Understanding the Revised Fourth Edition of the World Health Organization Classification of Tumours of the Central Nervous System (2016) for Clinical Decision-making: A Guide for Oncologists Managing Patients with Glioma

Back, Michael; Rodriguez, M. Gonzalez; Jayamanne, Dasantha; Khasraw, Mustafa; Lee, A.; Wheeler, Helen

doi:10.1016/j.clon.2018.06.005

Cited by 8 publications

(5 citation statements)

References 31 publications

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“…Glioblastoma multiforme (GBM), the most common primary malignant brain tumor in adults, is associated with poor prognosis and high lethality (1). Patient survival remains dismal owing to therapeutic resistance to clinically approved drugs Studies in human brain cancer models have identified a central role of CSCs in brain tumor initiation, progression and chemoresistance (3,5,6).…”

Section: Introductionmentioning

confidence: 99%

Targeting the ABC transporter ABCB5 sensitizes glioblastoma to temozolomide-induced apoptosis through a cell-cycle checkpoint regulation mechanism

Lee

Banerjee

Wilson

et al. 2020

Journal of Biological Chemistry

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Glioblastoma multiforme (GBM) is a malignant brain tumor with a poor prognosis resulting from tumor resistance to anticancer therapy and a high recurrence rate. Compelling evidence suggests that this is driven by subpopulations of cancer stem cells (CSCs) with tumor-initiating potential. ABC subfamily B member 5 (ABCB5) has been identified as a molecular marker for distinct subsets of chemoresistant tumor-initiating cell populations in diverse human malignancies. In the current study, we examined the potential role of ABCB5 in growth and chemoresistance of GBM. We found that ABCB5 is expressed in primary GBM tumors, in which its expression was significantly correlated with the CSC marker protein CD133 and with overall poor survival. Moreover, ABCB5 was also expressed by CD133-positive CSCs in the established human U-87 MG, LN-18, and LN-229 GBM cell lines. Antibody- or shRNA-mediated functional ABCB5 blockade inhibited proliferation and survival of GBM cells and sensitized them to temozolomide (TMZ)-induced apoptosis in vitro. Likewise, in in vivo human GBM xenograft experiments with immunodeficient mice, mAb treatment inhibited growth of mutant TP53, WT PTEN LN-229 tumors, and sensitized LN-229 tumors to TMZ therapy. Mechanistically, we demonstrate that ABCB5 blockade inhibits TMZ-induced G2/M arrest and augments TMZ-mediated cell death. Our results identify ABCB5 as a GBM chemoresistance marker and point to the potential utility of targeting ABCB5 to improve current GBM therapies.

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Section: Introductionmentioning

confidence: 99%

Targeting the ABC transporter ABCB5 sensitizes glioblastoma to temozolomide-induced apoptosis through a cell-cycle checkpoint regulation mechanism

Lee

Banerjee

Wilson

et al. 2020

Journal of Biological Chemistry

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“…This result is due to the small number of patients, which is not representative of the population. Traditionally, patients with glial tumors were classified using H-E, and in some cases, the search for the mutation in the gene that codes for Isocitrate Dehydrogenase (IDH) is performed by immunohistochemistry (IHC) according to the WHO 2016 criteria [12]. Based on these two analyses, we obtained the following results in the 31 patients with high-grade gliomas: 21 glioblastomas, five anaplastic astrocytomas, and five anaplastic oligoastrocytoma; see Supplementary Material 1.…”

Section: Discussionmentioning

confidence: 99%

Mutations in the PIK3C2B, ERBB3, KIT, and MLH1 Genes and their Relationship with Resistance to Temozolomide in Patients with High-grade Gliomas

Gómez¹,

Martínez²,

Flórez³

et al. 2023

Preprint

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Background. The treatment for patients with high-grade gliomas includes radiation therapy and temozolomide. However, some patients do not respond to temozolomide because they have a methylation reversal mechanism through the enzyme O6-methylguanine-DNA-methyltransferase. This biomarker has been used as a prognostic factor in patients receiving treatment with temozolomide. However, not all patients respond in the same way, which suggests the existence of other genes involved in resistance to temozolomide. Materials and Methods. A group of 31 patients with high-grade gliomas was recruited and were clinically, image pattern, and pathologically characterized. The sequencing of 324 genes related to different types of cancer was performed to detect mutations. Subsequently, a statistical analysis was conducted to determine the mutated genes that were most related to resistance to treatment. Results. The genes related to the second relapse of patients with high-grade glioma after the use of temozolomide according to Stupp protocol and metronomic dose were PIK3C2B, KIT, ERBB3, and MLH1. Conclusions. Considering the results obtained, we suggest that the mutations in the four genes and the methylation of the gene promoter that codes for MGMT protein could be related to the clinical evolution of patients with high-grade gliomas and its response to treatment with temozolomide.

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“…The proliferation index, Ki67 percentage positive (Ki67%), was recorded. Potential prognostic molecular profiles using protein sequencing for isocitrate dehydrogenase (IDH) mutation, O-6-methylguanine-DNA methyltransferase (MGMT) promoter status and EGFR amplification were gradually introduced into practice from 2012 as evidence improved for their utility [ 6 ].…”

Section: Methodsmentioning

confidence: 99%

Optimising Outcomes for Glioblastoma through Subspecialisation in a Regional Cancer Centre

et al. 2018

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Delivery of highly sophisticated, and subspecialised, management protocols for glioblastoma in low volume rural and regional areas creates potential issues for equivalent quality of care. This study aims to demonstrate the impact on clinical quality indicators through the development of a novel model of care delivering an outsourced subspecialised neuro-oncology service in a regional centre compared with the large volume metropolitan centre. Three hundred and fifty-two patients with glioblastoma were managed under the European Organisation for Research and Treatment of Cancer and National Cancer Institute of Canada Clinical Trials Group (EORTC-NCIC) Protocol, and survival outcome was assessed in relation to potential prognostic factors and the geographical site of treatment, before and after opening of a regional cancer centre. The median overall survival was 17 months (95% CI: 15.5–18.5), with more favourable outcome with age less than 50 years (p < 0.001), near-total resection (p < 0.001), Eastern Cooperative Oncology Group (ECOG) Performance status 0, 1 (p < 0.001), and presence of O-6 methylguanine DNA methyltransferase (MGMT) methylation (p = 0.001). There was no difference in survival outcome for patients managed at the regional centre, compared with metropolitan centre (p = 0.35). Similarly, no difference was seen with clinical quality process indicators of clinical trial involvement, rates of repeat craniotomy, use of bevacizumab and re-irradiation. This model of neuro-oncology subspecialisation allowed equivalent outcomes to be achieved within a regional cancer centre compared to large volume metropolitan centre.

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Understanding the Revised Fourth Edition of the World Health Organization Classification of Tumours of the Central Nervous System (2016) for Clinical Decision-making: A Guide for Oncologists Managing Patients with Glioma

Cited by 8 publications

References 31 publications

Targeting the ABC transporter ABCB5 sensitizes glioblastoma to temozolomide-induced apoptosis through a cell-cycle checkpoint regulation mechanism

Targeting the ABC transporter ABCB5 sensitizes glioblastoma to temozolomide-induced apoptosis through a cell-cycle checkpoint regulation mechanism

Mutations in the PIK3C2B, ERBB3, KIT, and MLH1 Genes and their Relationship with Resistance to Temozolomide in Patients with High-grade Gliomas

Optimising Outcomes for Glioblastoma through Subspecialisation in a Regional Cancer Centre

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