|
|
 Previous Article | Table of Contents | Next Article 
Blood, 1 November 2000, Vol. 96, No. 9, pp. 3209-3214
NEOPLASIA
A novel gene, MEL1, mapped to 1p36.3 is highly
homologous to the MDS1/EVI1 gene and is
transcriptionally activated in t(1;3)(p36;q21)-positive
leukemia cells
Naomi Mochizuki,
Seiichi Shimizu,
Toshiro Nagasawa,
Hideo Tanaka,
Masafumi Taniwaki,
Jun Yokota, and
Kazuhiro Morishita
From the Biology Division, National Cancer Center
Research Institute, Tokyo; the Division of Hematology, Institute of
Clinical Medicine, University of Tsukuba, Ibaraki; the Third Department
of Internal Medicine, Kyoto Prefectural University of Medicine, Kyoto;
the Department of Hematology and Oncology, Research Institute for
Radiation Biology and Medicine, Hiroshima University, Hiroshima, Japan.
The reciprocal translocation t(1;3)(p36;q21) occurs in a subset of
myelodysplastic syndrome (MDS) and acute myeloid leukemia (AML), which
is frequently characterized by trilineage dysplasia, in particular
dysmegakaryocytopoiesis, and poor prognosis. Previously, the breakpoint
cluster region (BCR) at 3q21 was identified within a 60-kilobase (kb)
region centromeric to the BCR of 3q21q26 syndrome and that at 1p36.3
within a 90-kb region. In this study, genes were searched near the
breakpoints at 1p36.3, and a novel gene was isolated that encoded a
zinc finger protein with a PR domain, which is highly homologous to the
MDS1/EVI1 gene. The novel gene, designated as
MEL1
(MDS1/EVI1-like gene
1), with 1257 amino acid residues is 64% similar in nucleotide and
63% similar in amino acid sequences to MDS1/EVI1 with the
same domain structure. The MEL1 gene is expressed in
leukemia cells with t(1;3) but not in other cell lines or bone marrow,
spleen, and fetal liver, suggesting that MEL1 is specifically in the
t(1;3)(p36;q21)-positive MDS/AML. On the basis of the positional
relationship between the EVI1 and MEL1 genes in
each translocation, it was suggested that both genes are
transcriptionally activated by the translocation of the 3q21 region with the Ribophorin I gene. Because of the transcriptional activation of the EVI1 family genes in both
t(1;3)(p36;q21)-positive MDS/AML and 3q21q26 syndrome, it is
suggested that they share a common molecular mechanism for the
leukemogenic transformation of the cells.
 CiteULike  Connotea  Del.icio.us  Digg  Reddit  Technorati What's this?
This article has been cited by other articles:
|
|
|
|
 
P. Seale, S. Kajimura, and B. M. Spiegelman
Transcriptional control of brown adipocyte development and physiological function--of mice and men
Genes & Dev.,
April 1, 2009;
23(7):
788 - 797.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
M. Takahata, Y. Inoue, H. Tsuda, I. Imoto, D. Koinuma, M. Hayashi, T. Ichikura, T. Yamori, K. Nagasaki, M. Yoshida, et al.
SKI and MEL1 Cooperate to Inhibit Transforming Growth Factor-{beta} Signal in Gastric Cancer Cells
J. Biol. Chem.,
January 30, 2009;
284(5):
3334 - 3344.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
S. Kajimura, P. Seale, T. Tomaru, H. Erdjument-Bromage, M. P. Cooper, J. L. Ruas, S. Chin, P. Tempst, M. A. Lazar, and B. M. Spiegelman
Regulation of the brown and white fat gene programs through a PRDM16/CtBP transcriptional complex
Genes & Dev.,
May 15, 2008;
22(10):
1397 - 1409.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
Y. Watanabe, M. Toyota, Y. Kondo, H. Suzuki, T. Imai, M. Ohe-Toyota, R. Maruyama, M. Nojima, Y. Sasaki, Y. Sekido, et al.
PRDM5 Identified as a Target of Epigenetic Silencing in Colorectal and Gastric Cancer
Clin. Cancer Res.,
August 15, 2007;
13(16):
4786 - 4794.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
A. Miremadi, M. Z. Oestergaard, P. D.P. Pharoah, and C. Caldas
Cancer genetics of epigenetic genes
Hum. Mol. Genet.,
April 15, 2007;
16(R1):
R28 - R49.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
C. A. Davis, M. Haberland, M. A. Arnold, L. B. Sutherland, O. G. McDonald, J. A. Richardson, G. Childs, S. Harris, G. K. Owens, and E. N. Olson
PRISM/PRDM6, a Transcriptional Repressor That Promotes the Proliferative Gene Program in Smooth Muscle Cells.
Mol. Cell. Biol.,
April 1, 2006;
26(7):
2626 - 2636.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
Y. Du, N. A. Jenkins, and N. G. Copeland
Insertional mutagenesis identifies genes that promote the immortalization of primary bone marrow progenitor cells
Blood,
December 1, 2005;
106(12):
3932 - 3939.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
M. Kobayashi-Osaki, O. Ohneda, N. Suzuki, N. Minegishi, T. Yokomizo, S. Takahashi, K.-C. Lim, J. D. Engel, and M. Yamamoto
GATA Motifs Regulate Early Hematopoietic Lineage-Specific Expression of the Gata2 Gene
Mol. Cell. Biol.,
August 15, 2005;
25(16):
7005 - 7020.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
M. Yoshida, K. Nosaka, J.-i. Yasunaga, I. Nishikata, K. Morishita, and M. Matsuoka
Aberrant expression of the MEL1S gene identified in association with hypomethylation in adult T-cell leukemia cells
Blood,
April 1, 2004;
103(7):
2753 - 2760.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
I. Nishikata, H. Sasaki, M. Iga, Y. Tateno, S. Imayoshi, N. Asou, T. Nakamura, and K. Morishita
A novel EVI1 gene family, MEL1, lacking a PR domain (MEL1S) is expressed mainly in t(1;3)(p36;q21)-positive AML and blocks G-CSF-induced myeloid differentiation
Blood,
November 1, 2003;
102(9):
3323 - 3332.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
H. Hirai
Molecular Mechanisms of Myelodysplastic Syndrome
Jpn. J. Clin. Oncol.,
April 1, 2003;
33(4):
153 - 160.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
J. Cools, N. Mentens, M. D. Odero, P. Peeters, I. Wlodarska, M. Delforge, A. Hagemeijer, and P. Marynen
Evidence for position effects as a variant ETV6-mediated leukemogenic mechanism in myeloid leukemias with a t(4;12)(q11-q12;p13) or t(5;12)(q31;p13)
Blood,
March 1, 2002;
99(5):
1776 - 1784.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
