Gatekeeper pathways and cellular background in the pathogenesis and therapy of AML

被引：14

作者：

Cammenga, J ^{[1
]}

机构：

[1] Heinrich Pette Inst Expt Virol & Immunol, Dept Mol Pathol, Hamburg, Germany

来源：

LEUKEMIA | 2005年 / 19卷 / 10期

关键词：

AML; gatekeepers; transcription factors; therapy; hematopoietic stem/progenitor cells;

D O I：

10.1038/sj.leu.2403894

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

Acute myelogenous leukemia (AML) is characterized by the accumulation of immature cells due to disturbed differentiation and proliferation of the myeloid lineage. Genetic alterations affecting transcription factors and receptor tyrosine kinases have been identified in AML and causally linked to the disease. The goal of this review is to address the role of the different genetic alterations in self-renewal and proliferation and to discuss the cellular background in which these events occur during the pathogenesis of AML. Data from AML samples, clinical studies and mouse models for AML will be used to support the different theories regarding the leukemogenesis of AML. Finally, this review wants to highlight the implication of these findings for the therapy of AML.

引用

页码：1719 / 1728

页数：10

共 97 条

[1] A clonogenic common myeloid progenitor that gives rise to all myeloid lineages [J].

Akashi, K ;

Traver, D ;

Miyamoto, T ;

Weissman, IL .

NATURE, 2000, 404 (6774) :193-197

[2] Transformation of myeloid progenitors by MLL oncoproteins is dependent on Hoxa7 and Hoxa9 [J].

Ayton, PM ;

Cleary, ML .

GENES & DEVELOPMENT, 2003, 17 (18) :2298-2307

[3]

Blackburn AC, 2003, CANCER RES, V63, P2364

[4] Human acute myeloid leukemia is organized as a hierarchy that originates from a primitive hematopoietic cell [J].

Bonnet, D ;

Dick, JE .

NATURE MEDICINE, 1997, 3 (07) :730-737

[5] A PMLRAR alpha transgene initiates murine acute promyelocytic leukemia [J].

Brown, D ;

Kogan, S ;

Lagasse, E ;

Weissman, I ;

Alcalay, M ;

Pelicci, PG ;

Atwater, S ;

Bishop, JM .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1997, 94 (06) :2551-2556

[6] EVI1 induces myelodysplastic syndrome in mice [J].

Buonamici, S ;

Li, DL ;

Chi, YQ ;

Zhao, R ;

Wang, XR ;

Brace, L ;

Ni, HY ;

Saunthararajah, Y ;

Nucifora, G .

JOURNAL OF CLINICAL INVESTIGATION, 2004, 114 (05) :713-719

[7] The role of EVI1 in normal and leukemic cells [J].

Buonamici, S ;

Chakraborty, S ;

Senyuk, V ;

Nucifora, G .

BLOOD CELLS MOLECULES AND DISEASES, 2003, 31 (02) :206-212

[8] Deregulated expression of HOXB4 enhances the primitive growth activity of human hematopoietic cells [J].

Buske, C ;

Feuring-Buske, M ;

Abramovich, C ;

Spiekermann, K ;

Eaves, CJ ;

Coulombel, L ;

Sauvageau, G ;

Hogge, DE ;

Humphries, RK .

BLOOD, 2002, 100 (03) :862-868

[9] Induction of C/EBPα activity alters gene expression and differentiation of human CD34+ cells [J].

Cammenga, J ;

Mulloy, JC ;

Berguido, FJ ;

MacGrogan, D ;

Viale, A ;

Nimer, SD .

BLOOD, 2003, 101 (06) :2206-2214

[10] Incidence and prognosis of c-KIT and FLT3 mutations in core binding factor (CBF) acute myeloid leukaemias [J].

Care, RS ;

Valk, PJM ;

Goodeve, AC ;

Abu-Duhier, FM ;

Geertsma-Kleinekoort, WMC ;

Wilson, GA ;

Gari, MA ;

Peake, IR ;

Löwenberg, B ;

Reilly, JT .

BRITISH JOURNAL OF HAEMATOLOGY, 2003, 121 (05) :775-777

← 1 2 3 4 5 6 7 8 9 10 →