Abstract
Aims
Glioma is a fatal disease that causes significant years of life lost to an individual. Mutations in the driver gene BRAF, such as the V600 alteration, may contribute to gliomagenesis in ...adults and children through abnormal signaling causing uncontrolled cell proliferation. The use of BRAF-inhibitor drugs including Vemurafenib and Dabrafenib have shown a favorable response in 48% and 50% of melanoma patients with BRAF V600 mutations respectively. BRAF inhibitors and MEK inhibitors have shown efficacy in certain paediatric gliomas in the recurrent setting.
Despite the potential benefit of BRAF inhibitors, the prevalence of BRAF V600 within primary gliomas is not fully discovered. Some studies identify the prevalence to be over 50%, while others find the prevalence to be around 1%. We performed a comprehensive systematic review to determine the prevalence of BRAF V600 within the adult and paediatric glioma population in different diagnostic groups.
Method
A systematic literature search was performed using Ovid MEDLINE and Embase from genesis to the 22nd October 2020. Studies were not restricted by language. Studies were eligible if patients were histologically diagnosed according to WHO guidelines as a primary glioma evaluating the prevalence of BRAF V600 and included ≥ 10 primary glioma patients. The review protocol was registered in PROSPERO (CRD42019127704). Search results were managed using Endnote. Two independent reviewers assessed the eligibility of the publications using Rayyan, conflicts were evaluated by a third reviewer. Included articles were extracted by one reviewer and confirmed by a second reviewer. Risk of bias assessments were conducted using Hoy et al’s risk of bias tool. Results were synthesized using “metaprop” in R. The meta-analysis was carried out in R which produced forest plots.
Results
Our cohort included 182 studies with a total of 13669 adult and paediatric glioma patients classified diagnostically according to WHO guidelines. Among 48 glioma entities, BRAF V600 was identified most commonly in epithelioid glioblastoma with a prevalence of 69% (95% confidence interval (CI): 45-89%), followed by pleomorphic xanthoastrocytoma with a prevalence of 56% (95% CI: 48-64%), anaplastic pleomorphic xanthoastrocytoma with a prevalence of 38% (95% CI: 23-54%), ganglioglioma with a prevalence of 40% (95% CI: 33-46%), and anaplastic ganglioglioma with a prevalence of 46% (95% CI: 18-76%). Other glioma entities were found to have a prevalence of BRAF V600, these include astroblastoma (24%), desmoplastic infantile astrocytoma (16%), subependymal giant cell astrocytoma (8%), dysembryoplastic neuroepithelial tumour (3%), diffuse astrocytoma (3%), and pilocytic astrocytoma (3%).
Conclusion
To our knowledge, this is the largest systematic review examining the prevalence of BRAF V600 in adult and paediatric glioma classified according to diagnostic WHO criteria. However, there were some limitations in this review. The sample sizes of some studies were very small, and the method of mutational analysis for BRAF V600 varied between papers. We found BRAF V600 in a significant prevalence of epithelioid glioblastoma, pleomorphic xanthoastrocytoma, anaplastic pleomorphic xanthoastrocytoma, ganglioglioma, and anaplastic ganglioglioma. Of interest, BRAF V600 mutation was found in a lower prevalence of astroblastoma, desmoplastic infantile astrocytoma, subependymal giant cell astrocytoma, dysembryoplastic neuroepithelial tumour, diffuse astrocytoma, and pilocytic astrocytoma. Consideration of assessment of BRAF V600 mutation may enable further treatment options with BRAF and/or MEK inhibitors in these particular diagnostic entities.
Abstract
Aims
The development of melanoma brain metastasis (MBM) occurs in ~50% of metastatic melanoma cases, and significantly worsens prognosis to a median survival of 12.8 months. Melanoma is ...often reported as an arginine auxotroph due to transcriptional silencing of argininosuccinate synthase 1 (ASS1). Arginine deiminase (ADI) is a non-mammalian enzyme which depletes blood arginine by converting it to citrulline and ammonia, and in its pegylated form ADI shows clinical efficacy in the treatment of a number of cancers via exploiting tumour arginine auxotrophy, resulting in targeted arginine deprivation of tumour cells. While cutaneous melanoma is the prototype cancer for this therapy, studies to date have excluded central nervous system metastasis.
We have demonstrated that patient derived primary MBM models are sensitive to arginine deprivation in vitro, confirmed suitable clinical biomarkers of sensitivity, and established the mechanism of tumour cell specific cytotoxicity.
Method
Patient derived primary cultures of MBM were established and subject to treatment with arginine deprivation. Gene expression and methylation analysis was examined by RT-qPCR, western blot, Illumina mRNA sequencing and Illumina methylated DNA immunoprecipitation-sequencing (MeDIP-seq) on ADI treated and untreated samples. Cell death, cytotoxicity induction and caspase-3 and-7 recruitment was analysed using an Incucyte S3 live-cell imager, by fluorescently labelling cells with Incucyte Cytolight Red Rapid dye, Cytotox Green dye and Caspase-3/7 Green dye, and imaging cells every 2 hours over the course of 2 weeks. 3D spheroid growth and invasion was measured by culturing cells as tumour spheroids before treating with ADI, and imaging spheroids every 2 hours for 2 weeks using an Incucyte S3 live-cell imager. Nuclear leakage and mitochondrial morphology was observed by fluorescently staining treated and untreated cells with DAPI and MitoTracker Red, and imaging on a Leica DMi8 confocal microscope.
Results
Primary MBMs differentially express ASS1 at substantially lower levels than non-cancerous melanocytes, however some models are capable of upregulating ASS1 following confrontation with arginine deprivation. Despite this, long-term sensitivity of primary MBMs to arginine deprivation was observed in both 2D and 3D models. In addition, arginine deprivation was seen to inhibit MBM invasion in a 3D model – an important feature in MBM pathogenesis. Initially, autophagy was induced in arginine deprived MBM, however in all models the induction of cytotoxicity correlated with recruitment of caspase-3 and -7, and intrinsic apoptotic cell death confirmed. Nuclear leakage, and eventually complete nuclear destruction was observed, in addition to mitochondrial fragmentation.
Conclusion
Arginine deprivation is highly effective in reducing 2D and 3D MBM growth, as well as limiting invasion. While apoptotic cell death was observed in all models, the initial induction of autophagy could pose threat of resistance development in a clinical setting, and so combinational therapies with autophagic inhibitors and/or additional apoptotic inducers should be investigated. It is unclear whether nuclear leakage and mitochondrial degradation are the cause or product of apoptosis. Considering the strong clinical evidence for the use of arginine deprivation in non-CNS metastatic melanoma and the results of this study, arginine deprivation is a highly suitable treatment for pre-surgical MBM to limit invasion and increase resection, and for post-surgical continuation.
Abstract
Aims
In patients with HGG, we know that QoL and physical function decline with progressive disease (PD) and fatigue is a strong predictor of survival in recurrent disease. Despite notable ...technical advances in therapy for in the past decade, survival has not improved. The role of physical function as a predictor of QoL, treatment tolerance and as an early indicator of worsening morbidity (e.g. tumour recurrence) is an area of growing importance.
Recent advancements in wearable technology allow us the opportunity to gather high-quality, continuous and objective data BrainWear is a feasibility study collecting longitudinal physical activity (PA) data from patients with primary and secondary brain tumours and we hypothesise changes in PA over time, are a potentially sensitive biomarker for PD both at diagnosis and relapse.
Method
Here we show early analysis of this novel dataset of 42 HGG patients and will present: 1) feasibility and acceptability 2) how digitally captured PA changes through treatment and at PD/hospitalization 3) the correlation between patient reported outcomes (PRO) and PA data 4) how PA in HGG patients compares with healthy UK Biobank participants.
PA data is collected via a wrist-worn accelerometer. Raw accelerometer data is processed using the UK Biobank Accelerometer Analysis pipeline in python 3.7, and evaluated for good quality wear-time. Overall activity is represented as vector magnitude in milligravity units(mg) and a machine-learning classifier classifies daily activity into 5 separate groups (walking, tasks-light, moderate, sedentary and sleep). Descriptive statistics summarise baseline characteristics and unadjusted mean used to present vector magnitude and accelerometer-predicted functional behaviours (in h/day) by age, sex, radiotherapy and weekend days. Mixed effect models for repeated measures are used for longitudinal data evaluation of PA.
Results
Between October 2018 and March 2021, 42 patients with a suspected HGG were recruited; 16 females and 26 males with a median age of 59. 40 patients had surgery and 35 patients had adjuvant primary radiotherapy, 23 of whom had a 6-week course. They have provided 3458 days of accelerometer data, 80% of which has been classified as good quality wear-time. There are no statistical differences in mean activity between gender, patients >60 years show statistical difference in time spent doing moderate activity compared to those <60 years, and there are significant differences in mean vector magnitude and walking between radiotherapy and non-radiotherapy days. In patients having a 6-week RT course, time spent in daily moderate activity falls 4-fold between week 1 and the second week following RT completion (70 minutes to 16 minutes). HGG versus healthy UK Biobank participants shows significant differences in all measures of PA.
Conclusion
Here we present preliminary analysis of this highly novel dataset in adult high grade glioma patients, and show digital remote health monitoring is feasible and acceptable with 80% of data classified as high quality wear-time suggesting good patient adherence. We are able to objectively describe how PA changes through standard treatments and understand the inter and intra-patient variation in PA, and whether there are correlates with patient-centred measures, clinical measures and early indicators of worsening disease. We will present further data on changes in PA prior to hospitalisation and at disease progression, and discuss some of the challenges of running a digital health trial. The passive and objective nature of wearable activity monitors gives clinicians the opportunity to evaluate and monitor the patient in motion, rather than the episodic snapshot we currently see, and in turn has the potential to improve our clinical decision making and potentially outcomes.
Abstract
Aims
Gliomas are the most frequent brain tumours, representing 75% of all primary malignant brain tumours in adults. IDH1 (and IDH2) driver mutations occur in >80% of low grade gliomas and ...secondary GBMs, in <10% of primary GBMs and other cancers. How IDH1/2 mutations contribute to tumorigenesis is mostly unknown. IDH1/2 convert isocitrate to α-ketoglutarate, but when mutated possess a novel enzymatic function that reduces α-ketoglutarate to D2-hydroxyglutarate (2HG). Indeed 2HG accumulates in IDH1/2-mutant tumours, and this discovery suggested that 2HG may have a role in IDH1/2-mutant tumours onset and progression, possibly by causing dysregulations of various enzymes in the cells. Studies are undergoing to clarify the causative role of 2HG in IDH1/2-mutant tumours, but it is still not clear whether 2HG is the driver/oncometabolite. Our aim is to understand the role of 2HG in developing and adult mouse tissues and whether its accumulation might cause features of gliomagenesis.
Method
A constitutive D2hgdh Knock-out mouse (D2hgdh KO) was generated and the relative molecular and cellular analysis were performed.
Results
Brains dissected from D2hgdh KO mice appeared to be histologically normal. No differences were found in the proliferation and labelling retaining capacity of neural stem and progenitors cells (NSC/NPC) of the D2hgdh KO mice compared to controls. A comprehensive metabolites analysis showed that D2hgdh KO mouse accumulated 2HG in various organs and tissues, included total brains and in the NSC/NPC microdissected from the subventricular zone, the site of origin of many human gliomas. The DNA amount of 5mC and 5hmC extracted from brains of D2hgdh KO mice was similar to controls. A normal number of haematopoietic progenitors was also found.
Conclusion
Although D2hgdh KO mice accumulated 2HG in all tissues analysed, they did not develop any abnormalities and remained completely asymptomatic. This suggests that a mere increment of 2HG in developing and adult tissues may be not sufficient to cause tumorigenesis (and gliomagenesis), leading some doubts on the oncogenic roles of the 2HG in IDH1/2-mutant tumours.
Abstract
Aims
There are approximately four thousand neuro-oncology procedures in the UK per annum. Many of these result in tissue and biofluid specimens that are surplus to diagnostic requirement and ...can be collected as standard of clinical care. However, developing technologies and treatments for precision medicine require access to a range of individualised biospecimens paired with deep clinical phenotyping data. Here, we present Brain Surgical Tissue for Advanced Tumour Models (BRAINSTAT) programme, an infrastructure that has been established between Queen Elizabeth Hospital, Birmingham and the University of Birmingham, to collect, structure and store these resources and also maximise their value for research over the long-term. Using this approach our aim is to provide high-quality, annotated resources to help develop novel treatments for patients with brain tumours.
Method
BRAINSTAT infrastructure allows:
Prospective consent
Biospecimens, including tumour tissue (brain and other primary in the case of metastasis), cyst fluid, dura, skin, CSF, blood (matched “germ-line” and for circulating cell free tumour DNA analysis), urine and saliva can be collected. Consent for long term follow-up, is either via clinic or NHS digital. More limited consent for non-oncological neurosurgical cohorts (e.g. epilepsy or vascular) and healthy volunteers allow healthy access-tissue and biofluids to be collected.
B. Rapid transfer of fresh surgical tissue samples:
Strong collaborative links and close physical proximity between operating theatre and laboratory allows rapid transfer of biospecimens minimising transit time.
C. Standardised annotation across disciplines
The RedCAP database system allows granular control over data-access, and each specialist research team is provided access only to the sub-sections relevant to them. All users must have Good Clinical Practice certification and GDPR training, prior to access of the BRAINSTAT database.
Results
Between 25/11/2019-16/03/2020 and 27/07/2020-16/11/2020, 65 patients were consented for BRAINSTAT at the weekly neurosurgical oncology clinic. (Recruitment gaps due to the SARS-COVID 19 pandemic). Pathological diagnosis of surplus tissue collected included: 37 high grade glioma, 3 low grade glioma and 16 brain metastasis including: (6 lung, 6 breast, 2 colorectal, 1 oesophageal, 1 endometrial). Meningioma (5 WHO I; 1 WHO III) 1 patient undergoing anterior temporal lobectomy for hippocampal sclerosis contributed access tissue from the lateral neocortex. 1 patient had a non- neoplastic, non-diagnostic sample. All patients had matched “germ-line” blood samples.
Median time from resection to arrival in the laboratory was 10 minutes (range 4-31). Standardised operating protocols to optimise this have been developed.
Glioblastoma and breast-brain metastasis tumourspheres and cerebral organoids are currently being validated.
Conclusion
Despite the challenges of the pandemic we have established a viable tissue pipeline from neurosurgical operating theatre to our university laboratories. We are developing clinically annotated human brain tumour cell lines, stem cells and 3D organoid models, principally for commonly encountered brain tumours such as glioma and metastasis.
The research sets the foundation for a multitude of downstream applications including:
- Building more complex organoid cultures e.g. by including other cell types such as healthy brain cells and endothelial cells allowing future experiments to more accurately model tumour growth.
- Developing high-throughput, patient-specific drug screens of novel drugs and drug combinations using these 3D tumour models aiming to more effectively treat tumour proliferation and spread. These patient avatars will help inform and test more “stratified” personal medical treatments and will provide opportunities to allow earlier intervention with the aim of improving survival, coupled with a better quality of life.
Abstract
Aims
It is common to have adjuvant chemo-radiotherapy after primary brain tumour resection. It is a known side effect that enhancing lesion could be seen in radiation territory after ...treatment, termed as pseudoprogression.
It has been a difficult task to distinguish brain between tumour recurrence from pseudoprogression after radiotherapy. Timing of occurrence of these can overlap. It is important to distinguish the two as management is completely different. Early intervention in recurrence could improve survival time while pseudoprogression could be self-limiting. Surgical resection of pseudoprogression could be counter-productive.
The radiological approach has been relying on multimodality investigation and close follow up. It has come to our institution notice that there is a new technique which could distinguish the two conditions efficiently. That's static permeability assessment method, also known as treatment response assessment maps (TRAMs). Our experience with it so far has been beneficial.
Method
This is a retrospective case series review of primary brain tumour treatment in our neurosurgical institution in 2020.
Two high resolution 3D T1-weighted brain MRI images were acquired after a standard dose of gadolinium based contrast agent was injected. The first acquisition began five minutes after injection, and the second began 60 – 105 minutes post contrast injection. The TRAMs technique is based on image subtraction that is post processed after acquisition.
The resultant subtracted image set was mapped to grey scale values, where voxels showing contrast clearance were light grey/white, and those showing contrast accumulation were dark grey/black. The zero value (i.e. no clearance or accumulation) was therefore mid-grey. Those with contrast clearance is associated with tumour recurrence.
TRAMs images were compared to serial follow up imaging and histopathology results to determine the diagnostic accuracy of the technique.
Results
We have identified 21 patients in this period who had concern of either of pseudoprogression or tumour recurrence/progression. There were 6 females and 15 males, mean age 51. There were 14 glioblastoma multiforme (GBM), 5 astrocytoma, 1 oligodendroglioma and 1 post radiotherapy arteriovenous malformation.
17 cases were found to have clear cut recurrence, pseudoprogression or mixture of both in TRAMS. These findings are backed up by histology or repeated follow up scan. 4 cases were considered as equivocal. In retrospect, these cases have challenging interpretation due to poor case selection. TRAMs could distinguish high grade transformation as well as detecting recurrence. In some difficult cases, it is found that both pseudoprogression and recurrence could happen together.
Conclusion
TRAMs is a useful adjunct to the multimodalities of diagnostic techniques in tricky situation. This has provided an efficient and easy to use tool for radiologists to come up with the answer. We are the first independent centre to report on this technique. This is still early days and fine-tuning of its use is still undergoing. It is clear this has saved precious resources and has given patients more suitable care. We think it would be beneficial for us to share our experience with others and hope to get future collaboration with other centres.
Abstract
Aims
Data on the treatment and outcomes of patients with primary brain tumours in England is sparse. The GlioCova project uses linked national data from England to explore the incidence, ...treatment, outcomes, and treatment costs of all adult brain tumour patients in all 50,000 patients in England from 2013 – 2018. Here we present initial results from patients with glioblastoma (GBM).
Method
We used a linked dataset from the national cancer registration system in England including all adult patients diagnosed with a malignant or benign brain tumour between 2013 and 2018 (51,775 patients in total).
Glioblastoma patients were selected based on ICD-10 codes (C70, C71, C72), morphology codes (9440, 9441, 9442), and grade (G4, G3, GX and NA) from the national cancer registry. We extracted data on treatment (radiotherapy, chemotherapy, brain surgery or biopsy) and measured how many patients who had adjuvant Temozolomide completed 6 cycles.
Results
We identified 15,294 glioblastoma patients. Most had glioblastoma morphology (14,924), followed by gliosarcoma (264) and giant cell glioblastoma (106). Almost all had a cranial tumour (C71) while 17 had a tumour originating in the spinal cord, cranial nerves or other part of central nervous system (C72). Median age was 66 (IQR=17) and 60% were male. 51.9% (7,935) underwent surgery; an additional 18.2% (2,784) had a biopsy; 3,701 (24.2%) out of 15,294 patients received radiotherapy (only) and 316 (2.1%) received chemotherapy (only). 5,520 (36.1%) received both radiotherapy and chemo. Out of 4,101 GBM patients receiving temozolomide after radiotherapy, only 1,535 (37.4%) completed 6 cycles. The 7,935 GBM patients who had surgery had a median length of stay in hospital of 5 days (IQR=6) while those that had a biopsy had a median of 3 days (IQR=6).
Conclusion
We have presented a description of treatment of all GBM patients in England over a five-year period. This is the first time we have been able to understand detailed treatment patterns at a national scale, and significantly extends previous analyses. Further work will look at patient safety indicators, variation across centres and costs of treatment.
Acknowledgements
We would like to thank the GlioCova Expert Advisory Group for their input and discussion.
This work uses data provided by patients and collected by the NHS as part of their care and support.
Abstract
Aims
Cerebellar mutism syndrome occurs in 25% of children following resection of posterior fossa tumours. Characterised by mutism, emotional lability and cerebellar motor signs, the syndrome ...is usually reversible over weeks to months. Its pathophysiology remains unclear, but evidence from diffusion MRI studies has implicated damage to the superior cerebellar peduncles in the development of this condition. The objective of this study was to describe the application of automated tractography of the cerebellar peduncles to provide a high-resolution spatiotemporal profile of diffusion MRI changes in cerebellar mutism syndrome.
Method
A retrospective case-control study was performed at Lucille Packard Children’s Hospital, Stanford University. Thirty children with midline medulloblastoma (mean age ± standard deviation 8.8 ± 3.8 years) underwent volumetric T1-weighted and diffusion MRI at four timepoints over one year. Forty-nine healthy children (9.0 ± 4.2 years), scanned at a single timepoint, were included as age- and sex-matched controls. Cerebellar mutism syndrome status was determined by contemporaneous casenote review. Automated Fibre Quantification was used to segment each subject’s cerebellar peduncles (Figure 1), and fractional anisotropy was computed at 30 nodes along each tract. A non-parametric permutation-based method was used to generate a critical cluster size and p-value for by-node ANOVA group comparisons. Z-scores for patients’ fractional anisotropy at each node were calculated based on values from controls’ corresponding nodes; these were analysed using mixed ANOVA with post-hoc false discovery rate-corrected pairwise t-tests.
Results
13 patients developed cerebellar mutism syndrome. Automated fibre segmentation successfully identified the cerebellar peduncles in the majority of participants, but was more robust at follow-up timepoints (78.7% vs. 44.7% pre-operatively). Fractional anisotropy was significantly lower in the distal regions of the left superior cerebellar peduncle pre-operatively (p=0.0137) in patients compared to controls, although patients could not be distinguished pre-operatively with respect to cerebellar mutism syndrome status (Figure 2). Post-operative reductions in fractional anisotropy in children with cerebellar mutism syndrome were highly specific to the distal left superior cerebellar peduncle, and were most pronounced at follow-up timepoints (p=0.006; Figure 3). There were no significant differences in other cerebellar peduncles, either in along-tract fractional anisotropy or Z-scores, with respect to cerebellar mutism syndrome status.
Conclusion
A novel application of an automated tool to extract diffusion MRI data along the length of the cerebellar peduncles is described in a longitudinal retrospective cohort of paediatric medulloblastoma. Changes in fractional anisotropy in the cerebellar peduncles following tumour resection are described in a heretofore unprecedented level of spatiotemporal detail. In particular, children with post-operative cerebellar mutism syndrome show changes in the distal regions of the left superior cerebellar peduncle, and these changes persist up to a year post-operatively. These findings will have direct clinical implications for neurosurgeons performing resection of midline paediatric posterior fossa tumours.
Abstract
Aims
Magnetic resonance imaging (MRI) is a valuable tool for non-invasive diagnosis of paediatric brain tumours. The rarity of the disease dictates multi-centre studies and imaging ...biomarkers that are robust to protocol variability. We investigated diffusion tensor MRI (DT-MRI), combined with machine learning, as an aid to diagnosis and evaluated the robustness of the imaging metrics.
Method
A multi-centre cohort of 52 clinical DT-MRI scans (20 medulloblastomas (MB), 21 pilocytic astrocytomas (PA), 11 ependymomas (EP)) were analysed retrospectively. Histograms for regions of solid tumour for fractional anisotropy (FA), mean diffusivity (MD), pure anisotropic diffusion (q) and pure isotropic diffusion (p) were compared to assess diagnostic capability. Linear discriminate analysis (LDA) was used for classification and validated using leave-one-out-cross-validation (LOOCV).
Results
Histogram medians for FA, MD, q and p were all different between tumor groups (P<.0001, Kruskal Wallis test). Median MD, p and q values were highest in PA, then EP and lowest in MB (P<.0001, Pairwise Wilcox test). FA median was higher for EP than PA (P=.004) with no significant difference between EP and MB (P=.591). ROC analysis showed that median MD, q and p perform best as a diagnostic marker (AUC= 0.92 to 0.99). LOOCV showed an overall accuracy of the LDA classification, ranging between 67% - 87%. FA values were highly dependent on protocol parameters, whereas pure anisotropic diffusion, q, was not.
Conclusion
DT-MRI metrics from multi-centre acquisitions can classify paediatric brain tumours. FA is the least robust metric to protocol variability and q provides the most robust quantification of anisotropic behaviour.
Abstract
Aims
Glioblastoma (GBM) is currently an incurable malignancy with a very poor prognosis for the majority of patients. Many patients undergo debulking surgery, radiotherapy and chemotherapy ...however therapeutic options are limited, and this can lead to patients sourcing their own treatments. There is some evidence that cannabinoids have the effect of inhibiting GBM tumour growth through a variety of pathways, some of which include CB2 cannabinoid receptor pathway activation. We undertook a patient questionnaire to understand what alternative therapies patients are accessing and why, with a focus on cannabinoid use.
Method
We undertook a prospective observational questionnaire based qualitative study of 50 … consecutive patients undergoing treatment for glioblastoma at our centre.
Results
43 patients responded to our questionnaire. 33% of patients were taking some kind of supplementary therapy with 25% taking cannabis derivatives, mainly CBD oil. There were no clear discriminators amongst our cohort including age or sex when considering the likelihood of taking cannabis derivatives. 6 out of 11 (55%) patients taking cannabis derivatives reported some positive effects with improved sleep and general wellbeing being most commonly reported. Patients reported spending between £10-£300 per month with an average of £42 per month. Cannabis products were obtained via the internet or from friends.
Conclusion
This small cohort of patients indicates that a significant proportion of glioblastoma patients investigate and use alternative therapies, in particular cannabis oil. NICE guidance for clinicians simply notes there is insufficient evidence to support the use of cannabis oil in the treatment of this disease. Given the publicity and interest in the utility of cannabis oil to treat cancers this leaves patients to research the use of these agents without access to robust clinical data to guide their use or indeed to conclude they are not beneficial. The accessing of these compounds, potentially by a sizeable number of patients, leaves them vulnerable to unregulated perhaps unscrupulous drug sources. This small study has further highlighted the unmet need for information and guidance on supplementary treatments for glioma patients and this poses a challenge to all those treating this group of patients to answer a question our patients are clearly wanting answered.
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