|
|
 Previous Article | Table of Contents | Next Article 
Hypermethylation of the 5' region of the calcitonin gene is a property of
human lymphoid and acute myeloid malignancies
SB Baylin, ER Fearon, B Vogelstein, A de Bustros, SJ Sharkis, PJ Burke, SP Staal and BD Nelkin
An abnormal increase in numbers of CCGG sites methylated in the 5' region
of the human calcitonin (CT) gene occurred in tumor cell DNA samples from
90% (17 of 19) of patients with non-Hodgkin's T and B cell lymphoid
neoplasms and in 95% (21 of 22) of tumor cell DNA samples from patients
with acute nonlymphocytic leukemia (ANLL). The changes were not seen in
patients with chronic myelogenous leukemia (0 of 9). The abnormal
methylation patterns appear to be a property only of transformed or
malignant cells since they were not found in DNA from nonneoplastic adult
tissues including sperm, early myeloid progenitor cells, benign lymphoid
hyperplasia, peripheral lymphocytes stimulated to divide, or early myeloid
progenitor cells (obtained by immunoaffinity using anti-My-10 antibody),
but they did appear after Epstein-Barr virus transformation of lymphocytes.
Moreover, during the course of therapy in patients with ANLL, the
hypermethylation pattern reflects the presence of the leukemic clone even
in normal-appearing granulocytes derived from this clone. The increased
methylation of the CT gene may then provide an important molecular marker
for biologic events in human cell transformation or tumor progression and
may prove clinically useful in monitoring patients with lymphoid and acute
myelogenous neoplasms.
Volume 70,
Issue 2,
pp. 412-417,
08/01/1987
Copyright © 1987 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. Liu, Z. Liu, Z. Xie, J. Pang, J. Yu, E. Lehmann, L. Huynh, T. Vukosavljevic, M. Takeki, R. B. Klisovic, et al.
Bortezomib induces DNA hypomethylation and silenced gene transcription by interfering with Sp1/NF-{kappa}B-dependent DNA methyltransferase activity in acute myeloid leukemia
Blood,
February 15, 2008;
111(4):
2364 - 2373.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
A. S. Yang, K. D. Doshi, S.-W. Choi, J. B. Mason, R. K. Mannari, V. Gharybian, R. Luna, A. Rashid, L. Shen, M. R.H. Estecio, et al.
DNA Methylation Changes after 5-Aza-2'-Deoxycytidine Therapy in Patients with Leukemia.
Cancer Res.,
May 15, 2006;
66(10):
5495 - 5503.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
F. E. Domann and B. W. Futscher
Flipping the Epigenetic Switch
Am. J. Pathol.,
June 1, 2004;
164(6):
1883 - 1886.
[Full Text]
[PDF]
|
|
|
|
|
|
|
J. F Costello and C. Plass
Methylation matters
J. Med. Genet.,
May 1, 2001;
38(5):
285 - 303.
[Abstract]
[Full Text]
|
|
|
|
|
|
|
S. A. Kuismanen, M. T. Holmberg, R. Salovaara, P. Schweizer, L. A. Aaltonen, A. de la Chapelle, M. Nystrom-Lahti, and P. Peltomaki
Epigenetic phenotypes distinguish microsatellite-stable and -unstable colorectal cancers
PNAS,
October 26, 1999;
96(22):
12661 - 12666.
[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]
|
|
|
|
|
