|
|
 Previous Article | Table of Contents | Next Article 
Frequent loss of heterozygosity at the TEL gene locus in acute
lymphoblastic leukemia of childhood
K Stegmaier, S Pendse, GF Barker, P Bray-Ward, DC Ward, KT Montgomery, KS Krauter, C Reynolds, J Sklar and M Donnelly
Division of Hematology/Oncology, Brigham and Women's Hospital, Harvard
Medical School, Boston, MA, USA.
TEL is a new member of the ETS family of transcription factors which is
rearranged in a number of hematologic malignancies with translocations
involving chromosome band 12p13. In some cases, both TEL alleles are
affected, resulting in loss of wild-type TEL function in the leukemic
cells. In addition, 5% of children with acute lymphoblastic leukemia (ALL)
have 12p12-p13 deletions, suggesting that a tumor suppressor gene resides
on 12p. These observations led us to consider whether TEL loss of function
may contribute to the pathogenesis of ALL. In this report we show that the
TEL gene maps between the polymorphic markers D12S89 and D12S98, and we use
these flanking markers to screen paired diagnosis and remission samples
from 81 children with ALL for loss of heterozygosity (LOH) at the TEL gene
locus. Fifteen percent of informative patients showed TEL LOH which was not
evident on cytogenetic analysis. Detailed examination of patients with LOH
at this locus showed that the critically deleted region included two
candidate tumor suppressor genes: TEL and KIP1, the gene encoding the
cyclin- dependent kinase inhibitor p27. These studies show that LOH at the
TEL locus is a frequent finding in childhood ALL.
Volume 86,
Issue 1,
pp. 38-44,
07/01/1995
Copyright © 1995 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. Hulit, R. J. Lee, Z. Li, C. Wang, S. Katiyar, J. Yang, A. A. Quong, K. Wu, C. Albanese, R. Russell, et al.
p27Kip1 Repression of ErbB2-Induced Mammary Tumor Growth in Transgenic Mice Involves Skp2 and Wnt/{beta}-Catenin Signaling.
Cancer Res.,
September 1, 2006;
66(17):
8529 - 8541.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
S. Kim, K. Chin, J. W. Gray, and J. M. Bishop
A screen for genes that suppress loss of contact inhibition: Identification of ING4 as a candidate tumor suppressor gene in human cancer
PNAS,
November 16, 2004;
101(46):
16251 - 16256.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
T. Motiwala, H. Kutay, K. Ghoshal, S. Bai, H. Seimiya, T. Tsuruo, S. Suster, C. Morrison, and S. T. Jacob
Protein tyrosine phosphatase receptor-type O (PTPRO) exhibits characteristics of a candidate tumor suppressor in human lung cancer
PNAS,
September 21, 2004;
101(38):
13844 - 13849.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
H. Kawagoe, M. Potter, J. Ellis, and G. C. Grosveld
TEL2, an ETS Factor Expressed in Human Leukemia, Regulates Monocytic Differentiation of U937 Cells and Blocks the Inhibitory Effect of TEL1 on Ras-Induced Cellular Transformation
Cancer Res.,
September 1, 2004;
64(17):
6091 - 6100.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
B. J. Irvin, L. D. Wood, L. Wang, R. Fenrick, C. G. Sansam, G. Packham, M. Kinch, E. Yang, and S. W. Hiebert
TEL, a Putative Tumor Suppressor, Induces Apoptosis and Represses Transcription of Bcl-XL
J. Biol. Chem.,
November 21, 2003;
278(47):
46378 - 46386.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
D. A. Sweetser, C.-S. Chen, A. A. Blomberg, D. A. Flowers, P. C. Galipeau, M. T. Barrett, N. A. Heerema, J. Buckley, W. G. Woods, I. D. Bernstein, et al.
Loss of heterozygosity in childhood de novo acute myelogenous leukemia
Blood,
August 15, 2001;
98(4):
1188 - 1194.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
A. T. Maia, A. M. Ford, G. R. Jalali, C. J. Harrison, G. M. Taylor, O. B. Eden, and M. F. Greaves
Molecular tracking of leukemogenesis in a triplet pregnancy
Blood,
July 15, 2001;
98(2):
478 - 482.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
R. Fenrick, L. Wang, J. Nip, J. M. Amann, R. J. Rooney, J. Walker-Daniels, H. C. Crawford, D. L. Hulboy, M. S. Kinch, L. M. Matrisian, et al.
TEL, a Putative Tumor Suppressor, Modulates Cell Growth and Cell Morphology of Ras-Transformed Cells While Repressing the Transcription of stromelysin-1
Mol. Cell. Biol.,
August 15, 2000;
20(16):
5828 - 5839.
[Abstract]
[Full Text]
|
|
|
|
|
|
|
R. Chiarle, L. M. Budel, J. Skolnik, G. Frizzera, M. Chilosi, A. Corato, G. Pizzolo, J. Magidson, A. Montagnoli, M. Pagano, et al.
Increased proteasome degradation of cyclin-dependent kinase inhibitor p27 is associated with a decreased overall survival in mantle cell lymphoma
Blood,
January 15, 2000;
95(2):
619 - 626.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
R. Fenrick, J. M. Amann, B. Lutterbach, L. Wang, J. J. Westendorf, J. R. Downing, and S. W. Hiebert
Both TEL and AML-1 Contribute Repression Domains to the t(12;21) Fusion Protein
Mol. Cell. Biol.,
October 1, 1999;
19(10):
6566 - 6574.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
L. C. Wang, W. Swat, Y. Fujiwara, L. Davidson, J. Visvader, F. Kuo, F. W. Alt, D. G. Gilliland, T. R. Golub, and S. H. Orkin
The TEL/ETV6 gene is required specifically for hematopoiesis in the bone marrow
Genes & Dev.,
August 1, 1998;
12(15):
2392 - 2402.
[Abstract]
[Full Text]
|
|
|
|
|
|
|
S. Faderl, H. M. Kantarjian, M. Talpaz, and Z. Estrov
Clinical Significance of Cytogenetic Abnormalities in Adult Acute Lymphoblastic Leukemia
Blood,
June 1, 1998;
91(11):
3995 - 4019.
[Full Text]
[PDF]
|
|
|
|
|
|
|
A. M. Ford, C. A. Bennett, C. M. Price, M. C. A. Bruin, E. R. Van Wering, and M. Greaves
Fetal origins of the TEL-AML1 fusion gene in identical twins with leukemia
PNAS,
April 14, 1998;
95(8):
4584 - 4588.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
S. Fears, M. Gavin, D.-E. Zhang, C. Hetherington, Y. Ben-David, J. D. Rowley, and G. Nucifora
Functional characterization of ETV6 and ETV6/CBFA2 in the regulation of the MCSFR proximal promoter
PNAS,
March 4, 1997;
94(5):
1949 - 1954.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
M Baens, P Peeters, C Guo, J Aerssens, and P Marynen
Genomic organization of TEL: the human ETS-variant gene 6.
Genome Res.,
May 1, 1996;
6(5):
404 - 413.
[Abstract]
[PDF]
|
|
|
|
|
