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1
Sevyan, N. V., V. B. Karakhan, D. R. Naskhletashvili, A. Kh Bekyashev, E. V. Prozorenko, D. M. Belov, A. A. Mitrofanov, A. A. Pogosova, and B. I. Polyakov. "Brain metastases from gynaecological cancers." Voprosy ginekologii, akušerstva i perinatologii 19, no. 4 (2020): 172–77. http://dx.doi.org/10.20953/1726-1678-2020-4-172-177.
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The spread of female genital tract tumours to the brain is a rare and insufficiently studied pathology. The problems of diagnosis and treatment of this group of patients still remain. The article gives a detail account of the clinical picture, radiological and morphological diagnosis, and the principles of treating patients with brain metastases from gynaecological cancers. Conclusion. A probable cause of a rare occurrence of brain metastases from gynaecological malignancies might be a high resistance of nervous tissue to various kinds of tumours. When local control over a brain tumour is achieved, this might improve the patient’s survival and quality of life in some particular cases. Key words: ovarian cancer, endometrial cancer, cervical cancer, brain metastases
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Dirks, Peter B. "Brain tumour stem cells: the undercurrents of human brain cancer and their relationship to neural stem cells." Philosophical Transactions of the Royal Society B: Biological Sciences 363, no. 1489 (February 19, 2007): 139–52. http://dx.doi.org/10.1098/rstb.2006.2017.
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Conceptual and technical advances in neural stem cell biology are being applied to the study of human brain tumours. These studies suggest that human brain tumours are organized as a hierarchy and are maintained by a small number of tumour cells that have stem cell properties. Most of the bulk population of human brain tumours comprise cells that have lost the ability to initiate and maintain tumour growth. Although the cell of origin for human brain tumours is uncertain, recent evidence points towards the brain's known proliferative zones. The identification of brain tumour stem cells has important implications for understanding brain tumour biology and these cells may be critical cellular targets for curative therapy.
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Chai-Adisaksopha, Chatree, Lori-Ann Linkins, Said Y. ALKindi, Matthew Cheah, Mark A. Crowther, and Alfonso Iorio. "Outcomes of low-molecular-weight heparin treatment for venous thromboembolism in patients with primary and metastatic brain tumours." Thrombosis and Haemostasis 117, no. 03 (2017): 589–94. http://dx.doi.org/10.1160/th16-09-0680.
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SummaryVenous thromboembolism (VTE) is one of the most common complications in patients with brain tumours. There is limited data available in the literature on VTE treatment in these patients. We conducted a matched retrospective cohort study of patients with primary or metastatic brain cancer who were diagnosed with cancer-associated VTE. Patients were selected after a retrospective chart review of consecutive patients who were diagnosed with cancer-associated VTE between January 2010 and January 2014 at the Juravinski Thrombosis Clinic, Hamilton, Canada. Controls were age- and gender-matched patients with cancer-associated VTE from the same cohort, but without known brain tumours. A total of 364 patients with cancer-associated VTE were included (182 with primary or metastatic brain tumours and 182 controls). The median follow-up duration was 6.7 (interquartile range 2.5–15.8) months. The incidence rate of recurrent VTE was 11.0 per 100 patient-years (95 % CI; 6.7–17.9) in patients with brain tumours and 13.5 per 100 patient-years (95 % CI; 9.3–19.7) in non-brain tumour group. The incidence of major bleeding was 8.6 per 100 (95 % CI; 4.8–14.7) patient-years in patients with brain tumours versus 5.0 per 100 patient-years (95 % CI; 2.8–9.2) in controls. Rate of intracranial bleeding was higher in brain tumour patients (4.4 % vs 0 %, p-value=0.004). In summary, rates of recurrent VTE and major bleeding were not significantly different in patients with cancer-associated VTE in the setting of primary or metastatic brain tumours compared those without known brain tumours. However, greater numbers of intracranial bleeds were observed in patients with brain tumours.
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Galati, Melissa, Li Li, Sumedha Sudhaman, Tatiana Lipman, Lucie Stengs, Dana Elshaer, Taylor Bridge, et al. "MODL-25. REPLICATION REPAIR DEFICIENT MOUSE MODELS PROVIDE INSIGHT ON HYPERMUTANT BRAIN TUMOURS, MECHANISMS OF IMMUNE EVASION, AND COMBINATORIAL IMMUNOTHERAPY." Neuro-Oncology 22, Supplement_3 (December 1, 2020): iii416. http://dx.doi.org/10.1093/neuonc/noaa222.598.
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Abstract Replication repair deficiency (RRD) is the leading cause of hypermutant brain tumours in children. RRD is caused by defects in one of four mismatch repair (MMR) genes and mutations in POLE or POLD1. Such tumours are resistant to common therapeutic agents and animal models are needed to study RRD in vivo and test novel therapies like immune checkpoint inhibitors (ICIs). To model RRD brain tumours specifically, we engineered a Pole mutant mouse model harbouring the S459F mutation (PoleS459F). We combined PoleS459F mice with conditional Msh2 knockout (Msh2LoxP) and Nestin-cre mice. All Nestin-cre+Msh2LoxP/LoxPPoleS459F/+ mice rapidly succumbed to posterior fossa brain tumours between 8.6 and 12.4 weeks. Importantly, tumours exhibited hallmark “ultrahypermutation” (~350 mutations/Mb) and the corresponding signatures characteristic of human combined MMR and POLE-proofreading glioblastoma. Interestingly, Nestin-cre+Msh2LoxP/LoxPPoleS459F/S459F mice failed to establish normal cerebella, suggesting such mutational loads may not support normal brain development. Furthermore, OLIG2-cre+Msh2LoxP/LoxPPoleS459F/+ mice failed to develop tumors. Tumors transplanted into syngeneic vs immunocompromised animals egrafted well orthotopically in the mouse hindbrain but significantly less efficiently when engrafted subcutaneously. Furthermore, immunocompromised and subcutaneous tumors revealed striking differences in mutational burden and clonal architecture, suggestive of nonautonomous immunoediting. Finally, anti-PD1 was sufficient to treat subcutaneously engrafted tumors in immunocompetent animals. This first mouse model of immunocompetent, hypermutant brain tumors can be used to uncover unique characteristics of RRD tumour evolution and allow for immune based therapeutic preclinical testing. Experiments to assess combinational ICIs and other therapeutic interventions in orthotopically transplanted tumors will also be presented.
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Nonaka, Motohiro, Misa Suzuki-Anekoji, Jun Nakayama, Hideaki Mabashi-Asazuma, Donald L. Jarvis, Jiunn-Chern Yeh, Kazuhiko Yamasaki, et al. "Overcoming the blood–brain barrier by Annexin A1-binding peptide to target brain tumours." British Journal of Cancer 123, no. 11 (September 14, 2020): 1633–43. http://dx.doi.org/10.1038/s41416-020-01066-2.
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Abstract Background Annexin A1 is expressed specifically on the tumour vasculature surface. Intravenously injected IF7 targets tumour vasculature via annexin A1. We tested the hypothesis that IF7 overcomes the blood–brain barrier and that the intravenously injected IF7C(RR)-SN38 eradicates brain tumours in the mouse. Methods (1) A dual-tumour model was generated by inoculating luciferase-expressing melanoma B16 cell line, B16-Luc, into the brain and under the skin of syngeneic C57BL/6 mice. IF7C(RR)-SN38 was injected intravenously daily at 7.0 μmoles/kg and growth of tumours was assessed by chemiluminescence using an IVIS imager. A similar dual-tumour model was generated with the C6-Luc line in immunocompromised SCID mice. (2) IF7C(RR)-SN38 formulated with 10% Solutol HS15 was injected intravenously daily at 2.5 μmoles/kg into two brain tumour mouse models: B16-Luc cells in C57BL/6 mice, and C6-Luc cells in nude mice. Results (1) Daily IF7C(RR)-SN38 injection suppressed tumour growth regardless of cell lines or mouse strains. (2) Daily injection of Solutol-formulated IF7C(RR)-SN38 led into complete disappearance of B16-Luc brain tumour in C57BL/6 mice, whereas this did not occur in C6-Luc in nude mice. Conclusions IF7C(RR)-SN38 crosses the blood–brain barrier and suppresses growth of brain tumours in mouse models. Solutol HS15-formulated IF7C(RR)-SN38 may have promoted an antitumour immune response.
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Gilbertson, R. "Paediatric embryonic brain tumours." European Journal of Cancer 38, no. 5 (March 2002): 675–85. http://dx.doi.org/10.1016/s0959-8049(01)00315-x.
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Sampson, John H., Michael D. Gunn, Peter E. Fecci, and David M. Ashley. "Brain immunology and immunotherapy in brain tumours." Nature Reviews Cancer 20, no. 1 (December 5, 2019): 12–25. http://dx.doi.org/10.1038/s41568-019-0224-7.
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Lindsell, Sarah. "Know the symptoms: diagnosing a brain tumour early is key." British Journal of Child Health 2, no. 1 (February 2, 2021): 10–11. http://dx.doi.org/10.12968/chhe.2021.2.1.10.
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Everyone has a role to play in reducing diagnosis times for childhood brain tumours, the biggest cancer killer of children and adults under 40 years old in the UK. The Brain Tumour Charity's HeadSmart campaign aims to inform parents and healthcare professionals about the key early signs and symptoms of brain tumours.
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Coyle, Beth, Maya Kessler, Durgagauri H. Sabnis, and Ian D. Kerr. "ABCB1 in children's brain tumours." Biochemical Society Transactions 43, no. 5 (October 1, 2015): 1018–22. http://dx.doi.org/10.1042/bst20150137.
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Tumours of the central nervous system are the most common solid tumour, accounting for a quarter of the 1500 cases of childhood cancer diagnosed each year in the U.K. They are the most common cause of cancer-related death in children. Treatment consists of surgery followed by adjuvant chemotherapy and/or radiotherapy. Survival rates have generally increased, but many survivors suffer from radiotherapy-related neurocognitive and endocrine side effects as well as an increased risk of secondary cancer. Adjuvant chemotherapy is normally given in combination to circumvent chemoresistance, but several studies have demonstrated it to be ineffective in the absence of radiotherapy. The identification of children with drug-resistant disease at the outset could allow stratification of those that are potentially curable by chemotherapy alone. Ultimately, however, what is required is a means to overcome this drug resistance and restore the effectiveness of chemotherapy. Medulloblastomas and ependymomas account for over 30% of paediatric brain tumours. Advances in neurosurgery, adjuvant radiotherapy and chemotherapy have led to improvements in 5-year overall survival rates. There remain, however, significant numbers of medulloblastoma patients that have intrinsically drug-resistant tumours and/or present with disseminated disease. Local relapse in ependymoma is also common and has an extremely poor prognosis with only 25% of children surviving first relapse. Each of these is consistent with the acquisition of drug and radiotherapy resistance. Since the majority of chemotherapy drugs currently used to treat these patients are transport substrates for ATP-binding cassette sub-family B member 1 (ABCB1) we will address the hypothesis that ABCB1 expression underlies this drug resistance.
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Arvanitis, Costas D., Gino B. Ferraro, and Rakesh K. Jain. "The blood–brain barrier and blood–tumour barrier in brain tumours and metastases." Nature Reviews Cancer 20, no. 1 (October 10, 2019): 26–41. http://dx.doi.org/10.1038/s41568-019-0205-x.
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Wanis, H. "P14.45 The incidence of major subtypes of primary brain tumours in adults in England 1995–2017." Neuro-Oncology 23, Supplement_2 (September 1, 2021): ii46—ii47. http://dx.doi.org/10.1093/neuonc/noab180.160.
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Abstract BACKGROUND Primary brain tumours are a complex heterogenous group of benign and malignant tumours. Reports on their occurrence in the English population by sex, age, and morphological subtype and on their incidence are currently not available. Using data from the National Cancer Registration and Analysis Service (NCRAS), the incidence of adult primary brain tumour by major subtypes in England will be described. METHODS Data on all adult English patients diagnosed with primary brain tumour between 1995 and 2017, excluding spinal, endocrinal and other CNS tumours, were extracted from NCRAS. Incidence rates were standardised to the 2013 European Standard Population. Results are presented by sex, age, and morphological subtype. RESULTS Between 1995 and 2017, a total of 133,669 cases of adult primary brain tumour were registered in England. Glioblastoma was the most frequent tumour subtype (31.8%), followed by meningioma (27.3%). The age-standardised incidence for glioblastoma increased from 3.27 per 100,000 population per year in 1995 to 7.34 in men in 2013 and from 2.00 to 4.45 in women. Meningioma incidence also increased from 1.89 to 3.41 per 100,000 in men and from 3.40 to 7.46 in women. The incidence of other astrocytic and unclassified brain tumours declined between 1995 and 2007 and remained stable thereafter. CONCLUSION Part of the increase in the incidence of major subtypes of brain tumours in England could be explained by advances in clinical practice including the adoption of new diagnostic tools, classifications and molecular testing, and improved cancer registration practices.
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Weber, Damien C., Pei S. Lim, Sebastien Tran, Marc Walser, Alessandra Bolsi, Ulrike Kliebsch, Jürgen Beer, Barbara Bachtiary, Tony Lomax, and Alessia Pica. "Proton therapy for brain tumours in the area of evidence-based medicine." British Journal of Radiology 93, no. 1107 (March 2020): 20190237. http://dx.doi.org/10.1259/bjr.20190237.
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Proton therapy (PT) has been administered for many years to a number of cancers, including brain tumours. Due to their remarkable physical properties, delivering their radiation to a very precise brain volume with no exit dose, protons are particularly appropriate for these tumours. The decrease of the brain integral dose may translate with a diminution of neuro-cognitive toxicity and increase of quality of life, particularly so in children. The brain tumour patient’s access to PT will be substantially increased in the future, with many new facilities being planned or currently constructed in Europe, Asia and the United States. Although approximately 150’000 patients have been treated with PT, no level I evidence has been demonstrated for this treatment. As such, it is this necessary to generate high-quality data and some new prospective trials will include protons or will be activated to compare photons to protons in a randomized design. PT comes however with an additional cost factor that may contribute to the ever-growing health’s expenditure allocated to cancer management. These additional costs and financial toxicity will have to be analysed in the light of a more conformal radiation delivery, non-target brain irradiation and lack of potential for dose escalation when compared to photons. The latter is due to the radiosensitivity of organs at risk in vicinity of the brain tumour, that photons cannot spare optimally. Consequentially, radiation-induced toxicities and tumour recurrences, which are cost-intensive, may decrease with PT resulting in an optimized photon/proton financial ratio in the end. Advances in knowledge: This review details the indication of brain tumors for proton therapy and give a list of the open prospective trials for these challenging tumors.
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Zalutsky, M. R. "Targeted radiotherapy of brain tumours." British Journal of Cancer 90, no. 8 (April 2004): 1469–73. http://dx.doi.org/10.1038/sj.bjc.6601771.
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Gatto, Francesca, Giacomo Milletti, Andrea Carai, Angela Mastronuzzi, and Francesca Nazio. "Recent Advances in Understanding the Role of Autophagy in Paediatric Brain Tumours." Diagnostics 11, no. 3 (March 9, 2021): 481. http://dx.doi.org/10.3390/diagnostics11030481.
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Autophagy is a degradative process occurring in eukaryotic cells to maintain homeostasis and cell survival. After stressful conditions including nutrient deprivation, hypoxia or drugs administration, autophagy is induced to counteract pathways that could lead to cell death. In cancer, autophagy plays a paradoxical role, acting both as tumour suppressor—by cleaning cells from damaged organelles and inhibiting inflammation or, alternatively, by promoting genomic stability and tumour adaptive response—or as a pro-survival mechanism to protect cells from stresses such as chemotherapy. Neural-derived paediatric solid tumours represent a variety of childhood cancers with unique anatomical location, cellular origins, and clinical presentation. These tumours are a leading cause of morbidity and mortality among children and new molecular diagnostics and therapies are necessary for longer survival and reduced morbidity. Here, we review advances in our understanding of how autophagy modulation exhibits antitumor properties in experimental models of paediatric brain tumours, i.e., medulloblastoma (MB), ependymoma (EPN), paediatric low-grade and high-grade gliomas (LGGs, HGGs), atypical teratoid/rhabdoid tumours (ATRTs), and retinoblastoma (RB). We also discuss clinical perspectives to consider how targeting autophagy may be relevant in these specific paediatric tumours.
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Chai-Adisaksopha, Chatree, Said Y. ALKindi, Matthew Cheah, Alfonso Iorio, Mark A. Crowther, and Lori Ann Linkins. "Outcomes of Low-Molecular-Weight Heparintreatment for Venous Thromboembolism in Patients with Primary and Metastatic Brain Tumors." Blood 126, no. 23 (December 3, 2015): 428. http://dx.doi.org/10.1182/blood.v126.23.428.428.
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Abstract Background: Venous thromboembolism (VTE) is one of the most common complications of patients with brain tumors. There is limited data available in the literature on VTE treatment in these patients compared to other cancer types. We evaluated the efficacy and safety of low-molecular weight heparin treatment for newly diagnosed VTE in patients with primary and metastatic brain tumours at a tertiary care centre. Methods: We conducted a matched retrospective cohort study of patients with primary or metastatic brain cancer who were diagnosed with cancer-associated VTE. Cases were selected after completion of a retrospective chart review of consecutive patients who were diagnosed with cancer-associated VTE between January 2010 and January 2014 at the Juravinski Thrombosis Clinic, Hamilton, Ontario, Canada. Controls were age- and gender-matched patients with cancer-associated VTE from the same cohort, but without brain tumours. The primary outcome was first recurrent VTE and secondary outcomes were major bleeding and clinically relevant bleeding. Results: A total of 364 patients with cancer-associated thrombosis were included (182 with primary or metastatic brain tumors and 182 controls). The median follow-up duration was 6.7 (inter quartile range 2.5-15.8) months. The incidence rate of recurrent VTE was 11.0 per 100 patient-year (95% confidence interval [CI]; 6.7-17.9) in patients with brain tumors and 13.5 per 100 patient-year (95% CI; 9.3-19.7) in controls, incidence rate ratio [IRR]; 0.8 (95% CI; 0.4-1.5, p-value=0.43). There was no significant difference in the rate of recurrent VTE in the two groups (log-rank p-value=0.26, Figure 1). The incidence of major bleeding was 8.9 per 100 (95% CI; 5.2-15.4) patient-year in patients with brain tumors versus 6.0 per 100 patient-year (95% CI; 3.4-10.9) in controls, IRR; 0.8 (95% CI; 0.4-1.5, p-value=0.51). There were no significant differences in the risk of major bleeding (Figure 2) and clinical relevant bleeding between the two groups, log-rank p-value 0.9 and 0.8, respectively. When compared to controls, the rate of major gastrointestinal bleeding was lower in patients with brain tumours (0.6% versus 6.0%, p-value=0.003) whereas the rate of intracranial bleeding was higher (4.4% versus 0%, p-value=0.004). Subgroup analysis revealed that the incidence of intracranial bleeding in patients with primary brain tumors was higher than those with metastatic brain tumors, but did not reach statistical significant (6.0% vs 3.5%, p=0.008). Conclusions: Recurrent VTE, major bleeding and clinical relevant bleeding were not significantly different in patients with cancer-associated VTE in the setting of primary or metastatic brain tumours compared with controls. However, intracranial bleedings occurred more frequently in patients with brain tumours. Disclosures Linkins: Pfizer: Honoraria; Bayer: Honoraria, Research Funding.
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Ismail, Heba M. S. "Overexpression of S6 Kinase 1 in Brain Tumours Is Associated with Induction of Hypoxia-Responsive Genes and Predicts Patients' Survival." Journal of Oncology 2012 (2012): 1–10. http://dx.doi.org/10.1155/2012/416927.
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mTOR/S6K pathway is a crucial regulator of cell growth and metabolism. Deregulated signalling via S6K has been linked to various human pathologies, including metabolic disorders and cancer. Many of the molecules signalling upstream of S6K have been shown to be either mutated or overexpressed in tumours, leading to S6K activation. The role of S6K1 in brain tumours is not fully investigated. In this study, we investigated the gene expression profile of S6 kinases in brain and CNS tumours using the publically available Cancer Microarray Database. We found that S6K1 but not S6K2 gene is overexpressed in brain tumours and this upregulation is associated with patients’ poor survival. Furthermore, we interrogated Oncomine database for the expression profile of hypoxia-induced genes using a literature-defined concept. This gene list included HIF1A, VEGFA, SOX4, SOX9, MMP2, and NEDD9. We show that those genes are upregulated in all brain tumour studies investigated. Additionally, we analysed the coexpression profile of S6K1 and hypoxia responsive genes. The analysis was done across 4 different brain studies and showed that S6K1 is co-overexpressed with several hypoxia responsive genes. This study highlights the possible role of S6K1 in brain tumour progression and prediction of patients’ survival. However, new epidemiological studies should be conducted in order to confirm these associations and to refine the role of S6K1 in brain tumours as a useful marker for patients’ survival.
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Yrysov, K. B., and M. B. Yrysova. "Epidemiology of brain tumours in Kyrgyz Republic: a population based study." Bulletin of Siberian Medicine 7, no. 5-2 (December 30, 2008): 481–86. http://dx.doi.org/10.20538/1682-0363-2008-5-2-481-486.
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Brain tumours cause considerable concern due to a high mortality and there are increasing efforts to provide adequate care. The goal of this study was to determine the incidence of brain tumours in Kyrgyz Republic. A population based study was performed. Patients from Kyrgyz Republic with incident intracranial tumours diagnosed in 2005 and 2007 (by CT, MRI or histology) were identified retrospectively using multiple sources. Differences in incidence by tumour type, age and sex were examined. Eight hundred and eighty four patients with incident brain tumours were identified (456 primary tumours and 428 secondary tumours). The commonest primary tumours were neuroepithelial tumours (53,5%), meningeal tumours (19,5%), and sellar tumours (16,5%). The crude yearly incidences of primary and secondary tumours were 30,3 and 28,3 per 100 000 respectively. About 50% of patients with secondary tumours had an underlying lung cancer. The incidence of primary and secondary tumours increased markedly with age. Meningeal tumours were more common in women. This study shows that the incidence of intracranial tumours in Kyrgyz Republic is considerably higher than previously thought. Brain tumours are a significant cause of morbidity and mortality in Kyrgyz Republic, and further research into their aetiology and treatment is urgently required.
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Cacciotti, Chantel, Adam Fleming, Hanna Tseitlin, JoAnn Duckworth, and Stacey Marjerrison. "QOL-02. PERCEPTIONS OF LATE EFFECTS CARE NEEDS AMONG SURVIVORS OF PEDIATRIC BRAIN TUMOURS." Neuro-Oncology 22, Supplement_3 (December 1, 2020): iii431. http://dx.doi.org/10.1093/neuonc/noaa222.668.
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Abstract OBJECTIVES Pediatric brain tumour survivors are at risk of long-term consequences of therapy. Comprehensive late effects care may mitigate these risks, but the best care model is unclear. We sought to describe the care experience and quality of life (QOL) of pediatric brain tumour survivors at the McMaster Children’s Hospital joint adult/pediatric Neuro-Oncology clinic. METHODS Cross-sectional survey data were collected. Care needs were assessed with the Cancer Care Experience Questionnaire (CCEQ), Cancer Worry Scale (CWS), and Self-Management Skills Scale (SMSS). Quality of life was measured utilizing the PedsQL Brain Tumor Module. Data were analyzed descriptively. RESULTS Thirty-two childhood brain tumor survivors and/or their parents participated. Their malignancies included embryonal tumors (medulloblastoma/ATRT) (62%), ependymoma (22%), and germ cell tumours (16%). Among 77%, therapy included chemotherapy, surgery and radiation. Most respondents reported high quality cancer care, although some could not recall discussions of late effects risks and health promotion. Mean cancer worry scores were low (71.8 (± 28.4)). Survivors reported limited self-management skills (58.5 (±18.2)), with support required in clinic visits, arranging medical appointments, filling prescriptions and tasks of daily living. Overall median QOL scores were in the ‘good’ range (parental report 72.3 (±17.7), survivor 68.2 (±16.6)). CONCLUSION In comparison to other childhood cancer survivor cohorts, this group of long-term brain tumour survivors appear to have similar QOL, fewer cancer worries, and increased need for aid with self-management. Given this, along with the positive care experience reported, this clinic model of care appears to meet the needs of this population.
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Garg, Neha, Thusyanth Vijayakumar, David Bakhshinyan, Chitra Venugopal, and Sheila K. Singh. "MicroRNA Regulation of Brain Tumour Initiating Cells in Central Nervous System Tumours." Stem Cells International 2015 (2015): 1–15. http://dx.doi.org/10.1155/2015/141793.
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CNS tumours occur in both pediatric and adult patients and many of these tumours are associated with poor clinical outcome. Due to a paradigm shift in thinking for the last several years, these tumours are now considered to originate from a small population of stem-like cells within the bulk tumour tissue. These cells, termed as brain tumour initiating cells (BTICs), are perceived to be regulated by microRNAs at the posttranscriptional/translational levels. Proliferation, stemness, differentiation, invasion, angiogenesis, metastasis, apoptosis, and cell cycle constitute some of the significant processes modulated by microRNAs in cancer initiation and progression. Characterization and functional studies on oncogenic or tumour suppressive microRNAs are made possible because of developments in sequencing and microarray techniques. In the current review, we bring recent knowledge of the role of microRNAs in BTIC formation and therapy. Special attention is paid to two highly aggressive and well-characterized brain tumours: gliomas and medulloblastoma. As microRNA seems to be altered in the pathogenesis of many human diseases, “microRNA therapy” may now have potential to improve outcomes for brain tumour patients. In this rapidly evolving field, further understanding of miRNA biology and its contribution towards cancer can be mined for new therapeutic tools.
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Shing, Matthew M. K., Dennis T. L. Ku, Godfrey C. F. Chan, C. W. Luk, Jeffrey P. W. Yau, Eric Fu, Carol L. S. Yan, and Alvin S. C. Ling. "LINC-20. INFANT BRAIN TUMOURS IN HONG KONG." Neuro-Oncology 22, Supplement_3 (December 1, 2020): iii382. http://dx.doi.org/10.1093/neuonc/noaa222.455.
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Abstract OBJECTIVES To review the clinical features, pathology and survivals of infants with brain tumours. METHODS A retrospective review of the clinical findings, pathology, treatment and survival outcome in infants with brain tumours. RESULTS From 1999 to 2018, there were 507 children (<18 years) who were diagnosed to have brain tumours in Hong Kong. The patients were treated in five public hospitals. The clinical data were collected by the Hong Kong Paediatric Haematology and Oncology Study Group, and were cross-checked with the data of the Hong Kong Cancer Registry. In this group of patients, there were 36 infants (birth to 365 days of age) i.e. 7.1% of the whole group. Both benign and malignant brain tumours were included, while non-neoplastic lesions were excluded. On average, there was 1.89 cases per year. The pathology of the tumours were astrocytoma (n= 8), medulloblastoma (n=6), germ cell tumour (n=6), PNET (n=5), ATRT (n=4), choroid plexus tumours (n=3), ependymoma (n=2), craniopharyngioma (n= 1) and ganglioglioma (n= 1). These infants were treated according to their clinical conditions and prognosis, with operation, chemotherapy or both. Radiotherapy was withheld or postponed to older age. Some patients only received palliative care due to the poor neurological status or prognosis. The overall survivals of children younger than 18 years old vs infants were 67.3% (±2.3) vs 50.5%(±9.2) respectively, while the event free survivals were 64.4% (±2.4) and 43.5% (±8.8) at 10-years respectively. CONCLUSION Infants with brain tumours have different pathology and inferior outcome.
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Alkins, RD, A. Burgess, R. Kerbel, WS Wels, and K. Hynynen. "Early treatment of HER2-amplified brain tumours with targeted nk-92 cells and focused ultrasound improves survival." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 42, S1 (May 2015): S11. http://dx.doi.org/10.1017/cjn.2015.76.
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Background: Malignant brain tumors have a dismal prognosis, with residual after surgery necessitating adjuvant chemoradiotherapy. We previously demonstrated that targeted Natural Killer (NK-92) cells could be delivered to the brain using a combination of MRI-guided focused ultrasound and Definity microbubbles. Once in the CNS, they can track to malignant tissues without inflicting collateral damage. The HER2 receptor is expressed by epithelial tumours including both breast and glioblastoma; breast tumors with HER2-amplification have a higher risk of CNS metastasis, and poorer prognosis. Methods: We investigated whether multiple combined treatments of targeted NK-92 cells and focused ultrasound with microbubbles could slow tumour growth and improve survival in an orthotopic HER2-amplified rodent brain tumour model using a human breast cancer line as a prototype. Results: Early daily treatments with targeted NK-92 cells and ultrasound improved survival and decreased tumour volumes compared with bi-weekly treatments, or either treatment alone. The intensive treatment paradigm resulted in cure in 50% of subjects. Conclusions: Many tumour proteins could be exploited for targeted therapy with the NK-92 cell line, and combined with the mounting safety evidence for transcranial ultrasound, this may soon provide a non-invasive and highly targeted treatment option for patients with brain tumours.
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Lee, Cathy, Sandra E. Dunn, and Stephen Yip. "Stem Cells in Brain Tumour Development and Therapy- Two-Sides of the Same Coin." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 39, no. 2 (March 2012): 145–56. http://dx.doi.org/10.1017/s0317167100013159.
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Primary brain tumours are difficult to manage clinically due to their abilities to invade adjacent tissue and infiltrate distant neuropil. These contribute to challenges in surgical management and also limit the effectiveness of radiotherapy. Despite initial responses to chemotherapy, most tumours become chemo-resistant, leading to relapse. Recent identification and isolation of brain cancer stem cells (BCSCs) have broadened our understanding of the molecular pathogenesis and potential Achilles' heel of brain tumours. BCSCs are thought to drive and propagate the tumour and therefore present an important target for further investigations. This review explores the history of the discovery of BCSCs and the evolving concept of “cancer stem cells” in neuro-oncology. We attempt to present a balanced view on the subject and also to update the readers on the molecular biology of BCSCs. Lastly, we outline the potential strategies to target BCSCs which will translate into specific and effective therapies for brain tumours.
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Joshi, Amit, Vijai Simha, Kumar Prabhash, Vanita Noronha, Santosh Menon, Vedang Murthy, Ganesh Bakshi, et al. "Clinical presentation and outcomes of patients with testicular tumors in cryptorchid testis." Journal of Clinical Oncology 38, no. 6_suppl (February 20, 2020): 428. http://dx.doi.org/10.1200/jco.2020.38.6_suppl.428.
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428 Background: Undescended testis which occurs in 2-4% of all boys confers a natural risk for development of testicular cancer. Cryptorchidism accounts for 10% of all testicular germ cell tumours. The presentation, natural history and outcomes of testicular tumours occurring in cryptorchid testis has not been described in literature so far. Methods: Case records of patients enlisted in the prospectively maintained ‘ testicular cancer database’ at our tertiary cancer care hospital were retrospectively reviewed. Any patient who presented with testicular germ cell tumour with the testis being absent in the scrotum was considered as ‘undescended testis’. Results: From our database of 490 patients with testicular tumours presenting from the year 2014 -2018, 42 patients had testicular cancer in cryptorchid testis. The mean age was 32.9 years (Range:17-56). 24(57.14%) had seminoma and 18(42.86%) had non seminomatous tumors. Orchidopexy was done in 22(52.3%) patients at median age of 30 yrs (Range 2-33). 23 patients had prior undescended testis underwent high inguinal orchidectomy, 13 patients had testis located in pelvis and 6 patient had testis located in the upper abdomen. The average maximum size of tumours presenting with after orchidopexy was 7.34cm (4-10.5cm), in those presenting with pelvic tumours was 9.86cm (7-12.6cm) and in those with intraabdominal tumours was 14.3cm (9-20cm). The median follow-up for these patients was 36 months (3-64 months). There were 6 patients who relapsed after front line therapy whom 3 were salvaged with second line chemotherapy and 2 patients had residual disease at their last follow up. There was one death due to disseminated tumour with brain metastasis. The disease free survival for the whole cohort was 92.85%. Conclusions: The tumours developing in intraabdominal location of testis presented with a larger size and orchiopexy apart from its role in prevention of testicular cancer also helps in surveillance and early detection leading to effective treatment of these highly curable cancers. In the first of its series on testicular tumours in the cryptorchid, we show that they are also as curable as the germ cell tumours developing in the descended testis.
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Sano, T., A. Asai, K. Mishima, T. Fujimaki, and T. Kirino. "Telomerase activity in 144 brain tumours." British Journal of Cancer 77, no. 10 (May 1998): 1633–37. http://dx.doi.org/10.1038/bjc.1998.267.
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Rahman, Ruman, David Walker, Emma Campbell, and Kristian Aquilina. "EPCT-08. TRIAL WORKING GROUPS FOR PAEDIATRIC BRAIN TUMOURS." Neuro-Oncology 23, Supplement_1 (June 1, 2021): i48. http://dx.doi.org/10.1093/neuonc/noab090.194.
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Abstract Introduction Brain tumours are the biggest cancer killer in children and young adults. Several recent developments have the potential to change the treatment of brain tumours in children. These include ultrasound-mediated blood-brain barrier disruption, convection enhanced delivery, polymer delivery systems and electric field therapy, as well as intra-arterial, intra-CSF and intra-nasal chemotherapy. To date, there have been very few clinical trials to evaluate any of these. The science and technology underlying these developments is not traditionally embedded within the standard paediatric neuro-oncology network. In addition, custom-built hardware, novel surgical procedures and, in some cases, the testing and licensing of implantable devices, add difficulty at the regulatory level. Methods The authors participated in an international workshop funded by the charity Children with Cancer UK in 2016, where different experimental techniques aimed at optimising CNS drug delivery were discussed. Following this workshop and two subsequent workshops run by the CBTDDC (Children’s Brain Tumour Drug Delivery Consortium) in 2018 and 2020, the CBTDDC and the recently developed ITCC (Innovative Therapies for Children with Cancer) brain tumour group started working together to set up a new initiative. This aims to develop CNS-delivery-focused trial working groups for paediatric brain tumours. Results We have assembled a prestigious steering group, comprising international researchers and clinicians with expertise in diverse aspects of translational and clinical research in CNS drug delivery. At our first group meeting in March, participants will discuss the most effective ways of translating the emerging drug delivery modalities into clinical trials. Prioritised actions will be taken forward and the group will reconvene to discuss developments and next steps at a workshop in the Autumn. Conclusion We present this abstract to the SNO Paediatric conference to raise awareness of this initiative with the large number of relevant stakeholders who will be attending the event.
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Lönnerblad, Malin, Eva Berglund, Ingrid van’t Hooft, and Klas Blomgren. "Can National Tests from the Last Year of Compulsory School Be Used to Obtain More Detailed Information about Academic Performance in Children Treated for Brain Tumours? A Nationwide, Population-Based Study from Sweden." Cancers 13, no. 1 (January 4, 2021): 135. http://dx.doi.org/10.3390/cancers13010135.
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Children treated for brain tumours often have late-appearing complications that may affect their school performance. Uneven skill profiles may help reveal late complications that can be compensated for but otherwise remain undetected. We investigated Swedish national school tests of oral, reading and writing skills in the first foreign language (English), the mother tongue (Swedish) and mathematics. Data were obtained from The Swedish Childhood Cancer Registry and Statistics Sweden. The results from 475 children diagnosed with a brain tumour before their 15th birthday and 2197 matched controls showed that children treated for brain tumours evinced more difficulties with national tests than controls in almost all subtests, especially in the subject English, and that they may perform better on oral than written tasks. There were larger differences between female cases and controls than between male cases and controls; age at diagnosis played a significant role for some subtests, whereas tumour grade did not. Missing information from national tests proved to be a strong predictor of poor academic performance. Our results show that regular educational follow-ups, as a complement to neuropsychological follow-ups, are important for all children treated for brain tumours, regardless of sex, age at diagnosis or tumour grade.
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Fares, Jawad, Ilya Ulasov, Peter Timashev, and Maciej S. Lesniak. "Emerging principles of brain immunology and immune checkpoint blockade in brain metastases." Brain 144, no. 4 (April 1, 2021): 1046–66. http://dx.doi.org/10.1093/brain/awab012.
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Abstract Brain metastases are the most common type of brain tumours, harbouring an immune microenvironment that can in principle be targeted via immunotherapy. Elucidating some of the immunological intricacies of brain metastases has opened a therapeutic window to explore the potential of immune checkpoint inhibitors in this globally lethal disease. Multiple lines of evidence suggest that tumour cells hijack the immune regulatory mechanisms in the brain for the benefit of their own survival and progression. Nonetheless, the role of the immune checkpoint in the complex interplays between cancers cells and T cells and in conferring resistance to therapy remains under investigation. Meanwhile, early phase trials with immune checkpoint inhibitors have reported clinical benefit in patients with brain metastases from melanoma and non-small cell lung cancer. In this review, we explore the workings of the immune system in the brain, the immunology of brain metastases, and the current status of immune checkpoint inhibitors in the treatment of brain metastases.
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McCartney, Aileen, Claire Butler, and Sue Acreman. "Exploring access to rehabilitation services from allied health professionals for patients with primary high-grade brain tumours." Palliative Medicine 25, no. 8 (March 10, 2011): 788–96. http://dx.doi.org/10.1177/0269216311398699.
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Primary brain tumours account for less than 2% of cancer diagnoses in the UK but more people under 40 die from a brain tumour than from any other cancer. Despite developments in some treatment options, survival remains poor and patients suffer with considerable functional and cognitive deficits. Rehabilitation for patients with primary brain tumours produces statistically and clinically significant improvements in function. When compared, similar functional gains are made following rehabilitation for brain tumour patients and for those following stroke and traumatic brain injury. There have been very few studies looking at access to rehabilitation for this group of patients as a primary objective. However, existing studies and clinical experience suggest that patients with brain tumours do not access rehabilitation services frequently or easily, either locally or nationally. Therefore, this qualitative study addressed the reasons for this through semi-structured interviews of healthcare professionals, investigating their experiences of rehabilitation for this patient group and describing commonly identified barriers under key themes. The interviews gauged the views of eight healthcare professionals representing three professions in different settings, including hospital and community based. The resultant barriers fell under the following themes: professional knowledge and behaviours; services and systems; and the disease and its effects. Suggested solutions were wide ranging and included education, multidisciplinary meetings and specialist clinicians to co-ordinate care. The barriers to accessing rehabilitation for this group of patients are complex, but some of the solutions could be reached through education and co-ordination of services. Further research into the benefits of, and access to, rehabilitation for this group of patients is essential to ensure that patients with brain tumours are given opportunity to gain from the benefits of rehabilitation in the same way as other diagnoses, both cancer and non-cancer.
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Walker, EV, and F. Davis. "55 Malignant primary brain and other central nervous system tumours diagnosed in the Canadian population from 2009 to 2013." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 45, S3 (June 2018): S16—S17. http://dx.doi.org/10.1017/cjn.2018.306.
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The Canadian Brain Tumour Registry (CBTR) project was established in 2016 with the aim of enhancing infrastructure for surveillance and clinical research to improve health outcomes for brain tumour patients in Canada. We present a national surveillance report on malignant primary brain and central nervous system (CNS) tumours diagnosed in the Canadian population from 2009-2013. Patients were identified through the Canadian Cancer Registry (CCR); an administrative dataset that includes cancer incidence data from all provinces/territories in Canada. Cancer diagnoses are coded using the ICD-O3 system. Tumour types were classified by site and histology using The Central Brain Tumour Registry of the United States definitions. Incidence rates (IR) and 95% confidence intervals (CI) were calculated per 100,000 person-years and standardized to the 2011 census population age-distribution. Overall, 12,115 malignant brain and CNS tumours were diagnosed in the Canadian population from 2009-2013 (IR:8.43;95%CI:8.28,8.58). Of these, 6,845 were diagnosed in males (IR:9.72;95%CI:9.49,9.95) and 5,270 in females (IR:7.20;95%CI:7.00,7.39). The most common histology overall was glioblastoma (IR:4.06;95%CI:3.95,4.16). Among those aged 0-19 years, 1,130 malignant brain and CNS tumours were diagnosed from 2009-2013 (IR:3.36;95%CI:3.16,3.56). Of these, 625 were diagnosed in males (IR:3.32;95%CI:3.34,3.92) and 505 in females (IR:3.08;95%CI:2.81,3.36). The most common histology among the paediatric population was pilocytic astrocytoma (IR:0.73;95%CI:0.64,0.83). The presentation will include: IRs for other histologies, the geographic distribution of cases and a comparison between Canada and the United States.
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Theakstone, Ashton, Paul Brennan, Michael Jenkinson, Samantha Mills, Khaja Syed, Christopher Rinaldi, Yun Xu, et al. "Rapid Spectroscopic Liquid Biopsy for the Universal Detection of Brain Tumours." Cancers 13, no. 15 (July 30, 2021): 3851. http://dx.doi.org/10.3390/cancers13153851.
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Background: To support the early detection and diagnosis of brain tumours we have developed a rapid, cost-effective and easy to use spectroscopic liquid biopsy based on the absorbance of infrared radiation. We have previously reported highly sensitive results of our approach which can discriminate patients with a recent brain tumour diagnosis and asymptomatic controls. Other liquid biopsy approaches (e.g., based on tumour genetic material) report a lower classification accuracy for early-stage tumours. In this manuscript we present an investigation into the link between brain tumour volume and liquid biopsy test performance. Methods: In a cohort of 177 patients (90 patients with high-grade glioma (glioblastoma (GBM) or anaplastic astrocytoma), or low-grade glioma (astrocytoma, oligoastrocytoma and oligodendroglioma)) tumour volumes were calculated from magnetic resonance imaging (MRI) investigations and patients were split into two groups depending on MRI parameters (T1 with contrast enhancement or T2/FLAIR (fluid-attenuated inversion recovery)). Using attenuated total reflection (ATR)-Fourier transform infrared (FTIR) spectroscopy coupled with supervised learning methods and machine learning algorithms, 90 tumour patients were stratified against 87 control patients who displayed no symptomatic indications of cancer, and were classified as either glioma or non-glioma. Results: Sensitivities, specificities and balanced accuracies were all greater than 88%, the area under the curve (AUC) was 0.98, and cancer patients with tumour volumes as small as 0.2 cm3 were correctly identified. Conclusions: Our spectroscopic liquid biopsy approach can identify gliomas that are both small and low-grade showing great promise for deployment of this technique for early detection and diagnosis.
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Rahman, Ruman, David Walker, Emma Campbell, and Kristian Aquilina. "CLRM-08. TRIAL WORKING GROUPS FOR PAEDIATRIC BRAIN TUMOURS." Neuro-Oncology Advances 3, Supplement_4 (September 21, 2021): iv2—iv3. http://dx.doi.org/10.1093/noajnl/vdab112.007.
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Abstract INTRODUCTION Brain tumours are the biggest cancer killer in children and young adults. Several recent developments have the potential to change the outlook for these children, including intra-CSF chemotherapy, ultrasound-mediated blood-brain barrier disruption, convection enhanced delivery, polymer delivery systems, electric field therapy, and intra-arterial and intra-nasal chemotherapy. To date, there have been very few clinical trials to evaluate these. In addition, custom-built hardware, novel surgical procedures and the testing and licensing of implantable devices add difficulty at the regulatory level. METHODS The authors participated in an international workshop funded by the charity Children with Cancer UK in 2016, where different experimental techniques aimed at optimising CNS drug delivery were discussed. Following this and two subsequent workshops run by the CBTDDC (Children’s Brain Tumour Drug Delivery Consortium), the CBTDDC and the ITCC (Innovative Therapies for Children with Cancer) brain tumour group launched the ‘Clinical Trials Working Group for Central Nervous System Drug Delivery’. This aims to accelerate clinical trials to assess the safety and effectiveness of drug delivery devices for the treatment of paediatric brain tumours. RESULTS On 1 March, 2021, CBTDDC and Mr Kristian Aquilina (Consultant Paediatric Neurosurgeon at Great Ormond Street Hospital) hosted the first steering group meeting, comprising 38 leading brain tumour research scientists and clinicians from the UK, EU and US. CONCLUSION The ideas generated during the March meeting are driving the agenda for a Clinical Trials Workshop that will be held in the autumn of 2021. In particular, there was agreed consensus that a ‘Roadmap’ document for pre-clinical to clinical translation needs to be created and shared with the paediatric neuro-oncology research community. We present this abstract to the CNS Clinical Trials Meeting to raise awareness of this initiative with the large number of relevant stakeholders who will be attending the event.
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SUTTER, R., G. YADIRGI, and S. MARINO. "Neural stem cells, tumour stem cells and brain tumours: Dangerous relationships?" Biochimica et Biophysica Acta (BBA) - Reviews on Cancer 1776, no. 2 (December 2007): 125–37. http://dx.doi.org/10.1016/j.bbcan.2007.07.006.
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Rengit, Ashy. "Longterm cognitive dysfunction in paediatric brain tumour survivors - the need for multifactorial risk screening." BJPsych Open 7, S1 (June 2021): S47. http://dx.doi.org/10.1192/bjo.2021.174.
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AimsIdentify common risk factors for longterm cognitive dysfunction in PBTS (paediatric brain tumour survivors) Examine how various paediatric cancer treatment modalities affect cognitive outcomes Consider baseline features which may increase the risk of cognitive dysfunction in PBTSMethodCurrent research into the neuropsychiatric sequelae of childhood brain tumours is limited, therefore review of the literature was conducted to identify research within this field.DatabasesGoogle Scholar - papers accessed via the University of Brighton or Sussex online libraryNICE HDAS - HMIC, AMED, MEDLINE, BNI, PsycINFO, CINAHL, Pubmed, EMBASE & EMCAREMendeley reference manager - papers for background readingSearch termsPICO(T) method - Population (Cancer Survivors), Intervention (Cancer Treatment), Comparison (Brain tumour), Outcome (Cognitive dysfunction) & Time (Childhood & adolescence) Boolean operators (AND/OR), truncation and wildcard search functions were also utilised.Inclusion criteria; no limits on date, study type or gender, however, study results were limited by age - as the research focus was restricted to children and adolescents.Excluded results; papers which did not meet inclusion criteria, duplicate studies, studies measuring non-cognitive cancer outcomes or investigating non-cortical tumours, non-English language studies with no available English translations.ResultCommon risk factors - certain tumour types (glioneuronal tumours or gliomas) or inner cortical tumour sites e.g. were more vulnerable to epileptogenesis. In particular, seizures which were prolonged and treatment-resistant were associated with a greater degree of cognitive dysfunction.Impact of various cancer treatment modalities - overall results understandably suggested that patients are more likely to develop cognitive deficits following brain tumour treatment. In particular, partial tumour resection (especially if epileptogenic), whole-brain irradiation, cranial radiotherapy and chemotherapy were more likely to impact cognitive function.Baseline features that may increase likelihood of cognitive dysfunction e.g. intellectual disability or education level were not noted in the reviewed literature.ConclusionCancer is one of the leading causes of global child mortality, and younger populations often present to paediatric oncology services with brain tumour involvement. Current childhood brain tumour research has begun to recognise that many young survivors develop into adulthood with cognitive sequelae impacting quality of life measures. However, existing evidence is also limited and requires further research to produce a standardised clinical tool for screening various risk factors which may increase longterm risk of cognitive dysfunction and subsequent difficulties with daily life.
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Drewes, Anne M., Maria E. Møller, Rasmus Hertzum-Larsen, Gerda Engholm, and Hans H. Storm. "Risk of primary brain tumour after breast cancer." Endocrine Connections 9, no. 1 (January 2020): 28–33. http://dx.doi.org/10.1530/ec-19-0498.
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Introduction Cancer registry data in the USA indicated that women diagnosed with breast cancer before the age of 40 were at increased risk of a new primary tumour within the brain and women aged 50 years or above were at lower risk than expected. Our aim was to investigate if similar results could be found in Danish population-based data, considering an explanatory role of hormonal status. Methods Our study cohort included all women diagnosed with breast cancer below the age of 60 between 1978 and 2013 in Denmark. A total of 47,920 women were followed up in the Danish Cancer Registry for primary brain cancer. Standardized incidence ratios (observed/expected cases (O/E)) were used to estimate the risk of getting a primary brain tumour in the breast cancer cohort. Results Data indicated an increased tendency of brain cancer following breast cancer at ages below 60 years (O/E = 1.24). For premenopausal women (age <49 at the diagnosis of breast cancer) the O/E was 1.25. Stratifying by time of breast cancer diagnosis, we observed an increased risk of being diagnosed with a brain tumour among women aged 49 years or younger at breast cancer diagnosis between 2004 and 2013. Conclusion The results indicate an increased tendency of developing a primary brain tumour in women with previous breast cancer history. Whereas the finding in premenopausal women is in line with the SEER data, the finding among postmenopausal is not. Primary brain tumours in breast cancer patients call for research in genetics and hormones to establish common risk factors.
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Withey, Stephanie, Lesley MacPherson, Adam Oates, Stephen Powell, Jan Novak, Laurence Abernethy, Barry Pizer, et al. "Multicentre study of perfusion magnetic resonance imaging in paediatric brain tumours." Neuro-Oncology 21, Supplement_4 (October 2019): iv10. http://dx.doi.org/10.1093/neuonc/noz167.041.
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Abstract Studies in adults have shown that brain tumour perfusion correlates with grade. These studies are dominated by gliomas grade II to IV which are rare in children. The standard method, Dynamic Susceptibility Contrast MRI, provides estimates of relative cerebral blood volume (rCBV) but contrast agent leakage affects rCBV accuracy. The majority of perfusion studies have been conducted at single centres and variation in acquisition protocols makes the generalizability of results questionable. The aim of this study was to compare leakage-corrected rCBV with grade in paediatric brain tumours at multiple centres. Scans were analysed from 85 patients at 4 centres on 6 scanners prior to treatment. MRI protocols varied between centres. Histological diagnoses including grade were obtained. Whole-tumour median rCBV was significantly higher in the 45 high grade than the 40 low grade tumours (2.54 ± 1.63 ml/100ml vs 1.68 ± 1.36 ml/100ml, p=0.010). Low grade tumours, particularly pilocytic astrocytomas (grade I), displayed more contrast agent leakage consistent with their appearance on contrast enhanced images and required more leakage correction than high grade tumours. This finding differs from that in adults where contrast agent uptake is usually associated with higher grade. A cut-off of 1.70 ml/100ml for rCBV gave sensitivity and specificity of 76% and 65% respectively for discriminating grade. In summary, perfusion MRI can be used to help distinguish between low and high grade paediatric brain tumours. This finding is robust across multiple centres and acquisition protocols but correction should be made for leakage of contrast agent from the vessels.
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Sastry, Jairam, Paul Van Siang Liang Mang, Dermot Murpy, Milind Ronghe, and Diana McIntosh. "QOL-56. THE RELAPSED AND OR PROGRESSED BRAIN TUMOURS IN CHILDREN: RHC, GLASGOW EXPERIENCE." Neuro-Oncology 22, Supplement_3 (December 1, 2020): iii441. http://dx.doi.org/10.1093/neuonc/noaa222.709.
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Abstract INTRODUCTION The outcome for children with relapsed or progressed brain tumours is poor. The aim of this project was to identify total number of children who have relapsed or progressed with Brain tumour and to determine the types of tumours, treatment offered and assess outcome. METHODS This is a retrospective study of all patients treated for relapsed or progressed brain tumours between 2007 and 2017 at the Royal Hospital for children. Patients were identified using the unit database. Clinical data included demographics, histologic diagnosis, treatment characteristics and outcome which was obtained from electronic records. RESULTS 46 children were included (22M:24F). The median age of diagnosis was 5 years. There were 16 histological subtypes of brain tumours: pilocytic astrocytoma (n=12, 26%), optic pathway glioma (n=4,7%), medulloblastoma (n=8, 17%), ependymoma (n=4, 9%), high grade glioma (n=3, 7%, DIPG (n=2, 4%) and others 13(32.2%). 28(61%) had relapsed at a median time of 18 months. Tumour progression occurred in 18(31%) at a median time of 21.5 months. Post-relapse or progression therapy included surgery (14, 30%), chemotherapy (17, 40%) and radiotherapy (5, 10.9%). 50% of the patients remain alive with 17(37%) being stable and 6(13%) with progression of disease. 50% had died of disease progression. CONCLUSIONS The relapse and or progression was seen 61% of patients. The commonest tumours in this cohort were pilocytic astrocytoma and medulloblastoma. Chemotherapy was the most used regimen followed by surgery and radiotherapy. Primary dissemination at the time of diagnosis was associated with poor prognosis.
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Phillips, Jo, and Mark Brougham. "QOL-14. A BIOPSYCHOSOCIAL APPROACH TO BRAIN INJURY REHABILITATION FOLLOWING TREATMENT FOR PAEDIATRIC BRAIN TUMOURS: CAN PHARMACOTHERAPY AID NEUROPSYCHOLOGICAL OUTCOME?" Neuro-Oncology 22, Supplement_3 (December 1, 2020): iii433. http://dx.doi.org/10.1093/neuonc/noaa222.677.
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Abstract Long term survival following paediatric brain tumours has vastly improved in recent decades. Consequently there is a drive towards improved quality of survivorship. Brain tumours, surgical resection and adjuvant therapies represent mechanisms for brain injury and can therefore negatively impact a child’s neuropsychological trajectory; affecting cognition, behaviour, emotional and adaptive functioning and educational/occupational outcomes. A biopsychosocial approach to rehabilitation should target each of these domains through supported remediation, environmental modification and psychoeducation for young people and the key systems around them (e.g. families, education). There is a growing evidence base for the role of concordant psychopharmacologies to improve neuropsychological outcome. Since 2015 children treated at RHSC Edinburgh for brain tumours have been offered pharmacotherapy alongside usual rehabilitation approaches if they demonstrate significant difficulties with Attention, Processing Speed and/or Executive Function on formal neuropsychological assessment. Patients are referred to a Consultant Psychiatrist or Paediatrician (as per local protocol) for medication selection, titration and monitoring. A short case series (N=14) is presented outlining brain tumour pathologies, treatment modalities, neuropsychological profile and rationale for recommending pharmacotherapy. Approximately 50% of patients took up the offer. The treatment/s offered and self or parents reported outcomes is summarised. Pharmacotherapy was broadly effective; “it’s been like night and day”, although for one case (N=1) the side effects outweighed any benefit; “she became even more emotional”. Findings indicate that pharmacotherapy should be considered alongside conventional neurorehabilitation techniques for CYP with specific cognitive difficulties following treatment for paediatric brain tumours.
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Calero-Pérez, Pilar, Shuang Wu, Carles Arús, and Ana Paula Candiota. "Immune System-Related Changes in Preclinical GL261 Glioblastoma under TMZ Treatment: Explaining MRSI-Based Nosological Imaging Findings with RT-PCR Analyses." Cancers 13, no. 11 (May 28, 2021): 2663. http://dx.doi.org/10.3390/cancers13112663.
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Glioblastomas (GB) are brain tumours with poor prognosis even after aggressive therapy. Previous work suggests that magnetic resonance spectroscopic imaging (MRSI) could act as a biomarker of efficient immune system attack onto GB, presenting oscillatory changes. Glioma-associated microglia/macrophages (GAMs) constitute the most abundant non-tumour cell type within the GB and can be polarised into anti-tumour (M1) or pro-tumour (M2) phenotypes. One of the mechanisms to mediate immunosuppression in brain tumours is the interaction between programmed cell death-1 ligand 1 (PD-L1) and programmed cell death-1 receptor (PD-1). We evaluated the subpopulations of GAMs in responding and control GB tumours to correlate PD-L1 expression to GAM polarisation in order to explain/validate MRSI-detected findings. Mice were evaluated by MRI/MRSI to assess the extent of response to treatment and with qPCR for GAMs M1 and M2 polarisation analyses. M1/M2 ratios and PD-L1 expression were higher in treated compared to control tumours. Furthermore, PD-L1 expression was positively correlated with the M1/M2 ratio. The oscillatory change in the GAMs prevailing population could be one of the key causes for the differential MRSI-detected pattern, allowing this to act as immune system activity biomarker in future work.
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Prasad, Maya, Ekta Chheda, Girish Chinnaswamy, Tejpal Gupta, Rahul Krishnatry, Tushar Vora, and Jayant Godashastri. "LINC-08. INCREASED TREATMENT TOXICITIES AND INFERIOR OUTCOMES IN UNDERNOURISHED CHILDREN WITH BRAIN TUMOURS." Neuro-Oncology 22, Supplement_3 (December 1, 2020): iii379. http://dx.doi.org/10.1093/neuonc/noaa222.443.
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Abstract BACKGROUND Children on treatment for brain tumours are known to be at high risk of undernutrition, the impact on outcome and toxicity is not well understood. METHODS Retrospective audit of children(<18 years)diagnosed January 2017-December 2018 with embryonal brain tumours (medulloblastoma, primitive neuro-ectodermal tumors, pinealoblastoma, atypical teratoid/rhabdoid tumour) and treated at our centre. Data was retrieved from case records and electronic medical records. Nutritional status(NS) was defined as per World Health Organization (WHO) into severe malnutrition (SAM),moderate malnutrition (MAM),well nourished (WN) and overweight. Undernutrition(UN) was defined as SAM/MAM.Toxicity was documented till end of treatment,defined as treatment delay>1week,significant infection or toxic death. RESULTS Of 124 eligible patients who received entire chemotherapy at our centre, NS data was available in 73 at diagnosis and 58 at follow-up. At diagnosis-29,16,26 and 2 and at follow-up-20,16,22 and 0 were SAM,MAM,WN and overweight. During treatment, weight gain was documented in 26%, stable weight in 55% and weight loss in 19%. Those UN at diagnosis had worse outcomes at follow-up with 70% alive in remission compared to 88% of WN(p-0.14). There was increased toxicity in UN group(50%) compared to WN(24%),p-0.04.All 3 toxic deaths were in UN. Those who lost weight during treatment had higher toxicities(70%) compared to those with stable weight (30%)or weight gain(20%),p-0.02. CONCLUSIONS In spite of nutritional intervention, children on treatment for brain tumours tend to lose weight. Increased treatment toxicities and inferior outcomes in undernourished children with brain tumours necessitates proactive and aggressive nutritional monitoring and intervention.
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Benito, Adrian, Nabil Hajji, Kevin O’Neill, Hector C. Keun, and Nelofer Syed. "Ketogenic diet and metabolic regulation of brain microglia." Neuro-Oncology 21, Supplement_4 (October 2019): iv8—iv9. http://dx.doi.org/10.1093/neuonc/noz167.035.
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Abstract Ketogenic diet (KD) has been proposed as a coadjuvant therapy in the treatment of brain tumours. Reduction of blood glucose and increase in ketone bodies concentration are amongst the most important changes induced by KD in patients. Preliminary data collected in our lab indicates that KD induces substantial changes in the immune system in mice bearing brain tumours. Microglia are brain-resident immune cells that account for around 30% of the tumour mass and play a major role in controlling tumour progression by adopting a protumour (M2 polarisation) or antitumour (M1 polarisation) phenotype. We are interested in understating the molecular and metabolic determinants of microglia polarisation and how these can be modulated by the metabolic microenvironment and KD. We report some initial findings that indicate microglia adapt to changes in the metabolic microenvironment and that nutrient availability can modulate microglia activation and polarisation. We believe that the study of microglia metabolism and nutritional interventions like KD can provide new knowledge about the regulation of the brain immune system and unveil novel routes for brain cancer treatment.
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Zaytseva, Olga, Nan-hee Kim, and Leonie M. Quinn. "MYC in Brain Development and Cancer." International Journal of Molecular Sciences 21, no. 20 (October 20, 2020): 7742. http://dx.doi.org/10.3390/ijms21207742.
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The MYC family of transcriptional regulators play significant roles in animal development, including the renewal and maintenance of stem cells. Not surprisingly, given MYC’s capacity to promote programs of proliferative cell growth, MYC is frequently upregulated in cancer. Although members of the MYC family are upregulated in nervous system tumours, the mechanisms of how elevated MYC promotes stem cell-driven brain cancers is unknown. If we are to determine how increased MYC might contribute to brain cancer progression, we will require a more complete understanding of MYC’s roles during normal brain development. Here, we evaluate evidence for MYC family functions in neural stem cell fate and brain development, with a view to better understand mechanisms of MYC-driven neural malignancies.
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Jallo, G. "Brain and Spinal Cord Tumours of Childhood." British Journal of Cancer 92, no. 2 (January 2005): 414. http://dx.doi.org/10.1038/sj.bjc.6602349.
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Mulligan, H. D., and M. J. Tisdale. "Metabolic substrate utilization by tumour and host tissues in cancer cachexia." Biochemical Journal 277, no. 2 (July 15, 1991): 321–26. http://dx.doi.org/10.1042/bj2770321.
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Utilization of metabolic substrates in tumour and host tissues was determined in the presence or absence of two colonic tumours, the MAC16, which is capable of inducing cachexia in recipient animals, and the MAC13, which is of the same histological type, but without the effect on host body composition. Glucose utilization by different tissues was determined in vivo by the 2-deoxyglucose tracer technique. Glucose utilization by the MAC13 tumour was significantly higher than by the MAC16 tumour, and in animals bearing tumours of either type the tumour was the second major consumer of glucose after the brain. This extra demand for glucose was accompanied by a marked decrease in glucose utilization by the epididymal fat-pads, testes, colon, spleen, kidney and, in particular, the brain, in tumour-bearing animals irrespective of cachexia. The decrease in glucose consumption by the brain was at least as high as the metabolic demand by the tumour. This suggests that the tissues of tumour-bearing animals adapt to use substrates other than glucose and that alterations in glucose utilization are not responsible for the cachexia. Studies in vitro showed that brain metabolism in the tumour-bearing state was maintained by an increased use of lactate and 3-hydroxybutyrate, accompanied by a 50% increase in 3-oxoacid CoA-transferase. This was supported by studies in vivo which showed an increased metabolism of 3-hydroxybutyrate in tumour-bearing animals. Thus ketone bodies may be utilized as a metabolic fuel during the cancer-bearing state, even though the nutritional conditions mimic the fed state.
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Schlehofer, B., I. Hettinger, P. Ryan, J. Little, S. Preston-Martin, A. Ahlbom, F. Menegoz, G. Howe, G. Giles, and M. Blettner. "Occupational risk factors for brain tumours in adults. Results from the international brain tumour case- control study." European Journal of Cancer 37 (April 2001): S23—S24. http://dx.doi.org/10.1016/s0959-8049(01)80569-4.
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Sun, Claire, Caroline Drinkwater, Dhanya Sooraj, Gabrielle Bradshaw, Claire Shi, Dasun Fernando, Sarah Parackal, Daniel Gough, Jason Cain, and Ron Firestein. "MODL-21. INTEGRATIVE APPROACHES IN FUNCTIONAL GENOMICS TO IDENTIFY GENETIC DEPENDENCIES IN PEDIATRIC BRAIN CANCER." Neuro-Oncology 22, Supplement_3 (December 1, 2020): iii415. http://dx.doi.org/10.1093/neuonc/noaa222.594.
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Abstract The precise decoding of human genomes facilitated by the advancements in next-generation sequencing has led to a better understanding of genetic underpinnings of pediatric brain cancers. Indeed, it is now evident that tumours of the same type harbour distinct driving mutations and molecular aberrations that can result in different prognosis and treatment outcomes. The profounder insight into the the identity, amount and types of molecular aberrations has paved the way for the advent of targeted therapies in precision medicine. Nevertheless, less than 10% of pediatric cancer patients harbour actionable mutations. Strictly limited therapeutic options that are firstly available for brain cancers and secondly acceptable for children’s development further impede the breakthrough in the survival rate in pediatric brain cancers. This underscores a desperate need to delve beyond genomic sequencing to identify biomarker coupled therapies that not only featured with treatment efficacy in the central nervous system but also acceptable side effects for children. The Hudson-Monash Paediatric Precision Medicine (HMPPM) Program focuses on utilising genetic profiles of patients’ tumour models to identify new therapeutic targets and repurpose existing ones using high-throughput functional genomics screens (2220 drugs and CRISPR screen of 300 oncogenic genes). Using a large compendium of over sixty patient derived paediatric brain cancer models, we provide proof-of-concept data that shows an integrative pipeline for functional genomics with multi-omics datasets to perform genotype-phenotype correlations and, therefore, identify genetic dependencies. Herein, using several examples in ATRT, DIPG and HGG, we show how functional interrogations can better define molecular subclassification of tumours and identify unique vulnerabilities.
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Li, H., J. Liu, M. Hofmann, M.-F. Hamou, and N. de Tribolet. "Differential CD44 expression patterns in primary brain tumours and brain metastases." British Journal of Cancer 72, no. 1 (July 1995): 160–63. http://dx.doi.org/10.1038/bjc.1995.294.
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Grist, James, Stephanie Withey, Lesley MacPherson, Adam Oates, Mr Stephen Powell, Jan Novak, Laurence Abernethy, et al. "Utilising functional imaging to predict survival in paediatric brain tumours." Neuro-Oncology 21, Supplement_4 (October 2019): iv5. http://dx.doi.org/10.1093/neuonc/noz167.018.
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Abstract Introduction Brain tumours are a common cause of death in the paediatric population. We have previously shown that MR imaging and spectroscopy can be used to non-invasively differentiate between tumour types. Here, we demonstrate that functional imaging can be highly predictive of survival and grade in a paediatric cohort. Methods Perfusion (PWI) and diffusion weighted imaging (DWI) were performed in a multi-site (Birmingham Children’s Hospital, Royal Victoria Infirmary, Alder Hey, Nottingham) cohort ([grade, 5-year survival alive:dead number] = [I,15:1],[II, 5:1],[III,2:3],[IV,8:11]). ROIs were drawn on T2 imaging and functional imaging features (mean, standard deviation, skewness, and kurtosis) were derived. Supervised machine learning was used to predict 5-year survival and tumour grade from features. ANOVA and post-hoc tests were used to assess differences in features between grade and 5-year survival status. Results 5-year survival was predicted with 89%, 85%, and 87% accuracy with all imaging, perfusion, or diffusion features, respectively. A significant difference in perfusion was found between surviving and diseased participants (1.71 ± 0.82 vs 2.62 ± 1 mL/100g/min, respectively, p < 0.05). A significant difference in ADC (mm2 s-1) between tumour grades was found (1 vs 4 (1533 ± 458 vs 857 ± 239), 4 vs 3 (857 ± 239 vs 1197 ± 137), 4 vs 2 (857 ± 239 vs 1440 ± 557), corrected p < 0.05). Conclusion We have shown that perfusion and diffusion imaging features can be used to non-invasively assess tumour grade and estimate 5-year survival status in a cohort of paediatric brain tumours.
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Albulescu, Radu, Elena Codrici, Ionela Daniela Popescu, Simona Mihai, Laura Georgiana Necula, Daniel Petrescu, Mihaela Teodoru, and Cristiana Pistol Tanase. "Cytokine Patterns in Brain Tumour Progression." Mediators of Inflammation 2013 (2013): 1–7. http://dx.doi.org/10.1155/2013/979748.
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Inflammation represents the immune system response to external or internal aggressors such as injury or infection in certain tissues. The body’s response to cancer has many parallels with inflammation and repair; the inflammatory cells and cytokines present in tumours are more likely to contribute to tumour growth, progression, and immunosuppression, rather than in building an effective antitumour defence. Using new proteomic technology, we have investigated serum profile of pro- (IL-1β, IL-6, IL-8, IL-12, GM-CSF, and TNF-α) and anti-inflammatory cytokines (IL-4, IL-10), along with angiogenic factors (VEGF, bFGF) in order to assess tumoural aggressiveness. Our results indicate significant dysregulation in serum levels of cytokines and angiogenic factors, with over threefold upregulation of IL-6, IL-1β, TNF-α, and IL-10 and up to twofold upregulation of VEGF, FGF-2, IL-8, IL-2, and GM-CSF. These molecules are involved in tumour progression and aggressiveness, and are also involved in a generation of disease associated pain.
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Parkins, Katie M., Amanda M. Hamilton, Veronica P. Dubois, Suzanne M. Wong, Paula J. Foster, and John A. Ronald. "Cellular MRI Reveals Altered Brain Arrest of Genetically Engineered Metastatic Breast Cancer Cells." Contrast Media & Molecular Imaging 2019 (January 8, 2019): 1–7. http://dx.doi.org/10.1155/2019/6501231.
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Purpose. The combined use of anatomical magnetic resonance imaging (MRI), cellular MRI, and bioluminescence imaging (BLI) allows for sensitive and improved monitoring of brain metastasis in preclinical cancer models. By using these complementary technologies, we can acquire measurements of viable single cell arrest in the brain after systemic administration, the clearance and/or retention of these cells thereafter, the growth into overt tumours, and quantification of tumour volume and relative cancer cell viability over time. While BLI is very useful in measuring cell viability, some considerations have been reported using cells engineered with luciferase such as increased tumour volume variation, changes in pattern of metastatic disease, and inhibition of in vivo tumour growth. Procedures. Here, we apply cellular and anatomical MRI to evaluate in vivo growth differences between iron oxide labeled naïve (4T1BR5) and luciferase-expressing (4T1BR5-FLuc-GFP) murine brain-seeking breast cancer cells. Balb/C mice received an intracardiac injection of 20,000 cells and were imaged with MRI on days 0 and 14. Mice that received 4T1BR5-FLuc-GFP cells were also imaged with BLI on days 0 and 14. Results. The number of signal voids in the brain (representing iron-labeled cancer cells) on day 0 was significantly higher in mice receiving 4T1BR5 cells compared to mice receiving 4T1BR5-FLuc-GFP cells (p<0.0001). Mice that received 4T1BR5 cells also had significantly higher total brain tumour burden and number of brain metastases than mice that received 4T1BR5-FLuc-GFP cells (p<0.0001). Conclusions. By employing highly sensitive cellular MRI tools, we demonstrate that engineered cells did not form tumours as well as their naïve counterparts, which appear to primarily be due to a reduction in cell arrest. These results indicate that engineering cancer cells with reporter genes may alter their tropism towards particular organs and highlight another important consideration for research groups that use reporter gene imaging to track metastatic cancer cell fate in vivo.
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Khairkar, Praveen, Srikanth Reddy, and Amit Agrawal. "Neuropsychiatric aspects of paediatric brain tumours: an update." Romanian Neurosurgery 30, no. 4 (December 1, 2016): 479–92. http://dx.doi.org/10.1515/romneu-2016-0077.
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Abstract The diagnosis and treatment of children and adolescents with cancer has a tremendous and lasting effect on the patients, their families, and other individuals in their social network. It carries a host of psychological and neurobehavioral ramifications, from questions of mortality to changes in levels of functioning in multiple domains. Childhood cancer remains the leading cause of illness-related death in childhood, but significant advances in survival have been made in the past 40 years. This review looks at the neuropsychiatric presentations, psychosocial and treatment-related issues that arise in children with brain tumors.