Antiepileptic drugs in patients with malignant brain tumor: beyond seizures and pharmacokinetics

被引:22
作者
Gefroh-Grimes, H. A. [1 ]
Gidal, B. E. [2 ,3 ]
机构
[1] Univ Wisconsin, Sch Pharm, Pharm Practice Div, Madison, WI 53705 USA
[2] Univ Wisconsin, Sch Pharm, Madison, WI 53705 USA
[3] Univ Wisconsin, Dept Neurol, Madison, WI 53705 USA
来源
ACTA NEUROLOGICA SCANDINAVICA | 2016年 / 133卷 / 01期
关键词
antiepileptic drugs; carbamazepine; epigenetics; histone deacetylase; glioblastoma; levetiracetam; valproic acid; HISTONE DEACETYLASE INHIBITORS; NEWLY-DIAGNOSED GLIOBLASTOMA; GLIOMA-CELL LINES; VALPROIC ACID USE; IN-VITRO; CHROMATIN MODIFICATIONS; RADIATION-THERAPY; GAMMA-H2AX FOCI; HDAC INHIBITORS; PHASE-II;
D O I
10.1111/ane.12437
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
In neurological malignancies, antiepileptic drugs (AEDs) are frequently used to control the seizure activity that accompanies the disorder. There is a growing body of evidence on the importance of AED selection for reasons other than pharmacokinetics (PK) properties. Epigenetic modifications may occur in glioblastomas, such as changes in gene methylation and histone acetylation states. Secondary mechanisms of AED drug action which impact these epigenetic modifications could play a significant role in patient survival outcomes. Both valproic acid (VPA) and carbamazepine have histone deacetylase (HDAC) inhibitory activities, and levetiracetam and VPA reduce the activity of O6-methylguanine-DNA methyltransferase (MGMT), a DNA-repair molecule implicated in resistance to alkylating agents used for chemotherapy. The use of AEDs for purposes other than seizure prophylaxis and their selection based on non-PK properties present a potential paradigm shift in the field of neuro-oncology.
引用
收藏
页码:4 / 16
页数:13
相关论文
共 82 条
[1]  
Alberta Provincial CNS Tumour Team, 2010, GLIOBL
[2]   Antiproliferative action of valproate is associated with aberrant expression and nuclear translocation of cyclin D3 during the C6 glioma G1 phase [J].
Bacon, CL ;
Gallagher, HC ;
Haughey, JC ;
Regan, CM .
JOURNAL OF NEUROCHEMISTRY, 2002, 83 (01) :12-19
[3]   Valproic Acid Use During Radiation Therapy for Glioblastoma Associated With Improved Survival [J].
Barker, Christopher A. ;
Bishop, Andrew J. ;
Chang, Maria ;
Beal, Kathryn ;
Chan, Timothy A. .
INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS, 2013, 86 (03) :504-509
[4]   Status Quo-Standard-of-Care Medical and Radiation Therapy for Glioblastoma [J].
Becker, Kevin P. ;
Yu, James .
CANCER JOURNAL, 2012, 18 (01) :12-19
[5]   Metabolic and endocrine effects of valproic acid chronic treatment [J].
Belcastro, Vincenzo ;
D'Egidio, Claudia ;
Striano, Pasquale ;
Verrotti, Alberto .
EPILEPSY RESEARCH, 2013, 107 (1-2) :1-8
[6]   Valproic acid for the treatment of malignant gliomas: review of the preclinical rationale and published clinical results [J].
Berendsen, Sharon ;
Broekman, Marike ;
Seute, Tatjana ;
Snijders, Tom ;
van Es, Corine ;
de Vos, Filip ;
Regli, Luca ;
Robe, Pierre .
EXPERT OPINION ON INVESTIGATIONAL DRUGS, 2012, 21 (09) :1391-1415
[7]   The mammalian epigenome [J].
Bernstein, Bradley E. ;
Meissner, Alexander ;
Lander, Eric S. .
CELL, 2007, 128 (04) :669-681
[8]   Carbamazepine is an inhibitor of histone deacetylases [J].
Beutler, AS ;
Li, SD ;
Nicol, R ;
Walsh, MJ .
LIFE SCIENCES, 2005, 76 (26) :3107-3115
[9]   VALPROIC ACID INDUCES THE GLUTAMATE TRANSPORTER EXCITATORY AMINO ACID TRANSPORTER-3 IN HUMAN OLIGODENDROGLIOMA CELLS [J].
Bianchi, M. G. ;
Franchi-Gazzola, R. ;
Reia, L. ;
Allegri, M. ;
Uggeri, J. ;
Chiu, M. ;
Sala, R. ;
Bussolati, O. .
NEUROSCIENCE, 2012, 227 :260-270
[10]   Levetiracetam enhances p53-mediated MGMT inhibition and sensitizes glioblastoma cells to temozolomide [J].
Bobustuc, George C. ;
Baker, Cheryl H. ;
Limaye, Arati ;
Jenkins, Wayne D. ;
Pearl, Gary ;
Avgeropoulos, Nicholas G. ;
Konduri, Santhi D. .
NEURO-ONCOLOGY, 2010, 12 (09) :917-927