|
|
 Previous Article | Table of Contents | Next Article 
Integration patterns of HTLV-I provirus in relation to the clinical course
of ATL: frequent clonal change at crisis from indolent disease
K Tsukasaki, H Tsushima, M Yamamura, T Hata, K Murata, T Maeda, S Atogami, H Sohda, S Momita, S Ideda, S Katamine, Y Yamada, S Kamihira and M Tomonaga
Department of Hematology, Nagasaki University School of Medicine, Japan.
We examined human T-lymphotropic virus type I (HTLV-I) DNA integration in
68 patients with adult T-cell leukemia/ lymphoma (ATL) by Southern blotting
using EcoRI, which does not cut within the 9 kb of the genome and probes
for pX and gag-pol region of HTLV-I. We detected defective proviral
integration as a monoclonal band of various sizes with the pX but not with
the gag-pol probe, or a monoclonal band of less than 9 kb with the pX
probe, in 20 patients (29.4%). These were designated defective (D) type.
With both probes, a single band greater than 9 kb was detected in 34
(50.0%), designated complete (C) type, and two or more bands greater than 9
kb, were designated multiple (M) type, in 14 (20.6%). Advanced age, a high
LDH value, and hypercalcemia were more frequent in D type patients. The
median survival time (MST) was 6.8, 24.4, and 33.3 months, for D, C, and M
types, respectively (log rank P = .006). Among 52 sequentially examined
patients, the HTLV-I integration patterns changed in 4 (7.5%). In three of
these four, the rearrangements of the T-cell receptor (TCR)b gene
concomitantly changed, suggesting the appearance of a new ATL clone.
Another patient had the same rearrangement of the TCRb gene, indicating
clonal evolution. The HTLV-I integration pattern changed at crisis from
indolent to aggressive ATL in three patients. These findings suggested that
the HTLV-I integration patterns have clinical implications in ATL
pathophysiology. In contrast to the clonal evolution characteristic of the
multistep carcinogenesis of most human malignancies, the frequent clonal
change of ATL at crisis is a peculiar phenomenon, probably reflecting the
emergence of multiple premalignant clones in viral leukemogenesis as
suggested in Epstein-Barr virus associated lymphomagenesis in the
immunocompromised host.
Volume 89,
Issue 3,
pp. 948-956,
02/01/1997
Copyright © 1997 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:
|
|
|
|
 
M. A. Rizvi, A. M. Evens, M. S. Tallman, B. P. Nelson, and S. T. Rosen
T-cell non-Hodgkin lymphoma
Blood,
February 15, 2006;
107(4):
1255 - 1264.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
K. Tsukasaki, J. Krebs, K. Nagai, M. Tomonaga, H. P. Koeffler, C. R. Bartram, and A. Jauch
Comparative genomic hybridization analysis in adult T-cell leukemia/lymphoma: correlation with clinical course
Blood,
June 15, 2001;
97(12):
3875 - 3881.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
M. Tanaka, B. Sun, J. Fang, T. Nitta, T. Yoshida, S. Kohtoh, H. Kikukawa, S. Hanai, K. Uchida, and M. Miwa
Human T-Cell Leukemia Virus Type 1 (HTLV-1) Infection of Mice: Proliferation of Cell Clones with Integrated HTLV-1 Provirus in Lymphoid Organs
J. Virol.,
May 1, 2001;
75(9):
4420 - 4423.
[Abstract]
[Full Text]
|
|
|
|
|
|
|
S. Tajima, Y. Ikawa, and Y. Aida
Complete Bovine Leukemia Virus (BLV) Provirus Is Conserved in BLV-Infected Cattle throughout the Course of B-Cell Lymphosarcoma Development
J. Virol.,
September 1, 1998;
72(9):
7569 - 7576.
[Abstract]
[Full Text]
[PDF]
|
|
|
| |
