Dexamethasone in Glioblastoma Multiforme Therapy: Mechanisms and Controversies

被引:71
作者
Cenciarini, Marta [1 ]
Valentino, Mario [2 ]
Belia, Silvia [3 ]
Sforna, Luigi [1 ]
Rosa, Paolo [4 ]
Ronchetti, Simona [5 ]
D'Adamo, Maria Cristina [2 ]
Pessia, Mauro [1 ,2 ]
机构
[1] Univ Perugia, Dept Expt Med, Sect Physiol & Biochem, Sch Med, Perugia, Italy
[2] Univ Malta, Fac Med & Surg, Dept Physiol & Biochem, Msida, Malta
[3] Univ Perugia, Dept Chem Biol & Biotechnol, Perugia, Italy
[4] Univ Rome Sapienza, Dept Med Surg Sci & Biotechnol, Latina, Italy
[5] Univ Perugia, Dept Med, Sect Pharmacol, Sch Med, Perugia, Italy
关键词
GBM; dexamethasone; cerebral oedema; pharmacogenomics; glioblastoma multiforme therapy; BLOOD-BRAIN-BARRIER; HYPOXIA-INDUCIBLE FACTORS; ENDOTHELIAL GROWTH-FACTOR; ISOCITRATE DEHYDROGENASE MUTATIONS; POTASSIUM CHANNEL EXPRESSION; INTEGRATED GENOMIC ANALYSIS; CENTRAL-NERVOUS-SYSTEM; HUMAN GLIOMA-CELLS; TUMOR BARRIER; MALIGNANT GLIOMA;
D O I
10.3389/fnmol.2019.00065
中图分类号
Q189 [神经科学];
学科分类号
071006 [神经生物学];
摘要
Glioblastoma multiforme (GBM) is the most common and malignant of the glial tumors. The world-wide estimates of new cases and deaths annually are remarkable, making GBM a crucial public health issue. Despite the combination of radical surgery, radio and chemotherapy prognosis is extremely poor (median survival is approximately 1 year). Thus, current therapeutic interventions are highly unsatisfactory. For many years, GBM-induced brain oedema and inflammation have been widely treated with dexamethasone (DEX), a synthetic glucocorticoid (GC). A number of studies have reported that DEX also inhibits GBM cell proliferation and migration. Nevertheless, recent controversial results provided by different laboratories have challenged the widely accepted dogma concerning DEX therapy for GBM. Here, we have reviewed the main clinical features and genetic and epigenetic abnormalities underlying GBM. Finally, we analyzed current notions and concerns related to DEX effects on cerebral oedema, cancer cell proliferation and migration and clinical outcome.
引用
收藏
页数:13
相关论文
共 170 条
[1]
EMP3, a myelin-related gene located in the critical 19q13.3 region, is epigenetically silenced and exhibits features of a candidate tumor suppressor in glioma and neuroblastoma [J].
Alaminos, M ;
Dávalos, V ;
Ropero, S ;
Setién, F ;
Paz, MF ;
Herranz, M ;
Fraga, MF ;
Mora, J ;
Cheung, NKV ;
Gerald, WL ;
Esteller, M .
CANCER RESEARCH, 2005, 65 (07) :2565-2571
[2]
Alexiou GA, 2010, NEUROL NEUROCHIR POL, V44, P80
[3]
Hypoxia Helps Glioma to Fight Therapy [J].
Amberger-Murphy, Verena .
CURRENT CANCER DRUG TARGETS, 2009, 9 (03) :381-390
[4]
Suberoylanilide hydroxamic acid limits migration and invasion of glioma cells in two and three dimensional culture [J].
An, Zhihua ;
Gluck, Christian B. ;
Choy, Megan L. ;
Kaufman, Laura J. .
CANCER LETTERS, 2010, 292 (02) :215-227
[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]
Effects of radiation on a model of malignant glioma invasion [J].
Bauman, GS ;
MacDonald, W ;
Moore, E ;
Ramsey, DA ;
Fisher, BJ ;
Amberger, VR ;
Del Maestro, RM .
JOURNAL OF NEURO-ONCOLOGY, 1999, 44 (03) :223-231
[7]
Beauchesne Patrick, 2011, Cancers (Basel), V3, P461, DOI 10.3390/cancers3010461
[8]
Microregional extracellular matrix heterogeneity in brain modulates glioma cell invasion [J].
Bellail, AC ;
Hunter, SB ;
Brat, DJ ;
Tan, C ;
Van Meir, EG .
INTERNATIONAL JOURNAL OF BIOCHEMISTRY & CELL BIOLOGY, 2004, 36 (06) :1046-1069
[9]
Histone deacetylase inhibitors in glioblastoma: pre-clinical and clinical experience [J].
Bezecny, Pavel .
MEDICAL ONCOLOGY, 2014, 31 (06)
[10]
Potential of diffusion imaging in brain tumors: A review [J].
Bode, M. K. ;
Ruohonen, J. ;
Nieminen, M. T. ;
Pyhtinen, J. .
ACTA RADIOLOGICA, 2006, 47 (06) :585-594