TY - JOUR
T1 - Dexamethasone in glioblastoma multiforme therapy
T2 - Mechanisms and controversies
AU - Cenciarini, Marta
AU - Valentino, Mario
AU - Belia, Silvia
AU - Sforna, Luigi
AU - Rosa, Paolo
AU - Ronchetti, Simona
AU - D’Adamo, Maria Cristina
AU - Pessia, Mauro
N1 - Funding Information:
This work was supported by the University of Malta—Research, Innovation and Development Trust (RIDT) and Internal Research Grant. MV was supported by the Alfred Mizzi Foundation, Malta through the RIDT.
Publisher Copyright:
© 2019 Cenciarini, Valentino, Belia, Sforna, Rosa, Ronchetti, D’Adamo and Pessia.
PY - 2019/2/12
Y1 - 2019/2/12
N2 - 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.
AB - 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.
KW - Cerebral oedema
KW - Dexamethasone
KW - GBM
KW - Glioblastoma multiforme therapy
KW - Pharmacogenomics
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U2 - 10.3389/fnmol.2019.00065
DO - 10.3389/fnmol.2019.00065
M3 - Review article
AN - SCOPUS:85064220556
SN - 1662-5099
VL - 12
JO - Frontiers in Molecular Neuroscience
JF - Frontiers in Molecular Neuroscience
M1 - 65
ER -