|
|
Previous Article | Table of Contents | Next Article 
Acceleration of chronic myeloid leukemia correlates with calcitonin gene
hypermethylation
T Malinen, A Palotie, S Pakkala, L Peltonen, T Ruutu and SE Jansson
Department of Clinical Chemistry, University of Helsinki, Finland.
Calcitonin gene methylation at CCGG sites were determined in 39 chronic
myeloid leukemia patients by isoschizomeric restriction endonuclease
analysis. A total of 27 patients were analyzed while still in the chronic
phase: 20 patients had a normal gene, and seven had a hypermethylated gene.
There were 12 patients initially studied in accelerated or blastic phases.
All but one patient showed gene hypermethylation, suggesting a good
correlation between gene methylation and disease stage. All five patients
who, while still in the chronic phase, had a major 3.1-kb hypermethylated
calcitonin gene fragment, accelerated within 2 to 27 months. In
consecutively analyzed patients, the initially normal calcitonin gene
changed to a hypermethylated state as the disease escalated. The
hypermethylation predicted disease acceleration with a median lead time of
6 months before any morphologic or clinical signs of disease progression
were seen. The disease progressed in 8 of 27 patients initially studied in
the chronic phase: in only two patients this occurred without predictive
methylation changes. The results suggest that the assessment of calcitonin
gene methylation status may be a promising tool for monitoring chronic
myeloid leukemia disease escalation.
Volume 77,
Issue 11,
pp. 2435-2440,
06/01/1991
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:

|
 |

|
 |
 
J. M. Brain, N. Goodyer, and P. Laneuville
Measurement of Genomic Instability in Preleukemic P190BCR/ABL Transgenic Mice Using Inter-Simple Sequence Repeat Polymerase Chain Reaction
Cancer Res.,
August 15, 2003;
63(16):
4895 - 4898.
[Abstract]
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
J. Roman-Gomez, J. A. Castillejo, A. Jimenez, F. Cervantes, C. Boque, L. Hermosin, A. Leon, A. Granena, D. Colomer, A. Heiniger, et al.
Cadherin-13, a Mediator of Calcium-Dependent Cell-Cell Adhesion, Is Silenced by Methylation in Chronic Myeloid Leukemia and Correlates With Pretreatment Risk Profile and Cytogenetic Response to Interferon Alfa
J. Clin. Oncol.,
April 15, 2003;
21(8):
1472 - 1479.
[Abstract]
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
B. Sun, G. Jiang, M.-A. A. Zaydan, V. F. La Russa, H. Safah, and M. Ehrlich
ABL1 Promoter Methylation Can Exist Independently of BCR-ABL Transcription in Chronic Myeloid Leukemia Hematopoietic Progenitors
Cancer Res.,
September 1, 2001;
61(18):
6931 - 6937.
[Abstract]
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
J. F Costello and C. Plass
Methylation matters
J. Med. Genet.,
May 1, 2001;
38(5):
285 - 303.
[Abstract]
[Full Text]
|
 |
|

|
 |

|
 |
 
F. A. Asimakopoulos, P. J. Shteper, S. Krichevsky, E. Fibach, A. Polliack, E. Rachmilewitz, Y. Ben-Neriah, and D. Ben-Yehuda
ABL1 Methylation Is a Distinct Molecular Event Associated With Clonal Evolution of Chronic Myeloid Leukemia
Blood,
October 1, 1999;
94(7):
2452 - 2460.
[Abstract]
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
S. Faderl, M. Talpaz, Z. Estrov, S. O'Brien, R. Kurzrock, and H. M. Kantarjian
The Biology of Chronic Myeloid Leukemia
N. Engl. J. Med.,
July 15, 1999;
341(3):
164 - 172.
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
D. Ben-Yehuda, S. Krichevsky, E. A. Rachmilewitz, A. Avraham, G. A. Palumbo, F. Frassoni, D. Sahar, H. Rosenbaum, O. Paltiel, M. Zion, et al.
Molecular Follow-Up of Disease Progression and Interferon Therapy in Chronic Myelocytic Leukemia
Blood,
December 15, 1997;
90(12):
4918 - 4923.
[Abstract]
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
M Heiskanen, A C Syvanen, H Siitari, S Laine, and A Palotie
A novel method to quantitate methylation of specific genomic regions.
Genome Res.,
August 1, 1994;
4(1):
26 - 30.
[Abstract]
[PDF]
|
 |
|
|
|