|
|
 Previous Article | Table of Contents | Next Article 
Rearrangement and expression of p53 in the chronic phase and blast crisis
of chronic myelogenous leukemia
R Mashal, M Shtalrid, M Talpaz, H Kantarjian, L Smith, M Beran, A Cork, J Trujillo, J Gutterman and A Deisseroth
Department of Hematology, University of Texas M.D. Anderson Cancer Center,
Houston 77030.
We tested a population of over 60 patients with chronic myelogenous
leukemia (CML) for changes in the structure and expression of the p53 gene,
which is located on chromosome 17. Six of 27 (22%) blast crisis samples and
3 of 5 (60%) accelerated phase samples had rearrangements of chromosome 17,
whereas only 3 of 42 (7%) chronic phase patients had cytogenetic changes in
chromosome 17. There was no loss of heterozygosity during the transition to
blastic crisis among seven individuals who were informative for polymorphic
probes for regions in or around the p53 gene on 17p. One patient in the
chronic phase and one patient in the blastic phase of the 61 CML patients
studied exhibited rearrangements of the p53 gene that were detectable by
Southern analysis. One p53 allele was rearranged in the chronic phase
patient and both p53 alleles were rearranged in the blastic phase patient.
The p53 messenger RNA (mRNA) was of normal size (2.8 kb) in chronic phase
and blast crisis, and the expression of the p53 gene was at least as high
or higher in blast crisis as in the chronic phase of CML. The high
incidence of abnormalities of chromosome 17 in blast-crisis CML found in
our studies and the discovery of rearrangements of the p53 gene in two CML
patients studied suggest that further study with probes for the p53 gene
and anonymous polymorphic sites in chromosome 17 should be conducted in
CML.
Volume 75,
Issue 1,
pp. 180-189,
01/01/1990
Copyright © 1990 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:
|
|
|
|
 
H.-G. Wendel, E. de Stanchina, E. Cepero, S. Ray, M. Emig, J. S. Fridman, D. R. Veach, W. G. Bornmann, B. Clarkson, W. R. McCombie, et al.
Loss of p53 impedes the antileukemic response to BCR-ABL inhibition
PNAS,
May 9, 2006;
103(19):
7444 - 7449.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
N. Kosugi, Y. Ebihara, T. Nakahata, H. Saisho, S. Asano, and A. Tojo
CD34+CD7+ Leukemic Progenitor Cells May Be Involved in Maintenance and Clonal Evolution of Chronic Myeloid Leukemia
Clin. Cancer Res.,
January 15, 2005;
11(2):
505 - 511.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
A. W. Goetz, H. van der Kuip, R. Maya, M. Oren, and W. E. Aulitzky
Requirement for Mdm2 in the Survival Effects of Bcr-Abl and Interleukin 3 in Hematopoietic Cells
Cancer Res.,
October 1, 2001;
61(20):
7635 - 7641.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
D. B. Zimonjic, J. L. Pollock, P. Westervelt, N. C. Popescu, and T. J. Ley
Acquired, nonrandom chromosomal abnormalities associated with the development of acute promyelocytic leukemia in transgenic mice
PNAS,
November 21, 2000;
97(24):
13306 - 13311.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
D. G. Tenen, R. Hromas, J. D. Licht, and D.-E. Zhang
Transcription Factors, Normal Myeloid Development, and Leukemia
Blood,
July 15, 1997;
90(2):
489 - 519.
[Full Text]
[PDF]
|
|
|
|
|
|
|
S. Baker, S Markowitz, E. Fearon, J. Willson, and B Vogelstein
Suppression of human colorectal carcinoma cell growth by wild-type p53
Science,
August 24, 1990;
249(4971):
912 - 915.
[Abstract]
[PDF]
|
|
|
|
|
