The role of glioma stem cells in chemotherapy resistance and glioblastoma multiforme recurrence

被引:278
作者
Auffinger, Brenda [1 ]
Spencer, Drew [1 ]
Pytel, Peter [1 ]
Ahmed, Atique U. [1 ]
Lesniak, Maciej S. [1 ]
机构
[1] Univ Chicago, Brain Tumor Ctr, Chicago, IL 60637 USA
关键词
chemoresistance; glioma stem cells; malignant glioma; mechanisms; plasticity recurrence; TUMOR-INITIATING CELLS; TYROSINE KINASE GENES; SIDE POPULATION; MULTIDRUG-RESISTANCE; CLONAL EVOLUTION; DRUG-RESISTANCE; SELF-RENEWAL; DNA-REPAIR; TEMOZOLOMIDE; BRAIN;
D O I
10.1586/14737175.2015.1051968
中图分类号
R74 [神经病学与精神病学];
学科分类号
100204 [神经病学];
摘要
Glioma stem cells (GSCs) constitute a slow-dividing, small population within a heterogeneous glioblastoma. They are able to self-renew, recapitulate a whole tumor, and differentiate into other specific glioblastoma multiforme (GBM) subpopulations. Therefore, they have been held responsible for malignant relapse after primary standard therapy and the poor prognosis of recurrent GBM. The failure of current therapies to eliminate specific GSC subpopulations has been considered a major factor contributing to the inevitable recurrence in GBM patients after treatment. Here, we discuss the molecular mechanisms of chemoresistance of GSCs and the reasons why complete eradication of GSCs is so difficult to achieve. We will also describe the targeted therapies currently available for GSCs and possible mechanisms to overcome such chemoresistance and avoid therapeutic relapse.
引用
收藏
页码:741 / 752
页数:12
相关论文
共 111 条
[1]
Ahmed AU, 2013, EXPERT REV NEUROTHER, V13, P545, DOI [10.1586/ern.13.42, 10.1586/ERN.13.42]
[2]
Aldea MD, 2014, J BUON, V19, P502
[3]
The Implications of Clonal Genome Evolution for Cancer Medicine [J].
Aparicio, Samuel ;
Caldas, Carlos .
NEW ENGLAND JOURNAL OF MEDICINE, 2013, 368 (09) :842-851
[4]
Conversion of differentiated cancer cells into cancer stem-like cells in a glioblastoma model after primary chemotherapy [J].
Auffinger, B. ;
Tobias, A. L. ;
Han, Y. ;
Lee, G. ;
Guo, D. ;
Dey, M. ;
Lesniak, M. S. ;
Ahmed, A. U. .
CELL DEATH AND DIFFERENTIATION, 2014, 21 (07) :1119-1131
[5]
Glioma stem cells promote radioresistance by preferential activation of the DNA damage response [J].
Bao, Shideng ;
Wu, Qiulian ;
McLendon, Roger E. ;
Hao, Yueling ;
Shi, Qing ;
Hjelmeland, Anita B. ;
Dewhirst, Mark W. ;
Bigner, Darell D. ;
Rich, Jeremy N. .
NATURE, 2006, 444 (7120) :756-760
[6]
Delineating the Cytogenomic and Epigenomic Landscapes of Glioma Stem Cell Lines [J].
Baronchelli, Simona ;
Bentivegna, Angela ;
Redaelli, Serena ;
Riva, Gabriele ;
Butta, Valentina ;
Paoletta, Laura ;
Isimbaldi, Giuseppe ;
Miozzo, Monica ;
Tabano, Silvia ;
Daga, Antonio ;
Marubbi, Daniela ;
Cattaneo, Monica ;
Biunno, Ida ;
Dalpra, Leda .
PLOS ONE, 2013, 8 (02)
[7]
Chk1 and Chk2 kinases in checkpoint control and cancer [J].
Bartek, J ;
Lukas, J .
CANCER CELL, 2003, 3 (05) :421-429
[8]
Replication stress and oxidative damage contribute to aberrant constitutive activation of DNA damage signalling in human gliomas [J].
Bartkova, J. ;
Hamerlik, P. ;
Stockhausen, M-T ;
Ehrmann, J. ;
Hlobilkova, A. ;
Laursen, H. ;
Kalita, O. ;
Kolar, Z. ;
Poulsen, H. S. ;
Broholm, H. ;
Lukas, J. ;
Bartek, J. .
ONCOGENE, 2010, 29 (36) :5095-5102
[9]
Temozolomide preferentially depletes cancer stem cells in glioblastoma [J].
Beier, Dagmar ;
Roehrl, Stefanie ;
Pillai, Deepu R. ;
Schwarz, Stefanie ;
Kunz-Schughart, Leoni A. ;
Leukel, Petra ;
Proescholdt, Martin ;
Brawanski, Alexander ;
Bogdahn, Ulrich ;
Trampe-Kieslich, Ariane ;
Giebel, Bernd ;
Wischhusen, Joerg ;
Reifenberger, Guido ;
Hau, Peter ;
Beier, Christoph P. .
CANCER RESEARCH, 2008, 68 (14) :5706-5715
[10]
Chemoresistance of glioblastoma cancer stem cells - much more complex than expected [J].
Beier, Dagmar ;
Schulz, Joerg B. ;
Beier, Christoph P. .
MOLECULAR CANCER, 2011, 10