann, P. C. Heinrich, V. Diehl, and H. Tesch
STAT3 is constitutively activated in Hodgkin cell lines
Blood,
August 1, 2001;
98(3):
762 - 770.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
U. Hasse, M. Tinguely, E. O. Leibundgut, J.-F. Cajot, A. M. Garvin, A. Tobler, B. Borisch, and M. F. Fey
Clonal Loss of Heterozygosity in Microdissected Hodgkin and Reed-Sternberg Cells
J Natl Cancer Inst,
September 15, 1999;
91(18):
1581 - 1583.
[Full Text]
[PDF]
|
|
|
|
|
|
|
S. Gravel, G. Delsol, and T. Al Saati
Single-Cell Analysis of the t(14;18)(q32;q21) Chromosomal Translocation in Hodgkin's Disease Demonstrates the Absence of This Translocation in Neoplastic Hodgkin and Reed-Sternberg Cells
Blood,
April 15, 1998;
91(8):
2866 - 2874.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
T. Ohno, B. N. Smir, D. D. Weisenburger, R. D. Gascoyne, S. D. Hinrichs, and W. C. Chan
Origin of the Hodgkin/Reed-Sternberg Cells in Chronic Lymphocytic Leukemia With "Hodgkin's Transformation"
Blood,
March 1, 1998;
91(5):
1757 - 1761.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
C. D. Jennings and K. A. Foon
Recent Advances in Flow Cytometry: Application to the Diagnosis of Hematologic Malignancy
Blood,
October 15, 1997;
90(8):
2863 - 2892.
[Full Text]
[PDF]
|
|
|
|
|
|
|
M. M. Morente, M. A. Piris, V. Abraira, A. Acevedo, B. Aguilera, C. Bellas, M. Fraga, R. Garcia-Del-Moral, F. Gomez-Marcos, J. Menarguez, et al.
Adverse Clinical Outcome in Hodgkin's Disease Is Associated With Loss of Retinoblastoma Protein Expression, High Ki67 Proliferation Index, and Absence of Epstein-Barr Virus-Latent Membrane Protein 1 Expression
Blood,
September 15, 1997;
90(6):
2429 - 2436.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
