Critical molecular pathways in cancer stem cells of chronic myeloid leukemia

被引：52

作者：

Chen, Y. ^{[1
]}

Peng, C. ^{[1
]}

Sullivan, C. ^{[2
]}

Li, D. ^{[3
]}

Li, S. ^{[1
]}

机构：

[1] Univ Massachusetts, Sch Med, Dept Med, Div Hematol Oncol, Worcester, MA 01605 USA

[2] Maine Inst Human Genet & Hlth, Dept Canc Res, Bangor, ME USA

[3] Edith Cowan Univ, Sch Comp & Secur Sci, Mt Lawley, WA, Australia

来源：

LEUKEMIA | 2010年 / 24卷 / 09期

关键词：

BCR-ABL; leukemic stem cells; CML; therapeutic agents; CHRONIC MYELOGENOUS LEUKEMIA; ACUTE LYMPHOBLASTIC-LEUKEMIA; HEDGEHOG-SIGNALING PATHWAY; COLONY-STIMULATING FACTOR; BCR-ABL; TYROSINE KINASE; BLAST-CRISIS; SONIC-HEDGEHOG; BETA-CATENIN; HEMATOPOIETIC-CELLS;

D O I：

10.1038/leu.2010.143

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

Inhibition of BCR-ABL with kinase inhibitors in the treatment of Philadelphia-positive (Ph+) chronic myeloid leukemia (CML) is highly effective in controlling but not curing the disease. This is largely due to the inability of these kinase inhibitors to kill leukemia stem cells (LSCs) responsible for disease relapse. This stem cell resistance is not associated with the BCR-ABL kinase domain mutations resistant to kinase inhibitors. Development of curative therapies for CML requires the identification of crucial molecular pathways responsible for the survival and self-renewal of LSCs. In this review, we will discuss our current understanding of these crucial molecular pathways in LSCs and the available therapeutic strategies for targeting these stem cells in CML. Leukemia (2010) 24, 1545-1554; doi:10.1038/leu.2010.143; published online 24 June 2010

引用

页码：1545 / 1554

页数：10

共 118 条

[1] beta-catenin is a target for the ubiquitin-proteasome pathway [J].

Aberle, H ;

Bauer, A ;

Stappert, J ;

Kispert, A ;

Kemler, R .

EMBO JOURNAL, 1997, 16 (13) :3797-3804

[2] Prospective identification of tumorigenic breast cancer cells [J].

Al-Hajj, M ;

Wicha, MS ;

Benito-Hernandez, A ;

Morrison, SJ ;

Clarke, MF .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2003, 100 (07) :3983-3988

[3]

Anderson KM, 1996, ANTICANCER RES, V16, P2589

[4] Selective inhibitors of 5-lipoxygenase reduce CML blast cell proliferation and induce limited differentiation and apoptosis [J].

Anderson, KM ;

Seed, T ;

Plate, JMD ;

Jajeh, A ;

Meng, J ;

Harris, JE .

LEUKEMIA RESEARCH, 1995, 19 (11) :789-801

[5] Targeting autophagy potentiates tyrosine kinase inhibitor-induced cell death in Philadelphia chromosome-positive cells, including primary CML stem cells [J].

Bellodi, Cristian ;

Lidonnici, Maria Rosa ;

Hamilton, Ashley ;

Helgason, G. Vignir ;

Soliera, Angela Rachele ;

Ronchetti, Mattia ;

Galavotti, Sara ;

Young, Kenneth W. ;

Selmi, Tommaso ;

Yacobi, Rinat ;

Van Etten, Richard A. ;

Donato, Nick ;

Hunter, Ann ;

Dinsdale, David ;

Tirro, Elena ;

Vigneri, Paolo ;

Nicotera, Pierluigi ;

Dyer, Martin J. ;

Holyoake, Tessa ;

Salomoni, Paolo ;

Calabretta, Bruno .

JOURNAL OF CLINICAL INVESTIGATION, 2009, 119 (05) :1109-1123

[6] Persistence of malignant hematopoietic progenitors in chronic myelogenous leukemia patients in complete cytogenetic remission following imatinib mesylate treatment [J].

Bhatia, R ;

Holtz, M ;

Niu, N ;

Gray, R ;

Snyder, DS ;

Sawyers, CL ;

Arber, DA ;

Slovak, ML ;

Forman, SJ .

BLOOD, 2003, 101 (12) :4701-4707

[7] Sertoli cell signaling by Desert hedgehog regulates the male germline [J].

Bitgood, MJ ;

Shen, LY ;

McMahon, AP .

CURRENT BIOLOGY, 1996, 6 (03) :298-304

[8] 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

[9] Akt promotes cell survival by phosphorylating and inhibiting a forkhead transcription factor [J].

Brunet, A ;

Bonni, A ;

Zigmond, MJ ;

Lin, MZ ;

Juo, P ;

Hu, LS ;

Anderson, MJ ;

Arden, KC ;

Blenis, J ;

Greenberg, ME .

CELL, 1999, 96 (06) :857-868

[10] The hematopoietic stem cell in chronic phase CML is characterized by a transcriptional profile resembling normal myeloid progenitor cells and reflecting loss of quiescence [J].

Bruns, I. ;

Czibere, A. ;

Fischer, J. C. ;

Roels, F. ;

Cadeddu, R-P ;

Buest, S. ;

Bruennert, D. ;

Huenerlituerkoglu, A. N. ;

Stoecklein, N. H. ;

Singh, R. ;

Zerbini, L. F. ;

Jaeger, M. ;

Kobbe, G. ;

Gattermann, N. ;

Kronenwett, R. ;

Brors, B. ;

Haas, R. .

LEUKEMIA, 2009, 23 (05) :892-899

← 1 2 3 4 5 6 7 8 9 10 →