Normal and transforming functions of RUNX1: A perspective

被引:49
作者
Mikhail, FM
Sinha, KK
Saunthararajah, Y
Nucifora, G
机构
[1] Univ Illinois, Dept Pathol, Chicago, IL 60607 USA
[2] Univ Illinois, Dept Med, Chicago, IL 60607 USA
[3] Univ Alabama Birmingham, Dept Genet, Birmingham, AL USA
[4] Univ Alexandria, Fac Med, Dept Clin Pathol, Alexandria, Egypt
关键词
D O I
10.1002/jcp.20538
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Converging studies from many investigators indicate that RUNX1 has a critical role in the correct maintenance of essential cellular functions during embryonic development and after birth. The discovery that this gene is also frequently mutated in human leukemia has increased the interest in the role that RUNX1 plays in both normal and transforming pathways. Here, we provide an overview of the many roles of RUNX1 in hematopoietic self-renewal and differentiation and summarize the information that is currently available on the many mechanisms of RUNX1 deregulation in human leukemia.
引用
收藏
页码:582 / 593
页数:12
相关论文
共 152 条
[31]   Intergenic splicing of MDS1 and EVI1 occurs in normal tissues as well as in myeloid leukemia and produces a new member of the PR domain family [J].
Fears, S ;
Mathieu, C ;
ZeleznikLe, N ;
Huang, S ;
Rowley, JD ;
Nucifora, G .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1996, 93 (04) :1642-1647
[32]  
FEINSTEIN PG, 1995, GENETICS, V140, P573
[33]  
Fenrick R, 1999, MOL CELL BIOL, V19, P6566
[34]   Absence of point mutations within the AML-1 gene in patients with MDS/AML and loss of chromosome 5q or 7 [J].
Ferrari, T ;
Weber, B ;
Pils, S ;
Harbott, J ;
Borkhardt, A .
ANNALS OF HEMATOLOGY, 2001, 80 (02) :72-73
[35]   Fetal origins of the TEL-AML1 fusion gene in identical twins with leukemia [J].
Ford, AM ;
Bennett, CA ;
Price, CM ;
Bruin, MCA ;
Van Wering, ER ;
Greaves, M .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1998, 95 (08) :4584-4588
[36]   Abnormal inside-out signal transduction-dependent activation of glycoprotein IIb-IIIa in a patient with impaired pleckstrin phosphorylation [J].
Gabbeta, J ;
Yang, X ;
Sun, L ;
McLane, MA ;
Niewiarowski, S ;
Rao, AK .
BLOOD, 1996, 87 (04) :1368-1376
[37]   The partner gene of AML1 in t(16;21) myeloid malignancies is a novel member of the MTG8(ETO) family [J].
Gamou, T ;
Kitamura, E ;
Hosoda, F ;
Shimizu, K ;
Shinohara, K ;
Hayashi, Y ;
Nagase, T ;
Yokoyama, Y ;
Ohki, M .
BLOOD, 1998, 91 (11) :4028-4037
[38]   Aberrant recruitment of the nuclear receptor corepressor-histone deacetylase complex by the acute myeloid leukemia fusion partner ETO [J].
Gelmetti, V ;
Zhang, JS ;
Fanelli, M ;
Minucci, S ;
Pelicci, PG ;
Lazar, MA .
MOLECULAR AND CELLULAR BIOLOGY, 1998, 18 (12) :7185-7191
[39]   INHERITED PLATELET-STORAGE POOL DEFICIENCY ASSOCIATED WITH A HIGH-INCIDENCE OF ACUTE MYELOID-LEUKEMIA [J].
GERRARD, JM ;
ISRAELS, ED ;
BISHOP, AJ ;
SCHROEDER, ML ;
BEATTIE, LL ;
MCNICOI, A ;
ISRAELS, SJ ;
WALZ, D ;
GREENBERG, AH ;
RAY, M ;
ISRAELS, LG .
BRITISH JOURNAL OF HAEMATOLOGY, 1991, 79 (02) :246-255
[40]   FUSION OF THE TEL GENE ON 12P13 TO THE AML1 GENE ON 21Q22 IN ACUTE LYMPHOBLASTIC-LEUKEMIA [J].
GOLUB, TR ;
BARKER, GF ;
BOHLANDER, SK ;
HIEBERT, SW ;
WARD, DC ;
BRAYWARD, P ;
MORGAN, E ;
RAIMONDI, SC ;
ROWLEY, JD ;
GILLILAND, DG .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1995, 92 (11) :4917-4921