2021
DOI: 10.1016/j.ctrv.2020.102124
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A basic review on systemic treatment options in WHO grade II-III gliomas

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Cited by 54 publications
(57 citation statements)
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References 58 publications
(86 reference statements)
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“…Malignant gliomas are heterogeneous, highly invasive primary brain tumors and are managed by surgical removal of as much of the tumor bulk as is considered safe, followed by fractionated radiotherapy (RT; typically 60 Gy in 30–35 fractions), and concurrent chemotherapy, which is given continuously for at least an additional six months after cessation of RT [7] . Asymptomatic benign brain tumors can be followed up frequently until they become symptomatic, and then surgically resected and treated with adjuvant radiotherapy (RT) [8] .…”
Section: Introductionmentioning
confidence: 99%
“…Malignant gliomas are heterogeneous, highly invasive primary brain tumors and are managed by surgical removal of as much of the tumor bulk as is considered safe, followed by fractionated radiotherapy (RT; typically 60 Gy in 30–35 fractions), and concurrent chemotherapy, which is given continuously for at least an additional six months after cessation of RT [7] . Asymptomatic benign brain tumors can be followed up frequently until they become symptomatic, and then surgically resected and treated with adjuvant radiotherapy (RT) [8] .…”
Section: Introductionmentioning
confidence: 99%
“…The concept of lower-grade glioma (LGG, WHO Grades II and III) was proposed after the update to classify the central nervous system tumors by WHO in 2016 [3]. Compared to glioblastoma, LGGs were known to have a better prognosis and more prolonged survival and shared some similar molecular alterations [21,22], clinical and pathological features [21], or even treatment modalities [22,23]. Therefore, LGGs could not be clustered in the group of low-grade gliomas or high-grade glioma simply, and both the research of Zhao et al [17] and the study of Yang et al [20] were not well applicable for LGGs.…”
Section: Discussionmentioning
confidence: 99%
“…The incidence of an IDH mutation is very high in patients with WHO grade II-III glioma (more than 80%) and secondary glioblastoma (GBM) (73%), while it is uncommon among patients with primary GBM (3.7%) [2][3][4][5]. Gain-of-function of the IDH gene results in increased intracellular levels of 2-hydroxyglutarate, which leads to alterations of DNA methylation [11]. The final biological effect is cellular dedifferentiation and growth promotion, mainly mediated by gene transcription deregulation.…”
Section: Introductionmentioning
confidence: 99%
“…The final biological effect is cellular dedifferentiation and growth promotion, mainly mediated by gene transcription deregulation. Clinically, IDH-mutated tumors present prolonged survival and an improved response to chemotherapy as compared to IDH-wild type gliomas [11]. Indeed, IDH-wild type gliomas often amplify epidermal growth factor receptor (EGFR), gain of chromosome 7 and loss of chromosome 10 and telomerase reverse transcriptase (TERT) promoter mutations [11,12].…”
Section: Introductionmentioning
confidence: 99%