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. 2015 Feb 13;6(Suppl 1):S9-S44.
doi: 10.4103/2152-7806.151331. eCollection 2015.

The future of high-grade glioma: Where we are and where are we going

Emilie Le Rhun, Emilie Le Rhun  1 , Sophie Taillibert  2 , Marc C Chamberlain  3
Affiliations

The future of high-grade glioma: Where we are and where are we going

Emilie Le Rhun et al. Surg Neurol Int. .

Erratum in

Abstract

High-grade glioma (HGG) are optimally treated with maximum safe surgery, followed by radiotherapy (RT) and/or systemic chemotherapy (CT). Recently, the treatment of newly diagnosed anaplastic glioma (AG) has changed, particularly in patients with 1p19q codeleted tumors. Results of trials currenlty ongoing are likely to determine the best standard of care for patients with noncodeleted AG tumors. Trials in AG illustrate the importance of molecular characterization, which are germane to both prognosis and treatment. In contrast, efforts to improve the current standard of care of newly diagnosed glioblastoma (GB) with, for example, the addition of bevacizumab (BEV), have been largely disappointing and furthermore molecular characterization has not changed therapy except in elderly patients. Novel approaches, such as vaccine-based immunotherapy, for newly diagnosed GB are currently being pursued in multiple clinical trials. Recurrent disease, an event inevitable in nearly all patients with HGG, continues to be a challenge. Both recurrent GB and AG are managed in similar manner and when feasible re-resection is often suggested notwithstanding limited data to suggest benefit from repeat surgery. Occassional patients may be candidates for re-irradiation but again there is a paucity of data to commend this therapy and only a minority of selected patients are eligible for this approach. Consequently systemic therapy continues to be the most often utilized treatment in recurrent HGG. Choice of therapy, however, varies and revolves around re-challenge with temozolomide (TMZ), use of a nitrosourea (most often lomustine; CCNU) or BEV, the most frequently used angiogenic inhibitor. Nevertheless, no clear standard recommendation regarding the prefered agent or combination of agents is avaliable. Prognosis after progression of a HGG remains poor, with an unmet need to improve therapy.

Keywords: Anaplastic glioma; anti-angiogenic agents; bevacizumab; chemotherapy; glioblastoma; high grade glioma; immunotherapy; nitrosourea; targeted therapy; temozolomide.

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Figures

Figure 1
Figure 1
Biomarker interactive model based upon NOA-04. IDH: Isocitrate dehydrogenase MGMT: 0-6 methylguanine DNA methyltransferase
Figure 2
Figure 2
NO 04-design. n Number of patients, R: Randomization; PD: Progression disease; TMZ: Temozolomide; PCV: Lomustine, vincristine, procarbazine. PCV: Lomustine 110 mg/m2 on day1, vincristine 2 mg on days 8 and 29, and procarbazine 60 mg/m2 on days 8 through 21 TMZ: 200 mg/m2 on days 1 through 5, every 28 days
Figure 3
Figure 3
RTOG 94-02 and EORTC 26951 trial design. AO: Anaplastic oligodendroglioma; AOA: Anaplastic oligoastrocytoma; n: Number of patients; PCV: Lomustine, vincristine, procarbazine
Figure 4
Figure 4
CATNON trial design. R: Randomization; RT: Radiotherapy, TMZ: Temozolomide
Figure 5
Figure 5
RTOG 0825 and AVAglio trial design. Tx: Treatment; RPA: Recursive Partitioning Analysis; RT: Radiotherapy; TMZ: Temozolomide; BEV: Bevacizumab; N: Number of patients; qd: Every day; q2w: Every 2 weeks; qd28: Every 28 days; q3w: Every 3 weeks; Tx:Treatment; PD: Progression disease
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