Relevant bibliographies by topics / Cancer; Brain tumours

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Academic literature on the topic 'Cancer; Brain tumours'

Author: Grafiati
Published: 4 June 2021
Last updated: 8 February 2022

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Journal articles on the topic "Cancer; Brain tumours"

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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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Dissertations / Theses on the topic "Cancer; Brain tumours"

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Maxwell, Marius. "Expression of proto-oncogenes and growth factors in glioblastoma multiforme." Thesis, University of Oxford, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.259967.

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Florian, Catarina Ligia. "Proton nuclear magnetic resonance studies of human glioma cell lines." Thesis, University College London (University of London), 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.309218.

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Gill, Simrandip Kaur. "Single voxel proton magnetic resonance spectroscopy of childhood brain tumours." Thesis, University of Birmingham, 2014. http://etheses.bham.ac.uk//id/eprint/4899/.

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Conventional magnetic resonance imaging (MRI) is essential for the management of childhood brain tumours. However, it is increasingly being supplemented with functional techniques such as magnetic resonance spectroscopy (MRS). This thesis investigates how pre-treatment single voxel MRS can aid in diagnosis and surveillance of paediatric brain tumours and identify prognostic biomarkers. Data from multiple centres, scanners from three leading manufacturers and field strengths of 1.5 T and 3 T are incorporated. MRS was analysed using TARQUIN software with metabolite peaks fitted using a simulated basis set to provide metabolite concentrations. Univariate and multivariate statistical tests were used to compare variables. Multi-scanner spectroscopy detected significant differences in common and rare paediatric brain tumours. Diagnostic metabolite profiles were able to confirm tumour on follow-up imaging. Elevated creatine and total choline determined good prognosis in medulloblastoma. Myo-inositol and citrate aided in the characterisation of diffuse pontine gliomas (DIPG). While conventional MRI was unable to identify prognostic markers for DIPG, elevated taurine was found to be significantly associated with a better prognosis. The results encourage the use of MRS as an adjunct to conventional MRI in routine clinical practice. For future studies, accurate assignment of biomarkers will be determined in tumour tissue using in vitro high-resolution spectroscopy methods.
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Schmiegelow, Marianne. "Endocrinological late effects following radiotherapy and chemotherapy of childhood brain tumours. /." København : Lægeforeningens Forlag, 2005. http://bvbr.bib-bvb.de:8991/F?func=service&doc_library=BVB01&doc_number=014566238&line_number=0001&func_code=DB_RECORDS&service_type=MEDIA.

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Punjaruk, Wiyada. "The contribution of drug resistant cancer stem cells to paediatric brain tumours." Thesis, University of Nottingham, 2010. http://eprints.nottingham.ac.uk/13403/.

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Introduction: Recent studies have revealed that cancer stem cells (CSCs) exist in malignant disease. Additionally, it is proposed that these cells may survive following chemotherapy, and hence contribute to tumour relapse. A significant mechanism of drug resistance in CSCs is believed to be the expression of ATP-binding cassette (ABC) transporters that efflux cytotoxic agents out of cells. The objective of this study was to study the existence of CSCs in a panel of primary paediatric brain tumours (PBTs) and to determine if these were drug resistant via functional ABC transporters. Materials and Methods: The main cell lines characterised were: EPN-2 (primary ependymoma); MED-2 (recurrent medulloblastoma); SPNET-1 [primary CNS primitive neuroectodermal tumour (CNS PNET)]; and a commercial CNS PNET (PFSK-1). Basic characterisation of our cell lines were assessed by Telomeric Repeat Amplification Protocol (TRAP) assay, Terminal Restriction Fragments (TRF) assay, metaphase spread analysis and doubling time. To determine the proportion of cancer stem-like cells in the parental cell lines, CD133 and SOX2 co-staining immunofluorescence was performed and validated by Western blotting analysis. The expression of ABC transporters (ABCB1, ABCC1 and ABCG2) was also investigated by co-staining for CD133 and ABC transporters using immunofluorescence and Western blotting analysis. Flow cytometry was performed to examine ABCB1 function. Four clinically relevant drugs (etoposide, cisplatin, irinotecan and methotrexate) were used to assess the degree of drug resistance of these lines. Clonnogenic assay and neurosphere formation assay were then performed to investigate colony survival and the ability of cells to form neurospheres, respectively, after drug treatment. Finally, the potential to increase chemosensitivity by drug treatment in the presence of the ABCB1 inhibitor, Verapamil, was assessed. Results: Basic characterisation results demonstrated that a high level of telomerase activity and maintenance of telomere length was found in all cell lines (grown both as monolayers and neurospheres). Metaphase spread analysis showed a wide range of aberrant chromosome numbers in PFSK-1 cells whereas our cell lines demonstrated a more stable chromosome number. Neurospheres grew slower than monolayers and monolayers had constant growth rate with increasing passage number. It was found that for each cell line, a small subpopulation (8-12%) of cultured monolayer cells are positive for both CD133 and SOX-2 immunofluorescent staining whilst cultured neurospheres contained 35-45% of co-stained cells. No co-stained cells were identified in the commercial PFSK-1 line and these findings were consistent with the results from Western blotting analysis. Approximately 10% of the parental cell lines comprised cells co-expressing CD133 and ABCB1 or ABCC1 at a low level whilst none of our cell lines were positive for ABCG2. Additionally, the parental cell lines contained a small proportion of cells expressing functional endogenous ABCB1 (34±5.2% in EPN-2, 26.5±3.9% in MED-2 and 13.9±3.2% in SPNET-1). During multiple rounds of drug treatment, ABCB1 was consistently expressed at a high level throughout and the proportion of functional ABCB1 expressing cells increased in all cell lines almost 2 fold compared to the parental cell lines and the selected control sublines. Whilst ABCC1 expression was gradually upregulated after multiple rounds of treatment but ABCG2 expression remained negative. Drug combined with Verapamil treatment significantly decrease survival rate approximately 5 fold compared to drug treatment alone although the majority of surviving cells were still CD133 and ABCB1 positive. Conclusion: Newly established paediatric cell lines (EPN-2, MED-2 and SPNET-1) represented significant histological and biological features of the original tumours from which they were derived and were stable in standard culture condition for a prolonged period of time. The parental cell lines contained a small proportion of cells expressing endogenous functional ABCB1 at a low level indicating intrinsic drug resistance. After multiple rounds of drug treatment, ABCB1 was the major mechanism of drug resistance in our cell lines. ABCC1 were upregulated later in our cell lines after multiple rounds of drug treatment whereas none of our cell lines expressed ABCG2 during drug treatment.
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Neal, Anthony James. "Optimisation of radiotherapy treatment planning for tumours of the breast, prostate and brain." Thesis, King's College London (University of London), 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.306922.

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Gorgolewski, Krzysztof Jacek. "Using functional magnetic resonance imaging to plan surgical resections of brain tumours." Thesis, University of Edinburgh, 2013. http://hdl.handle.net/1842/7861.

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Brain tumours, even though rare, are one of the deadliest types of cancer. The five year survival rate for the most malignant type of brain tumours is below 5%. Modern medicine provides many options for treating brain cancer such as radiotherapy and chemotherapy. However, one of the most effective ways of fighting the disease is surgical resection. During such a procedure the tumour is partially or completely removed. Unfortunately, even after a complete resection some tumourous tissue is left behind and can grow back or metastasise to a different location in the brain. It has been shown, however, that more aggressive resections lead to longer life expectancy. This does not come without risks. Depending on tumour location, extensive resections can lead to transient or permanent post-operative neurological deficits. Therefore, when planning a procedure, the neurosurgeon needs to find balance between extending patients life and maintaining its quality. Recent developments in Magnetic Resonance Imaging (MRI) fueled by the field of human cognitive neuroscience have led to improved methods of non-invasive imaging of the brain function. Such methods allow the creation of functional brain maps of populations or individual subjects. Adapting this technique to the clinical environment enables the assessment of the risks and to plan surgical procedures. The following work aims at improving the use of functional MRI with a specific clinical goal in mind. The thesis begins with description of etiology, epidemiology and treatment options for brain tumours. This is followed by a description of MRI and related data processing methods, which leads to introduction of a new technique for thresholding statistical maps which improves upon existing solutions by adapting to the nature of the problem at hand. In contrast to methods used in cognitive neuroscience our approach is optimized to work on single subjects and maintain a balance between false positive and false negative errors. This balance is crucial for accurate assessment of the risk of a surgical procedure. Using this method a test-retest reliability study was performed to assess five different behavioural paradigms and scanning parameters. This experiment was performed on healthy controls and was aimed at selecting which paradigms produce reliable results and therefore can be used for presurgical planning. This allowed the creation of a battery of task that was applied to glioma patients. Functional maps created before the surgeries were compared with electrocortical stimulation performed during the surgeries. The final contribution of this work focuses on technical aspects of performing neuroimaging data analysis. A novel data processing framework which provides means for rapid prototyping and easy translation and adaptation of already existing methods taken from cognitive neuroscience field is introduced. The framework enables fully automatic processing of patient data and therefore greatly reduced costs while maintaining quality control. A discussion of future directions and challenges in using functional MRI for presurgical planning concludes the thesis.
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Tomson, Derek. "Evaluating the association between adult primary brain tumours and a family history of cancer." Thesis, University of Ottawa (Canada), 2006. http://hdl.handle.net/10393/27301.

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There are very few established causes of primary brain tumours in adults. Associated with short survival times, increasing effort is being put forth in an attempt to better understand the risk factors of these neoplasms, including investigating the possible relationship with a family history of cancer and germline genetic polymorphisms. This thesis was conducted to evaluate both of these potential associations. Using an international population-based case-control study, the self-reported family histories of cancer were compared between 1089 glioma cases and 1922 matched controls and between 307 meningioma cases and 1095 controls. Significantly lowered odds of glioma were associated with the reporting of any type of cancer in a first degree relative (OR = 0.8, 95% CI = 0.7-0.99) and with any type of cancer excluding brain tumours (OR = 0.8, 95% CI = 0.7-0.9). No significant associations were found amongst the meningioma cases and controls, though elevated point estimates were found for those reporting parental lung and genitourinary cancers, while the presence of breast, lip, oral, pharyngeal and unspecified cancers all produced great reductions in meningioma odds, suggesting that further study is required. In order to evaluate the association between adult brain tumours and genetic polymorphisms, a systematic review of the literature was completed. A total of 41 case-control studies were included, covering 46 separate genes and more than 100 different single nucleotide polymorphisms. When possible, quantitative data synthesis was performed to establish a more refined point estimate and confidence intervals. Heterogeneity across the studies and variability in the subject matter often prevented any possible data synthesis so establishing associations that were statistically significant was difficult. All told, there were 41 significant associations found amongst the included studies and each varied by the particular polymorphism or histology studied. None of the estimates produced in the quantitative data syntheses suggested a statistically significant association. The results of this thesis suggest that a family history of cancer is not a risk factor for primary brain tumours in adults and that further work is necessary to better establish the possible association between various genetic polymorphisms and adult brain tumours.
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Balathasan, Lukxmi. "Characterising the role of circulating immune cells in brain metastasis." Thesis, University of Oxford, 2012. http://ora.ox.ac.uk/objects/uuid:e7620d30-7e4a-468b-b819-db4cf27eaef6.

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Brain metastasis is a frequent occurrence in cancer patients and carries a high mortality rate. The incidence of brain metastasis is on the rise, highlighting the need for improved therapeutic intervention. Immune cells have been shown to promote disseminated tumour cells to colonise the lung and liver. Therefore, we aim to determine whether immune cells also facilitate brain metastasis by describing the host immune response to tumour cells attached to the brain vasculature. We developed a model of brain metastasis by using ultrasound guidance to perform intracardiac injection of tumour cells. Using this method, we identified highly and weakly brain metastatic cell lines. To understand how cancer cells develop into brain metastases, we analysed brains harvested 4 h- 14 d after tumour injections. At 4 h after intracardiac injection, only cell lines that developed into brain metastases were found adhered to the brain vasculature in high numbers. A small number of arrested tumour cells clustered with CD45⁺ immune cells. These tumour-CD45 clusters persisted over time whilst the frequency of solitary tumour cells declined. Tumour-associated CD45⁺ immune cells were identified to be Ly6G⁺Gr-1⁺CD11c⁻ myeloid cells. Considerably more tumour-CD45⁺ immune cell clusters were found within the brain vasculature when tumour cells were injected into mice bearing a primary tumour. Increased tumour-CD45⁺ immune cells clusters correlated with an increased number of brain metastases in the same group of mice. We also found a positive association between increased tumour-immune clusters and levels of tumour and host derived G-CSF. To establish a causal relationship between tumour cell-CD45 clusters and metastases, we developed an experimental setup for transcranial imaging. Our results suggest that tumour recruited immune cells may promote tumour cell colonisation of the brain and provides a framework for further investigation.
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Ferguson, Anthea Elizabeth Women's &amp Children's Health Faculty of Medicine UNSW. "Gene polymorphisms influencing the cause and disease outcome of childhood central nervous system tumours." Awarded By:University of New South Wales. Women's & Children's Health, 2009. http://handle.unsw.edu.au/1959.4/44816.

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Tumours of the central nervous system (CNS) are the second most common cancers diagnosed in children, yet the cause of this disease remains largely unknown. This thesis examines whether polymorphisms in folate-metabolising and glutathione S transferase (GST) genes influence the risk and disease outcome of childhood CNS tumours. 204 children aged ≤18 years diagnosed with a CNS tumour at the Sydney Children??s Hospital between 1989 and 2004 were included in the study. DNA samples were isolated from archival frozen and formalin-fixed paraffin-embedded tumour tissue. Polymorphisms in GST and folate pathway genes were examined using real-time PCR. Genotype distributions in children with CNS tumours were compared to those observed in a control panel of cord blood samples from 363 healthy newborns. Children carrying at least one variant allele for each of MTHFR 677 C>T, MTHFR 1298 A>C, MTR 2756 A>G, MTRR 66 A>G, and RFC 80 G>A were found to have a 2.8-fold greater risk of developing a CNS tumour than non-carriers (OR=2.80; 95%CI: 1.08-7.56, P=0.022), an association which was even more apparent in those children with an embryonal tumour (OR=4.54; 95%CI: 1.13-15.85, P=0.016). Results also showed that children with the GSTP1 105 Val/Val genotype were three times more likely to develop a CNS tumour of embryonal cell origin than children with the GSTP1 105 Ile/Ile or Ile/Val genotypes (OR=3.02; 95%CI: 1.34-6.46, P=0.005). No such association was observed for CNS tumours of glial cell origin. The GSTM1, GSTT1, and GSTP1 Ala114Val polymorphisms did not appear to be associated with the development of a childhood CNS tumour. In addition, children with the MTHFR 677 TT or RFC 80 AA genotypes were found to have a higher risk of death within 5 years of diagnosis compared to children with one or more MTHFR 677 C or RFC 80 G alleles, respectively (HR=5.52, 95%CI: 1.00-30.37, P=0.049 and HR=5.69, 95%CI: 1.38-23.51, P=0.016, respectively), after adjusting for other prognostic factors such as sex, age at diagnosis, period of diagnosis, and tumour grade. Conversely, children with the MTR 2756 AG or GG genotypes, or MTRR 66 AG or GG genotypes, were more likely to survive compared to those with the MTR 2756 AA or MTRR 66 AA genotypes, respectively (HR=0.21, 95%CI: 0.05-0.93, P=0.040 and HR=0.11, 95%CI: 0.02-0.53, P=0.006). Results presented in this thesis indicate that polymorphisms in folate-metabolising and GST genes may play a role in the aetiology and survival of childhood CNS tumours, and that this may vary depending on the histological sub-type of tumour.
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Books on the topic "Cancer; Brain tumours"

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1940-, Tabuchi K., ed. Biological aspects of brain tumors: Proceedings of the 8th Nikko Brain Tumor Conference, Karatsu (Saga) 1990. Tokyo: Springer-Verlag, 1991.

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Brain tumors: Leaving the Garden of Eden : a survival guide to diagnosis, learning the basics, getting organized and finding your medical team. Encino, Cal: Shilysca Press, 2004.

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Gillespie, Joanne. Brave heart. London: Century, 1989.

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Disrupted: On fighting death & keeping faith. Eugene, Or: Cascade Books, 2011.

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Kressel, Duffner Patricia, ed. Brain tumors in children: Principles of diagnosis and treatment. 2nd ed. New York: Raven Press, 1994.

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Kline, Jerry D. An unremarkable man: A survivor's story. Enumclaw, WA: Pleasant Word, a division of WinePress Group, 2010.

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Károly, Lapis, Eckhardt S, and International Union Against Cancer, eds. Radiotherapy, paediatric oncology, neurooncology. Budapest: Akadémiai Kiadó, 1987.

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Gutiérrez, Lucía M. Neuro-oncology and cancer targeted therapy. New York: Nova Biomedical Books, 2010.

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Iwata, Takanobu. Isha ga makki gan kanja ni natte wakatta koto: Aru nōgekai ga nōshōshō to tatakata seizetsu na hibi. Tōkyō: Chūkei Shuppan, 1998.

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Virginia. General Assembly. Joint Legislative Audit & Review Commission. Evaluation of House Bill 2156: mandated coverage of second opinions for primary malignant brain tumor patients at NCI Comprehensive Cancer Center. Richmond, Va: Commonwealth of Virginia, 2007.

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Book chapters on the topic "Cancer; Brain tumours"

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Nomura, K., and A. B. M. F. Karim. "Neuroepithelial Tumours of Brain." In Prognostic Factors in Cancer, 257–62. Berlin, Heidelberg: Springer Berlin Heidelberg, 1995. http://dx.doi.org/10.1007/978-3-642-79395-0_29.

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Kaye, Andrew H. "Photodynamic Therapy of Brain Tumours." In Progress in Neutron Capture Therapy for Cancer, 613–17. Boston, MA: Springer US, 1992. http://dx.doi.org/10.1007/978-1-4615-3384-9_133.

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Porter, D. G., and D. G. T. Thomas. "Non-Curative Neurosurgery for Malignant Brain Tumours." In Focus on Cancer, 71–82. London: Springer London, 1998. http://dx.doi.org/10.1007/978-1-4471-1509-0_5.

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Crilly, Shane M., and Philip J. O’Halloran. "Targeted Therapies in Brain Tumours: An Overview." In Resistance to Targeted Anti-Cancer Therapeutics, 1–23. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-46505-0_1.

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Kalofonos, H., and A. A. Epenetos. "Radioimmunotherapy with Iodine 131-Labelled Antibodies in Ovarian, Colonic and Brain Tumours." In Cancer Therapy, 18–26. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-73721-3_3.

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Hill, Richard, Samantha A. Murray, Zaynah Maherally, Samantha C. Higgins, and Geoffrey J. Pilkington. "Drug Repurposing to Circumvent Chemotherapy Resistance in Brain Tumours." In Resistance to Targeted Anti-Cancer Therapeutics, 107–44. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-46505-0_6.

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Sirai, Eiji, Hidetake Takahashi, Masahiko Issiki, Kenji Arigane, Masao Iwaya, Hiroshi Hatanaka, Yoshinori Hayakawa, and Yoshinobu Nakagawa. "Clinical Experience of Bnct for Brain Tumours at Jaeri." In Progress in Neutron Capture Therapy for Cancer, 569–76. Boston, MA: Springer US, 1992. http://dx.doi.org/10.1007/978-1-4615-3384-9_125.

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Workman, Paul. "Tumours in the Brain: A Special Case for Drug Delivery." In Drug Delivery in Cancer Treatment III, 97–125. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-75938-3_8.

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Julià-Sapé, Margarida, Carles Majós, and Carles Arús. "Diagnosis and Staging of Brain Tumours: Magnetic Resonance Single Voxel Spectra." In Methods of Cancer Diagnosis, Therapy, and Prognosis, 227–43. Dordrecht: Springer Netherlands, 2010. http://dx.doi.org/10.1007/978-90-481-8665-5_19.

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Ujeno, Y., K. Akuta, H. Hatanaka, Y. Mishima, Y. Oda, and Y. Nakagawa. "Clinical Experience of Bnct for Brain and Skin Tumours at Kyoto University Reactor." In Progress in Neutron Capture Therapy for Cancer, 593–96. Boston, MA: Springer US, 1992. http://dx.doi.org/10.1007/978-1-4615-3384-9_129.

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Conference papers on the topic "Cancer; Brain tumours"

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Hood, R. Lyle, Tobias Ecker, John Rossmeisl, John Robertson, and Christopher G. Rylander. "Improving Convection-Enhanced Delivery Through Photothermal Augmentation of Fluid Dispersal." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80720.

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Malignant tumors of the central nervous system are the third leading cause of cancer-related deaths in adolescents and adults between the ages of 15 and 34; in children, brain tumors are the leading cause of cancer death. Convection-enhanced delivery (CED) has emerged as a promising method for the transport of high concentrations of chemotherapeutic macromolecules to brain tumors. CED is a minimally-invasive surgical procedure wherein a stereotactically-guided small-caliber catheter is inserted into the brain parenchyma, to a tumor site, for low flowrate infusion of chemotherapy [1]. This direct-delivery method bypasses obstacles to systemic chemotherapy caused by the selective impermeability of the blood-brain barrier. Although preliminary studies were favorable, CED recently failed Phase III FDA trials because clinical goals for tumor regression were not met [2]. This was primarily attributed to insufficient diffuse delivery of the drug throughout tumor masses and their surrounding margins.
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Stokol, Tracy, Mandy B. Esch, Nozomi Nishimura, Chris Schaffer, Janelle L. Daddona, David J. Post, and Dhruv P. Desai. "Little Channels, Big Disease: Using Microfluidics to Investigate Cancer Metastasis." In ASME 2011 9th International Conference on Nanochannels, Microchannels, and Minichannels. ASMEDC, 2011. http://dx.doi.org/10.1115/icnmm2011-58298.

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The leading cause of death in human patients with malignant cancer is the dissemination of the primary tumor to secondary sites throughout the body. It is well known that cancers metastasize to certain tissues (e.g. breast cancer typically spreads to the lungs. brain and bone), in a pattern that cannot be explained by blood flow from the primary tumor or simple mechanical arrest. Circulating tumor cells usually arrest in the microvasculature of target tissues. At these sites, they must adhere to the endothelium, survive, proliferate and extravasate in order to form a secondary tumor. In vitro tools that appropriately mimic the microvasculature in which cancer metastasis occurs have been largely unavailable. With the advent of microfluidic and nanotechnology, we can now more accurately model the complexity of the microvascular environment, in terms of representative endothelial cells, geometry, shear stress and exposure to organ-specific environmental cues. This talk will focus on the use of microfluidic devices to explore mechanisms involved in tumor-endothelial cell interactions that govern cancer metastasis to organ specific sites.
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Pishko, Gregory L., Morad Nasseri, Seymur Gahramanov, Leslie L. Muldoon, and Edward A. Neuwelt. "Blood-Tumor Barrier Normalization Effects on Cytotoxic Drug Delivery to Brain Tumors." In ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14648.

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The blood-brain barrier (BBB) restricts delivery of anti-cancer drugs to brain tumors, but the leaky neovasculature of the blood-tumor barrier (BTB) permits systemically delivered cytotoxic agents to reach the tumor. Anti-angiogenic therapies such as bevacizumab (BEV) have been shown to “normalize” brain tumor vasculature,1 but the impact on chemotherapy delivery remains unclear.2 The goal of this study was to use magnetic resonance imaging (MRI) to investigate the consequences of BTB normalization, via BEV, on temozolomide (TMZ) chemotherapy. Non-invasive MRI techniques were used to track the transport of a chemotherapy surrogate, a low molecular contrast agent (Gd-DTPA), in an intracerebrally implanted human glioma. MRI-derived Gd-DTPA concentration curves were fit to a transvascular exchange model to measure vascular permeability changes and were used to quantify initial area under the gadolinium curve (IAUGC) over the course of treatment.
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Pappafotis, Nicholas, Wojciech Bejgerowski, Rao Gullapalli, J. Marc Simard, Satyandra K. Gupta, and Jaydev P. Desai. "Towards Design and Fabrication of a Miniature MRI-Compatible Robot for Applications in Neurosurgery." In ASME 2008 International Design Engineering Technical Conferences and Computers and Information in Engineering Conference. ASMEDC, 2008. http://dx.doi.org/10.1115/detc2008-49587.

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Brain tumors are among the most feared complications of cancer and they occur in 20–40% of adult cancer patients. Despite numerous advances in treatment, the prognosis for these patients is poor, with a median survival of 4–8 months. The primary reasons for poor survival rate are the lack of good continuous imaging modality for intraoperative intracranial procedures and the inability to remove the complete tumor tissue due to its placement in the brain and the corresponding space constraints to reach it. Intraoperative magnetic resonance imaging (MRI) supplements the surgeon’s visual and tactile senses in a way that no other imaging device can achieve resulting in less trauma to surrounding healthy brain tissue during surgery. To minimize the trauma to surrounding healthy brain tissue, it would be beneficial to operate through a narrow surgical corridor dissected by the neurosurgeon. Facilitating tumor removal by accessing regions outside the direct “line-of-sight” of the neurosurgical corridor will require a highly dexterous, small cross section, and MRI-compatible robot. Developing such a robot is extremely challenging task. In this paper we report a preliminary design of 6-DOF robot for possible application in neurosurgery. The robot actuators and body parts are constructed from MRI compatible materials. The current prototype is 0.36” in diameter and weighs only 0.0289 N (2.95 grams). The device was actuated using Flexinol® which is a shape memory alloy manufactured by Dynalloy, Inc. The end-effector forces ranged from 12 mN to 50 mN depending on the robot configuration. The end-effector force to robot weight ratio varied from 0.41 to 1.73. During trials the robot motion was repeatable and the range of motion of the robot was about 90 degrees for the end-effector when one side shape memory alloy (SMA) channel was actuated. The actuation time from the start to finish was about 2.5 s.
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Biniazan, Maral, and Kamran Mohseni. "Inverse Heat Transfer Analysis of Micro Heater Strength and Locations for Hyperthermia Treatment of Brain Tumors." In ASME 2007 2nd Frontiers in Biomedical Devices Conference. ASMEDC, 2007. http://dx.doi.org/10.1115/biomed2007-38046.

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Hyperthermia, also called thermal therapy or thermotherapy, is a type of cancer treatment in which the aim is to maintain the surrounding healthy tissue at physiologically normal temperatures and expose the cancerous region to high temperatures between 43°C–45°C. Several methods of hyperthermia are currently under study, including local, regional, and whole-body hyperthermia. In local hyperthermia, Interstitial techniques are used to treat tumors deep within the body, such as brain tumors. heat is applied to the tumor, usually by probes or needles which are inserted into the tumor. The heat source is then inserted into the probe. Invasive interstitial heating technique offer a number of advantages over external heating approaches for localizing heat into small tumors at depth. e. g interstitial technique allows the tumor to be heated to higher temperatures than external techniques. This is why an innovative internal hyperthermia research is being conducted in the design of an implantable microheater [1]. To proceed with this research we need complete and accurate data of the strength, number and location of the micro heaters, which is the objective of this paper. The location, strength, and number of implantable micro heaters for a given tumor size is calculated by solving an Inverse Heat Transfer Problem (IHTP). First we model the direct problem by calculating the transient temperature field via Pennies bioheat transfer equation. A nonlinear least-square method, modified by addition of a regularization term, Levenberg Marquardt method is used to determine the inverse problem [2].
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Ho, Mingyen, and Jaydev P. Desai. "Towards the Development of a Tendon-Driven Neurosurgical Robot." In ASME 2011 Dynamic Systems and Control Conference and Bath/ASME Symposium on Fluid Power and Motion Control. ASMEDC, 2011. http://dx.doi.org/10.1115/dscc2011-6075.

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Brain tumors are among the most feared complications of cancer and their treatment is challenging due to the lack of good continuous imaging modality during the procedure and the inability to remove the complete tumor due to obstructions. A highly dexterous, small cross-section robot is being developed to overcome these limitations. The robot is being designed to remove the tumor which is outside the direct “line-of-sight” of the physician. In this paper, we report the design of a Minimally Invasive Neurosurgical Intracranial Robot (MINIR) using a tendon-driven mechanism. In the current prototype presented in this paper, the actuators for actuating the robot are not MRI compatible. The primary goal of this paper is to evaluate the performance of the robot motion and not the MRI compatibility of the entire system. The robot contains four links and four revolute joints. Pulleys and cables are put inside the robot to make the robot compact. The four revolute joints are placed orthogonally to have out-of-plane motion capability and can be controlled independently.
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Stepp, Herbert, Ronald Sroka, and Walter Stummer. "Intra-operative Brain Tumor Imaging." In Cancer Imaging and Therapy. Washington, D.C.: OSA, 2016. http://dx.doi.org/10.1364/cancer.2016.jm2a.1.

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Leblond, Frederic. "Intraoperative Optical Spectroscopy of Brain Tumors for Guiding Resection." In Cancer Imaging and Therapy. Washington, D.C.: OSA, 2016. http://dx.doi.org/10.1364/cancer.2016.jm2a.4.

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Chasiotis, I., D. C. Street, H. L. Fillmore, and G. T. Gillies. "AFM Studies of Tumor Cell Invasion." In ASME 2003 International Mechanical Engineering Congress and Exposition. ASMEDC, 2003. http://dx.doi.org/10.1115/imece2003-43293.

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Our recent investigations on human brain tumor (glioma) cell micro and nanodynamics via AFM methodologies have shown that brain tumor invadopodia (malignant cytostructural cell extensions with sensory, motility, and invasive characteristics extended by tumor cells into their environment) can assume specific geometries based on cell plating density and the location/distance of neighboring cells indicating strong cell sensing and signaling mechanisms between malignant cells and their surroundings. In certain occasions, cancer cell processes (extensions) have been found to be highly directional measuring more than 80 μm while invading neighboring cells by following a connecting straight path. Moreover, strong chemical gradients are suggested to influence the growth and motility of cell processes allowing for gradual adjustments of the direction of the invasive tumor extension. In response to external signals, tumor cell invadopodia develop micron-sized side-ligaments that follow the chemical gradients in their neighborhood and assist the reorientation of their main intrusive elements.
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Liu, Haowen, Jianting Sheng, HONG ZHAO, and Stephen Wong. "Abstract C108: Systematic identification of astrocyte-tumor crosstalk regulating brain metastatic tumors." In Abstracts: AACR-NCI-EORTC International Conference on Molecular Targets and Cancer Therapeutics; October 26-30, 2019; Boston, MA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1535-7163.targ-19-c108.

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