You searched for subject:(Glioblastoma GBM ).
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Boston University
1.
Jindani, Rajika.
Glioblastoma multiforme: etiology, progression, and treatment.
Degree: MS, Medical Sciences, 2017, Boston University
URL: http://hdl.handle.net/2144/26730 
► Glioblastoma multiforme is the most common and malignant brain tumor, accounting for more than 52% of all primary brain tumors. The molecular heterogeneity of the…
(more)
▼ Glioblastoma multiforme is the most common and malignant brain tumor, accounting for more than 52% of all primary brain tumors. The molecular heterogeneity of the tumor has made it difficult to treat, and even more difficult to cure. Due to the high mortality rate associated with the current treatments used, new innovative medical techniques are being explored. Prominent treatments that are currently being investigated are immune based therapies, focused on checkpoint inhibitors and biomarkers, the use of 2-deoxy-D-glucose to initiate tumor cell apoptosis, and the induction of alterations in DNA and miRNA to inhibit glioblastoma stem cell accelerated growth and tumorigenesis. Throughout the paper, various ongoing studies are summarized and discussed to compare the outcomes of different treatments. The goal of this paper is to present the different therapies and analyze which one of them is the most effective in treating and prolonging survival for patients with glioblastoma multiforme.
This thesis reviewed the large collection of publications about glioblastoma multiforme and treatments for the disease. The use of immune based therapies, such as checkpoint inhibitors and biomarkers, are increasingly delivering promising results as an immunotherapy approach, but it is necessary to complete the phase III trials in order to truly know if these products are successful as anticancer agents or if further research into the matter is required. More research must be done to find the best route of treatment. In addition, the use of 2-deoxy-D-glucose has been successful in treating other types of cancer, such as breast cancer, and now studies look promising in GBM patients. This treatment is still in its initial stages of testing, so more work will need to be done to determine how efficacious this treatment is.
By comparing the results of the different therapeutic agents, it was determined that genetic alterations seemed to be the most promising avenue of treatment with current information. The data showed that the greatest increase in survival time and least recurrence was achieved by MGMT promoter methylation and gene modifications of the tumor. Though these treatments have varying results in their efficacy and there are many different combinations of medications that have yet to be assessed, research in the area is greatly advancing and increasing the lives of GBM patients. By allocating resources in the best possible treatment, researchers can change the fatal prognosis of this illness.
Subjects/Keywords: Medicine; GBM; Glioblastoma
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APA (6th Edition):
Jindani, R. (2017). Glioblastoma multiforme: etiology, progression, and treatment. (Masters Thesis). Boston University. Retrieved from http://hdl.handle.net/2144/26730
Chicago Manual of Style (16th Edition):
Jindani, Rajika. “Glioblastoma multiforme: etiology, progression, and treatment.” 2017. Masters Thesis, Boston University. Accessed March 05, 2021.
http://hdl.handle.net/2144/26730.
MLA Handbook (7th Edition):
Jindani, Rajika. “Glioblastoma multiforme: etiology, progression, and treatment.” 2017. Web. 05 Mar 2021.
Vancouver:
Jindani R. Glioblastoma multiforme: etiology, progression, and treatment. [Internet] [Masters thesis]. Boston University; 2017. [cited 2021 Mar 05].
Available from: http://hdl.handle.net/2144/26730.
Council of Science Editors:
Jindani R. Glioblastoma multiforme: etiology, progression, and treatment. [Masters Thesis]. Boston University; 2017. Available from: http://hdl.handle.net/2144/26730
University of Alberta
2.
Alnaami, Ibrahim.
Evaluation of Concomitant Temozolomide Treatment in
Glioblastoma Multiforme Patients in Two Canadian Tertiary Care
Centers.
Degree: MS, Public Health Sciences, 2010, University of Alberta
URL: https://era.library.ualberta.ca/files/g158bh56v
► The study evaluated the survival of 364 glioblastoma multiforme (GBM) patients who received different modalities of treatment in two Canadian tertiary care centres. Retrospective and…
(more)
▼ The study evaluated the survival of 364 glioblastoma
multiforme (GBM) patients who received different modalities of
treatment in two Canadian tertiary care centres. Retrospective and
prospective databases were utilized to do a retrospective
population based cohort study. The thesis question was “among
treated GBM patients in Edmonton and Halifax; does the survival
rate differ with introduction of concomitant temozolomide and
radiation therapy (RT) versus non concomitant treatment?” Our
results indicate that concomitant temozolomide with radiation
therapy and surgery was associated with longer survival in
comparison to radiation therapy with surgery. We also found that
age; surgical resection and shorter time to radiation therapy are
important factors for longer survival.
Subjects/Keywords: Glioblastoma multiforme GBM, Radiation Therapy
RT
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APA (6th Edition):
Alnaami, I. (2010). Evaluation of Concomitant Temozolomide Treatment in
Glioblastoma Multiforme Patients in Two Canadian Tertiary Care
Centers. (Masters Thesis). University of Alberta. Retrieved from https://era.library.ualberta.ca/files/g158bh56v
Chicago Manual of Style (16th Edition):
Alnaami, Ibrahim. “Evaluation of Concomitant Temozolomide Treatment in
Glioblastoma Multiforme Patients in Two Canadian Tertiary Care
Centers.” 2010. Masters Thesis, University of Alberta. Accessed March 05, 2021.
https://era.library.ualberta.ca/files/g158bh56v.
MLA Handbook (7th Edition):
Alnaami, Ibrahim. “Evaluation of Concomitant Temozolomide Treatment in
Glioblastoma Multiforme Patients in Two Canadian Tertiary Care
Centers.” 2010. Web. 05 Mar 2021.
Vancouver:
Alnaami I. Evaluation of Concomitant Temozolomide Treatment in
Glioblastoma Multiforme Patients in Two Canadian Tertiary Care
Centers. [Internet] [Masters thesis]. University of Alberta; 2010. [cited 2021 Mar 05].
Available from: https://era.library.ualberta.ca/files/g158bh56v.
Council of Science Editors:
Alnaami I. Evaluation of Concomitant Temozolomide Treatment in
Glioblastoma Multiforme Patients in Two Canadian Tertiary Care
Centers. [Masters Thesis]. University of Alberta; 2010. Available from: https://era.library.ualberta.ca/files/g158bh56v
Victoria University of Wellington
3.
Venkatesh, Varun.
Investigating the role of the apelinergic system in glioblastoma.
Degree: 2018, Victoria University of Wellington
URL: http://hdl.handle.net/10063/7804
► Elucidating the molecular signalling circuitry that underpins the pathogenesis of cancers is critical to understanding and developing effective treatment paradigms for cancer. The apelinergic system…
(more)
▼ Elucidating the molecular signalling circuitry that underpins the pathogenesis of cancers is critical to understanding and developing effective treatment paradigms for cancer. The apelinergic system is a signalling pathway primarily consisting of the apelin peptide (APLN) and the apelin receptor (APLNR). The apelinergic system has been implicated in the pathophysiology of several cancers. However, there have been very few reports regarding the role of the apelinergic system in the brain cancer
glioblastoma.
Glioblastoma is a highly recalcitrant malignancy with a poor prognosis which makes understanding the underlying molecular pathogenesis critical for developing new treatments. The goal of this thesis was to investigate the role of the apelinergic system in
glioblastoma. This primary goal was divided into three specific aims that comprised of the following.
i) Determine the expression of APLN and APLNR mRNA in
glioblastoma and
glioblastoma-derived cell lines as well as use public data to investigate the expression of APLN and APLNR in other astrocytic and oligodendroglial tumours.
ii) Develop a cellular model for the apelinergic system in
glioblastoma.
iii) Determine the response of the apelinergic system to common
glioblastoma stressors.
APLN, but not APLNR, mRNA expression was elevated in
glioblastoma compared to normal tissue. Analysis of mRNA expression from several public data sources through the GLIOVIS portal demonstrated that both APLN and APLNR were upregulated in
glioblastoma relative to lower grade tumours. Significantly, it was also noted that APLN expression was strongly associated with regions of hypoxia whilst APLNR expression was elevated in astrocytes, tumour cells and vascular cells.
The mRNA expression of APLNR and APLN was high in resected
glioblastoma tissue but 100 – 1000 fold lower in
glioblastoma-derived cell lines. The low expression of APLNR in
glioblastoma-derived cells suggested that these cell lines would not be a suitable model for testing the apelinergic system in
glioblastoma. To overcome this limitation, the established
glioblastoma-derived cell line U87MG was stably transfected with a plasmid expressing an APLNR-GFP fusion protein to recapitulate the expression of APLNR seen in resected tissue, and this cell line was used as a model of the apelinergic system in
glioblastoma. This U87.APLNR cell line demonstrated that exogenous [Pyr1]apelin-13 could induce migration in the transwell migration assays, indicating a possible role in
glioblastoma tumour cell migration.
Glioblastomas like other solid tumours are exposed to significant stresses from sources such as hypoxia, nutrient deprivation and chemotherapeutic treatment. The apelinergic system has been reported to protect against cell death caused by several stressors, including hypoxia and glucose deprivation, but this has not been investigated in
glioblastoma cells. The effects of hypoxia and glucose deprivation and chemotherapeutic treatments were investigated in regard to mRNA expression of APLN and APLNR in…
Advisors/Committee Members: Day, Darren, Miller, John.
Subjects/Keywords: Glioblastoma; Apelinergic system; Apelin; Hypoxia; GBM; cancer
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APA (6th Edition):
Venkatesh, V. (2018). Investigating the role of the apelinergic system in glioblastoma. (Doctoral Dissertation). Victoria University of Wellington. Retrieved from http://hdl.handle.net/10063/7804
Chicago Manual of Style (16th Edition):
Venkatesh, Varun. “Investigating the role of the apelinergic system in glioblastoma.” 2018. Doctoral Dissertation, Victoria University of Wellington. Accessed March 05, 2021.
http://hdl.handle.net/10063/7804.
MLA Handbook (7th Edition):
Venkatesh, Varun. “Investigating the role of the apelinergic system in glioblastoma.” 2018. Web. 05 Mar 2021.
Vancouver:
Venkatesh V. Investigating the role of the apelinergic system in glioblastoma. [Internet] [Doctoral dissertation]. Victoria University of Wellington; 2018. [cited 2021 Mar 05].
Available from: http://hdl.handle.net/10063/7804.
Council of Science Editors:
Venkatesh V. Investigating the role of the apelinergic system in glioblastoma. [Doctoral Dissertation]. Victoria University of Wellington; 2018. Available from: http://hdl.handle.net/10063/7804
University of Ottawa
4.
Jilesen, Zachary Keavin.
Discovery and Application of Neoepitopes in an Oncolytic Rhabdovirus Vaccine Approach to Treat Glioblastoma Multiforme
.
Degree: 2019, University of Ottawa
URL: http://hdl.handle.net/10393/39688
► Glioblastoma multiforme is the most common and lethal primary brain tumour in adults. Its aggressive and invasive phenotype makes it resistant to current standards of…
(more)
▼ Glioblastoma multiforme is the most common and lethal primary brain tumour in adults. Its aggressive and invasive phenotype makes it resistant to current standards of care, with a patient median survival following treatment of only 14 months. Potent and safe therapeutics are necessary to improve patient prognosis. Globally, efforts are being made in immunotherapies to combat such deleterious tumours. Preliminary work in the Stojdl lab has developed a novel oncolytic virus platform for brain cancer therapy that is non-toxic and exhibits potent anti-tumour efficacy. This platform is based on the rhabdovirus Farmington, identified for its potent oncolytic properties and engineering malleability. Herein, we begin to show our capability to discover and vaccinate against immunogenic neoepitopes derived from a mouse cancer mutanome. Engineering Farmington virus to express neoepitopes, allows for robust tumour specific immune proliferation following a prime vaccination. Overcoming problems of targeting self-antigen and antigen loss variants, a multi-neoepitope vaccine, presented here, is one of many alternative approaches to help combat cancer resistance. Despite achieving robust anti-tumour immunity by vaccination, selectivity of the tumour microenvironment remains an enormous challenge. Cumulative efforts in immunotherapy research will help drive novel therapeutics, like Farmington, into clinic and, ultimately, improve patient’s prognosis and quality of life.
Subjects/Keywords: Glioblastoma multiforme;
GBM;
Oncolytic virus;
Immunotherapy
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APA ·
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APA (6th Edition):
Jilesen, Z. K. (2019). Discovery and Application of Neoepitopes in an Oncolytic Rhabdovirus Vaccine Approach to Treat Glioblastoma Multiforme
. (Thesis). University of Ottawa. Retrieved from http://hdl.handle.net/10393/39688
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Jilesen, Zachary Keavin. “Discovery and Application of Neoepitopes in an Oncolytic Rhabdovirus Vaccine Approach to Treat Glioblastoma Multiforme
.” 2019. Thesis, University of Ottawa. Accessed March 05, 2021.
http://hdl.handle.net/10393/39688.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Jilesen, Zachary Keavin. “Discovery and Application of Neoepitopes in an Oncolytic Rhabdovirus Vaccine Approach to Treat Glioblastoma Multiforme
.” 2019. Web. 05 Mar 2021.
Vancouver:
Jilesen ZK. Discovery and Application of Neoepitopes in an Oncolytic Rhabdovirus Vaccine Approach to Treat Glioblastoma Multiforme
. [Internet] [Thesis]. University of Ottawa; 2019. [cited 2021 Mar 05].
Available from: http://hdl.handle.net/10393/39688.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Jilesen ZK. Discovery and Application of Neoepitopes in an Oncolytic Rhabdovirus Vaccine Approach to Treat Glioblastoma Multiforme
. [Thesis]. University of Ottawa; 2019. Available from: http://hdl.handle.net/10393/39688
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
University of Toronto
5.
Elsehemy, Ahmed Ali Ahmed Ali.
The role of Norrie Disease Pseudoglioma (NDP) signaling in glioblastoma.
Degree: PhD, 2018, University of Toronto
URL: http://hdl.handle.net/1807/97783
► Norrin is a WNT ligand that binds Frizzled-4 (FZD4) and Low-density lipoprotein receptor-related protein (LRP5/6) receptor complex to activate canonical WNT/ β-Catenin signaling. Norrin/FZD4 signaling…
(more)
▼ Norrin is a WNT ligand that binds Frizzled-4 (FZD4) and Low-density lipoprotein receptor-related protein (LRP5/6) receptor complex to activate canonical WNT/ β-Catenin signaling. Norrin/FZD4 signaling is involved in the regulation of vasculature in several tissues including retina, inner ear and for blood-brain barrier function. The role of Norrin in cancer is not very well characterized. Here, we show that NDP is expressed in a wide range of cancer types, with a particular enrichment in glioblastoma (GBM) and lower grade glioma (LGG). Kaplan-Meier survival analysis of publicly available datasets revealed a significant correlation between NDP expression and survival in GBM, LGG and neuroblastoma. To investigate the function of NDP in GBM, we performed a set of NDP and FZD4 gain and loss of function experiments in patient-derived GBM stem cell (GNS) lines. Recently ASCL1 expression was shown to stratify GNS lines into two cohorts with different tumorigenic, proliferation and differentiation dynamics. Surprisingly, we found that NDP manipulation resulted in opposite effects in ASCL1hi versus ASCL1lo lines. NDP inhibited proliferation and sphere formation in ASCL1lo lines through WNT- dependent mechanisms, while it stimulated proliferation and sphere formation in ASCL1hi lines through WNT-independent mechanisms. Immunocytochemistry staining for proliferation markers indicated that NDP affects cycle kinetics and cell cycle exit in both cohorts. Interestingly, RNA-Seq analysis of NDP knockdown ASCL1hi and ASCL1lo lines revealed a remarkable effect of NDP knockdown on cell cycle controlling genes. In addition, the library revealed a significant number of uniquely expressed genes in each cell line, consistent with the divergence of NDP molecular functions between the two lines. Collectively, our results indicate that NDP is involved in the regulation of GBM progression, and that NDP function in GBM stratifies with ASCL1 expression.
2019-11-16 00:00:00
Advisors/Committee Members: Wallace, Valerie A, Laboratory Medicine and Pathobiology.
Subjects/Keywords: ASCL1; GBM; Glioblastoma; NDP; Norrin; WNT; 0992
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APA ·
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Manager
APA (6th Edition):
Elsehemy, A. A. A. A. (2018). The role of Norrie Disease Pseudoglioma (NDP) signaling in glioblastoma. (Doctoral Dissertation). University of Toronto. Retrieved from http://hdl.handle.net/1807/97783
Chicago Manual of Style (16th Edition):
Elsehemy, Ahmed Ali Ahmed Ali. “The role of Norrie Disease Pseudoglioma (NDP) signaling in glioblastoma.” 2018. Doctoral Dissertation, University of Toronto. Accessed March 05, 2021.
http://hdl.handle.net/1807/97783.
MLA Handbook (7th Edition):
Elsehemy, Ahmed Ali Ahmed Ali. “The role of Norrie Disease Pseudoglioma (NDP) signaling in glioblastoma.” 2018. Web. 05 Mar 2021.
Vancouver:
Elsehemy AAAA. The role of Norrie Disease Pseudoglioma (NDP) signaling in glioblastoma. [Internet] [Doctoral dissertation]. University of Toronto; 2018. [cited 2021 Mar 05].
Available from: http://hdl.handle.net/1807/97783.
Council of Science Editors:
Elsehemy AAAA. The role of Norrie Disease Pseudoglioma (NDP) signaling in glioblastoma. [Doctoral Dissertation]. University of Toronto; 2018. Available from: http://hdl.handle.net/1807/97783
University of Sydney
6.
Hallal, Susannah.
Extracellular Vesicles as Surrogates for Understanding and Monitoring Glioblastoma Progression
.
Degree: 2019, University of Sydney
URL: http://hdl.handle.net/2123/21238
► Glioblastoma (GBM; WHO grade IV glioma), is the most common and lethal adult primary brain tumour. Lack of sensitive monitoring methods contributes to poor patient…
(more)
▼ Glioblastoma (GBM; WHO grade IV glioma), is the most common and lethal adult primary brain tumour. Lack of sensitive monitoring methods contributes to poor patient outcomes. Extracellular vesicles (EVs) are stable nanoparticles that carry molecules from their cell-of-origin and cross the blood-brain barrier into the circulation. EV release is upregulated in neoplasia, offering access to GBM molecular phenotypes by blood sampling. While blood-EVs are attractive for biomarker discovery, highly abundant serum proteins complicate proteomic studies. SWATH-MS allowed deep coverage of glioma plasma-EV proteins, with 4909 proteins identified using a custom spectral library; 463 proteins significantly changed across glioma cohorts and controls, including TRiC subunits. This work is the first to analyse glioma blood-EVs by SWATH-MS and shows promise for patient stratification. A rich clinical source of GBM-EVs was identified to substantiate blood-based studies. Neurosurgical aspirates, isolated directly from tumour microenvironments, are a novel and abundant source of tumour-EVs. EVs were enriched from the aspirates for protein and miRNA analyses. Comparison of EVs from GBM and glioma II-III surgeries identified 298 significant proteins, including all TRiC subunits, and 68 miRNAs, of which 21 were detected in a GBM serum-EV study. Profiling rich clinical EVs enhances our understanding of EV molecules released into the periphery and verifies GBM biomarkers identified in blood-EVs. GBM-EVs also play critical signaling roles and can influence non-neoplastic cells to support GBM invasion. Astrocytes internalise GBM-EVs and induce podosome formation. Bioinformatics of proteome changes in GBM-EV treated astrocytes predicted changes to MYC and TP53 signaling, confirmed by qPCR. Measured p53-isoform changes implicated a shift towards a pro-inflammatory, tumour-promoting senescence-associated secretory phenotype, shedding light on GBM-astrocyte interactions in assisting GBM progression.
Subjects/Keywords: glioblastoma;
GBM;
cancer;
exosomes;
extracellular vesicles
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APA (6th Edition):
Hallal, S. (2019). Extracellular Vesicles as Surrogates for Understanding and Monitoring Glioblastoma Progression
. (Thesis). University of Sydney. Retrieved from http://hdl.handle.net/2123/21238
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Hallal, Susannah. “Extracellular Vesicles as Surrogates for Understanding and Monitoring Glioblastoma Progression
.” 2019. Thesis, University of Sydney. Accessed March 05, 2021.
http://hdl.handle.net/2123/21238.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Hallal, Susannah. “Extracellular Vesicles as Surrogates for Understanding and Monitoring Glioblastoma Progression
.” 2019. Web. 05 Mar 2021.
Vancouver:
Hallal S. Extracellular Vesicles as Surrogates for Understanding and Monitoring Glioblastoma Progression
. [Internet] [Thesis]. University of Sydney; 2019. [cited 2021 Mar 05].
Available from: http://hdl.handle.net/2123/21238.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Hallal S. Extracellular Vesicles as Surrogates for Understanding and Monitoring Glioblastoma Progression
. [Thesis]. University of Sydney; 2019. Available from: http://hdl.handle.net/2123/21238
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
University of New South Wales
7.
Lee, Chung Gyo.
Roles of Sphingosine Kinases and Regulation of Sphingosine 1-Phosphate in Glioblastoma Multiforme Cells.
Degree: Biotechnology & Biomolecular Sciences, 2012, University of New South Wales
URL: http://handle.unsw.edu.au/1959.4/52012
;
https://unsworks.unsw.edu.au/fapi/datastream/unsworks:10682/SOURCE01?view=true
► Sphingosine 1-phosphate (S1P) is a mitogenic lipid molecule formed by the enzymes, sphingosine kinase (SphK) 1 and 2. SphK1, which is commonly overexpressed in malignant…
(more)
▼ Sphingosine 1-phosphate (S1P) is a mitogenic lipid molecule formed by the enzymes, sphingosine kinase (SphK) 1 and 2. SphK1, which is commonly overexpressed in malignant tumours, is recognised as a significant contributor to cancer cell survival and tumour angiogenesis, and is accordingly implicated in the pathogenesis of various types of cancer. We investigated the roles of SphK1 and 2 in
glioblastoma multiforme (
GBM), the most common and most aggressive malignant primary brain cancer. Using RNA interference, our research confirmed that both SphKs are vital for the proliferation of
GBM cell lines, T98G and U87MG. Interestingly, suppressing the gene expression of SphK2 produced a more potent inhibition of cell proliferation, reduction of viability, and G1 cell cycle arrest than suppressing SphK1. We subsequently tested if a reduced intracellular S1P level was responsible for such anti-proliferative effects. However, intracellular lipid measurements by mass spectrometry and in situ SphK activity measurements revealed that the total S1P generation by each SphK isoform was independent of the effect on cell growth, and was determined by the particular cell line used and the presence or absence of serum. Furthermore, supplying the cells with a high concentration of exogenous S1P could not rescue the anti-proliferative effect of SphK suppression, and overexpressing SphK1 could not compensate the loss of SphK2. Thus, our data highlight the significance of specifically localised or compartmentalised S1P signalling in cell proliferation and survival.Potential targets of S1P required for the growth of
GBM cells include the S1P receptors, which are expressed on the cell surface. Once generated, S1P is thought to be secreted through efflux transporters such as ATP-binding cassette transporters, leading to autocrine or paracrine stimulation of S1P receptors. The regulation of extracellular S1P levels by cells is not thoroughly understood despite abundant literature emphasising the importance of S1P receptors. Therefore, we investigated the regulation of extracellular S1P on
GBM cells using mass spectrometry and thin layer chromatography. We present data indicating that U87MG cells actively import S1P across the cell membrane through an as-yet unidentified transporter. These findings will contribute to our deeper understanding of the mechanisms of S1P signalling.
Advisors/Committee Members: Don, Anthony, Clinical School - Prince of Wales Hospital, Faculty of Medicine, UNSW.
Subjects/Keywords: Sphingosine; Cancer; Glioblastoma; Lipid; S1P; GBM
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APA ·
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MLA ·
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Manager
APA (6th Edition):
Lee, C. G. (2012). Roles of Sphingosine Kinases and Regulation of Sphingosine 1-Phosphate in Glioblastoma Multiforme Cells. (Masters Thesis). University of New South Wales. Retrieved from http://handle.unsw.edu.au/1959.4/52012 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:10682/SOURCE01?view=true
Chicago Manual of Style (16th Edition):
Lee, Chung Gyo. “Roles of Sphingosine Kinases and Regulation of Sphingosine 1-Phosphate in Glioblastoma Multiforme Cells.” 2012. Masters Thesis, University of New South Wales. Accessed March 05, 2021.
http://handle.unsw.edu.au/1959.4/52012 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:10682/SOURCE01?view=true.
MLA Handbook (7th Edition):
Lee, Chung Gyo. “Roles of Sphingosine Kinases and Regulation of Sphingosine 1-Phosphate in Glioblastoma Multiforme Cells.” 2012. Web. 05 Mar 2021.
Vancouver:
Lee CG. Roles of Sphingosine Kinases and Regulation of Sphingosine 1-Phosphate in Glioblastoma Multiforme Cells. [Internet] [Masters thesis]. University of New South Wales; 2012. [cited 2021 Mar 05].
Available from: http://handle.unsw.edu.au/1959.4/52012 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:10682/SOURCE01?view=true.
Council of Science Editors:
Lee CG. Roles of Sphingosine Kinases and Regulation of Sphingosine 1-Phosphate in Glioblastoma Multiforme Cells. [Masters Thesis]. University of New South Wales; 2012. Available from: http://handle.unsw.edu.au/1959.4/52012 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:10682/SOURCE01?view=true
University of New South Wales
8.
Adams, Seray.
The involvement of the kynurenine pathway in brain tumour pathogenesis.
Degree: Clinical School - St Vincent's Hospital, 2012, University of New South Wales
URL: http://handle.unsw.edu.au/1959.4/52433
;
https://unsworks.unsw.edu.au/fapi/datastream/unsworks:11106/SOURCE1?view=true
► Glioblastoma multiforme (GBM) is the most prevalent type of primary brain tumour in adults and the prognosis for patients remains dismal. The kynurenine pathway (KP)…
(more)
▼ Glioblastoma multiforme (
GBM) is the most prevalent type of primary brain tumour in adults and the prognosis for patients remains dismal. The kynurenine pathway (KP) is the principal route of L-tryptophan (TRP) catabolism leading to the production of kynurenine (KYN), the neuroprotectants, kynurenic acid (KYNA) and picolinic acid (PIC), the neurotoxin, quinolinic acid (QUIN) and quinaldic acid (QA). The enzymes indoleamine 2,3-dioxygenase-1 (IDO-1), indoleamine 2,3-dioxygenase-2 (IDO-2) and tryptophan 2,3-dioxygenase (TDO-2) initiate the first step of the KP. Mounting evidence directly implicates that the induction of IDO-1 in various tumours is a crucial mechanism facilitating tumour immune evasion and persistence. TDO-2 has recently been shown to be a mechanism of tumoural immune resistance. However, the involvement of the downstream machinery of the KP in brain tumour progression has been virtually unexplored. Further, a full characterisation of the KP in brain tumours and the role of the KP in terms of the balance between neuroprotection and neurodegeneration in
GBM has not yet been investigated. Here we report the first comprehensive characterisation of the KP in human primary
GBM in vitro and in vivo. qRT-PCR revealed that IFN-γ stimulation significantly potentiated the expression of IDO-1 and IDO-2 in
GBM cells. HPLC analysis revealed that IFN-γ stimulation significantly increased KP activity (KYN/TRP ratio) and significantly lowered the KYNA/KYN neuroprotective ratio in
GBM cells. Using both HPLC and GC/MS, it was revealed that KP activation (KYN/TRP) and QA production was shown to be significantly higher and the concentrations of TRP, KYNA, QUIN and PIC and the KYNA/KYN ratio were shown to be significantly lower in
GBM patient plasma (n=18) compared to controls. In conclusion, this study has confirmed that the KP is up-regulated and that both neuroprotective branches of the KP are impaired in
GBM patients. These results provide strong evidence which implicates the involvement of the KP in
GBM pathophysiology and highlights that pharmacological approaches aimed at restoring the physiological balance of these imbalanced metabolites and augmented enzymes may be promising novel therapeutic targets for the treatment of brain cancer.
Advisors/Committee Members: Guillemin, Gilles, Medical Sciences, Faculty of Medicine, UNSW, Bruce, Brew, St Vincent's Centre for Applied Medical Research, NSW.
Subjects/Keywords: Glioblastoma multiforme (GBM); Pathogenisis; Kynurenine pathway; Brain tumour; GBM pathophysiology
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APA (6th Edition):
Adams, S. (2012). The involvement of the kynurenine pathway in brain tumour pathogenesis. (Doctoral Dissertation). University of New South Wales. Retrieved from http://handle.unsw.edu.au/1959.4/52433 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:11106/SOURCE1?view=true
Chicago Manual of Style (16th Edition):
Adams, Seray. “The involvement of the kynurenine pathway in brain tumour pathogenesis.” 2012. Doctoral Dissertation, University of New South Wales. Accessed March 05, 2021.
http://handle.unsw.edu.au/1959.4/52433 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:11106/SOURCE1?view=true.
MLA Handbook (7th Edition):
Adams, Seray. “The involvement of the kynurenine pathway in brain tumour pathogenesis.” 2012. Web. 05 Mar 2021.
Vancouver:
Adams S. The involvement of the kynurenine pathway in brain tumour pathogenesis. [Internet] [Doctoral dissertation]. University of New South Wales; 2012. [cited 2021 Mar 05].
Available from: http://handle.unsw.edu.au/1959.4/52433 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:11106/SOURCE1?view=true.
Council of Science Editors:
Adams S. The involvement of the kynurenine pathway in brain tumour pathogenesis. [Doctoral Dissertation]. University of New South Wales; 2012. Available from: http://handle.unsw.edu.au/1959.4/52433 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:11106/SOURCE1?view=true
University of Cambridge
9.
Parkins, Christopher Charles.
Bypassing the Blood-Brain Barrier: Cucurbit[8]uril-based Hydrogels Towards Drug Delivery Reservoirs.
Degree: PhD, 2020, University of Cambridge
URL: https://www.repository.cam.ac.uk/handle/1810/303174
► Hydrogels formed from supramolecular crosslinking are an exciting class of soft materials that exhibit attractive properties lending themselves towards biomedical applications, specifically as drug delivery…
(more)
▼ Hydrogels formed from supramolecular crosslinking are an exciting class of soft materials that exhibit attractive properties lending themselves towards biomedical applications, specifically as drug delivery reservoirs. Dynamic crosslinks form materials that can be stimuli-responsive, shear-thinning and self-healing. It is the application of these materials in the local delivery of cargo to post-resection tumour cavities that is the focus of this thesis.
In the first chapter the host-guest interactions of cucurbit[8]uril in aqueous assemblies, with a particular emphasis on those systems forming hydrogels, are summarised. The application of hydrogels towards delivery devices in glioblastoma and ependymoma are outlined and discussed.
The second chapter focuses on the preparation of peptide-functionalised hyaluronic acid hydrogels dynamically crosslinked using the macrocylic host molecule cucurbit[8]uril (CB[8]). The host facilitates supramolecular crosslinks between the polymer chains drastically increasing the viscoelastic properties of the materials. By tuning the temporary chain entanglement (molecular weight) and the crosslinking density, control over the network mechanics, flow properties and relaxation is demonstrated. Matrix metalloproteinase cleavable linkers were introduced to produce environment-responsive networks that would lower the mechanical properties on demand. Conversely, light-triggered guest moieties were introduced to spatially and temporally modulate mechanical stiffness.
The third chapter builds upon this initial work through the employment of peptide functionalised hyaluronic acid (HA(CF)) hydrogels as delivery devices. The binding dynamics of small-molecule chemotherapies is analysed through proton nuclear magnetic resonance (NMR) titrations and isothermal titration calorimetry (ITC). The in vitro and ex vivo release of each molecule from HA(CF) hydrogels is analysed using UV/vis spectroscopy, confocal microscopy and mass spectrometry imaging. Biocompatibility of the hydrogel and the constituents were demonstrated through a variety of in vitro viability and immunocytochemistry based assays.
Moving forward, the in vivo validation of injectable HA(CF) hydrogels using patient derived xenografts (PDXs) of glioblastoma tumours, was undertaken in chapter four. The mechanical and viscoelastic properties of native human and mouse tissues are measured over 8 hours via oscillatory rheology under physiological conditions. Tissue stiffness matching of the hydrogels enables a significant survival impact of 45% (55.5 to 80.5 days) due to improved tissue apposition and subsequently increased local repurposed drug bioavailability. A relationship between the type of PDX tumour formed—a consequence of the heterogeneic nature of GB tumours—and changes in the initial survival is observed owing to greater local pressure from stiffer tumours.
Chapter five highlights the utility of HA(CF) hydrogels within glioblastoma PDXs and supratentorial fusion-negative ependymoma resection models. Patient derived GB cells…
Subjects/Keywords: cucurbit[8]uril; hydrogel; glioblastoma; gbm; ependymoma; glioblastoma multiforme; hyaluronic acid
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APA (6th Edition):
Parkins, C. C. (2020). Bypassing the Blood-Brain Barrier: Cucurbit[8]uril-based Hydrogels Towards Drug Delivery Reservoirs. (Doctoral Dissertation). University of Cambridge. Retrieved from https://www.repository.cam.ac.uk/handle/1810/303174
Chicago Manual of Style (16th Edition):
Parkins, Christopher Charles. “Bypassing the Blood-Brain Barrier: Cucurbit[8]uril-based Hydrogels Towards Drug Delivery Reservoirs.” 2020. Doctoral Dissertation, University of Cambridge. Accessed March 05, 2021.
https://www.repository.cam.ac.uk/handle/1810/303174.
MLA Handbook (7th Edition):
Parkins, Christopher Charles. “Bypassing the Blood-Brain Barrier: Cucurbit[8]uril-based Hydrogels Towards Drug Delivery Reservoirs.” 2020. Web. 05 Mar 2021.
Vancouver:
Parkins CC. Bypassing the Blood-Brain Barrier: Cucurbit[8]uril-based Hydrogels Towards Drug Delivery Reservoirs. [Internet] [Doctoral dissertation]. University of Cambridge; 2020. [cited 2021 Mar 05].
Available from: https://www.repository.cam.ac.uk/handle/1810/303174.
Council of Science Editors:
Parkins CC. Bypassing the Blood-Brain Barrier: Cucurbit[8]uril-based Hydrogels Towards Drug Delivery Reservoirs. [Doctoral Dissertation]. University of Cambridge; 2020. Available from: https://www.repository.cam.ac.uk/handle/1810/303174
NSYSU
10.
Shui, Wan-pin.
Quantitative analysis of intra-lesional susceptibility signal of ring-enhanced lesions using susceptibility weighted imaging.
Degree: Master, Electrical Engineering, 2013, NSYSU
URL: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0601113-163100
► Susceptibility-weighted imaging (SWI) has been used to enhance the variation of magnetic susceptibility among human tissues and is very sensitive to the accumulation of paramagnetic…
(more)
▼ Susceptibility-weighted imaging (SWI) has been used to enhance the variation of
magnetic susceptibility among human tissues and is very sensitive to the accumulation of paramagnetic compounds like hemorrhage, which is in appearance of low gray levels in SWI. In this study, an objective method was proposed to determine the intra-lesional susceptibility signal (ILSS) for ring-enhanced lesions. The procedure of image processing can be divided into three steps, including selection of region of interest (ROI) on post-contrast images, Ostuâs segmentation of the lesion, and determination of ILSS by using normalized difference, in which the information from non-ILSS and normal
white matter was considered. Therefore, the volume of ILSS and lesion, and the
corresponding ratio, can be measured.
A total of 44 subjects, including 21 with abscess, 13 with
glioblastoma
multiforme(
GBM), and 10 with brain metastasis, was enrolled in this study. For abscess,
GBM, and metastasis, the mean volume of ILSS is 1.0cm3 , 5.3 cm3 , and 2.5 cm3 and the mean lesion size is 19.5 cm3 , 47.3 cm3 , and 29.4 cm3 , respectively, and the corresponding ratio on average is 7.1%, 11.8%, and 8.8%. As a result, the volume of ILSS and lesion, and the ratio of abscess are obviously the smallest among three types of ring-enhanced lesions when
GBM has the largest numbers. In comparison, the statistical results of brain metastasis were found between abscess and
GBM with a comparatively small simple size of ten.
Advisors/Committee Members: Hsiao-Wen Chung (chair), Tzu-Chao Chuang (committee member), Ping-Hong Lai (chair), Ming-Long Wu (chair), Shang-Yueh Tsai (chair).
Subjects/Keywords: SWI; abscess; glioblastoma multiforme(GBM); hemorrhage; brain metastasis
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APA (6th Edition):
Shui, W. (2013). Quantitative analysis of intra-lesional susceptibility signal of ring-enhanced lesions using susceptibility weighted imaging. (Thesis). NSYSU. Retrieved from http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0601113-163100
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Shui, Wan-pin. “Quantitative analysis of intra-lesional susceptibility signal of ring-enhanced lesions using susceptibility weighted imaging.” 2013. Thesis, NSYSU. Accessed March 05, 2021.
http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0601113-163100.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Shui, Wan-pin. “Quantitative analysis of intra-lesional susceptibility signal of ring-enhanced lesions using susceptibility weighted imaging.” 2013. Web. 05 Mar 2021.
Vancouver:
Shui W. Quantitative analysis of intra-lesional susceptibility signal of ring-enhanced lesions using susceptibility weighted imaging. [Internet] [Thesis]. NSYSU; 2013. [cited 2021 Mar 05].
Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0601113-163100.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Shui W. Quantitative analysis of intra-lesional susceptibility signal of ring-enhanced lesions using susceptibility weighted imaging. [Thesis]. NSYSU; 2013. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0601113-163100
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
University of Alberta
11.
Heydari, Maysam.
Prognosis of Glioblastoma Multiforme Using Textural
Properties on MRI.
Degree: MS, Department of Computing Science, 2009, University of Alberta
URL: https://era.library.ualberta.ca/files/bv73c2154
► This thesis addresses the challenge of prognosis, in terms of survival prediction, for patients with Glioblastoma Multiforme brain tumors. Glioblastoma is the most malignant brain…
(more)
▼ This thesis addresses the challenge of prognosis, in
terms of survival prediction, for patients with Glioblastoma
Multiforme brain tumors. Glioblastoma is the most malignant brain
tumor, which has a median survival time of no more than a year.
Accurate assessment of prognostic factors is critical in deciding
amongst different treatment options and in designing stratified
clinical trials. This thesis is motivated by two observations.
Firstly, clinicians often refer to properties of glioblastoma
tumors based on magnetic resonance images when assessing prognosis.
However, clinical data, along with histological and most recently,
molecular and gene expression data, have been more widely and
systematically studied and used in prognosis assessment than image
based information. Secondly, patient survival times are often used
along with clinical data to conduct population studies on brain
tumor patients. Recursive Partitioning Analysis is typically used
in these population studies. However, researchers validate and
assess the predictive power of these models by measuring the
statistical association between survival groups and survival times.
In this thesis, we propose a learning approach that uses historical
training data to produce a system that predicts patient survival.
We introduce a classification model for predicting patient survival
class, which uses texture based features extracted from magnetic
resonance images as well as other patient properties. Our prognosis
approach is novel as it is the first to use image-extracted
textural characteristics of glioblastoma scans, in a classification
model whose accuracy can be reliably validated by cross validation.
We show that our approach is a promising new direction for
prognosis in brain tumor patients.
Subjects/Keywords: prognosis; machine learning; MRI; GBM; texture; survival; glioblastoma; decision tree
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Manager
APA (6th Edition):
Heydari, M. (2009). Prognosis of Glioblastoma Multiforme Using Textural
Properties on MRI. (Masters Thesis). University of Alberta. Retrieved from https://era.library.ualberta.ca/files/bv73c2154
Chicago Manual of Style (16th Edition):
Heydari, Maysam. “Prognosis of Glioblastoma Multiforme Using Textural
Properties on MRI.” 2009. Masters Thesis, University of Alberta. Accessed March 05, 2021.
https://era.library.ualberta.ca/files/bv73c2154.
MLA Handbook (7th Edition):
Heydari, Maysam. “Prognosis of Glioblastoma Multiforme Using Textural
Properties on MRI.” 2009. Web. 05 Mar 2021.
Vancouver:
Heydari M. Prognosis of Glioblastoma Multiforme Using Textural
Properties on MRI. [Internet] [Masters thesis]. University of Alberta; 2009. [cited 2021 Mar 05].
Available from: https://era.library.ualberta.ca/files/bv73c2154.
Council of Science Editors:
Heydari M. Prognosis of Glioblastoma Multiforme Using Textural
Properties on MRI. [Masters Thesis]. University of Alberta; 2009. Available from: https://era.library.ualberta.ca/files/bv73c2154
University of California – San Francisco
12.
Yeh, Alex.
Serial MRI/MRSI of Patients with Gliomas Being Treated with Novel Therapies.
Degree: Biomedical Imaging, 2014, University of California – San Francisco
URL: http://www.escholarship.org/uc/item/5rd3r5pm
► Background: Glioblastoma multiforme (GBM) is a primary brain tumor that typically results in poor outcomes. A number of combination therapies are being considered for improving…
(more)
▼ Background: Glioblastoma multiforme (GBM) is a primary brain tumor that typically results in poor outcomes. A number of combination therapies are being considered for improving the prognosis for such patients. In this study serial MRI data were evaluated from patients with newly diagnosed GBM who were participating in a single-arm, Phase II clinical trial for an autologous heat-shock protein peptide complex-96 (HSPPC-96) vaccine.Methods: Patients underwent surgical resection, radiation with temozolomide, and concurrent administrations of heat-shock protein peptide complex-96 (HSPPC-96) vaccine and temozolomide. Anatomical, diffusion-weighted, and perfusion-weighted imaging parameters were examined starting after radiation therapy/temozolomide and before the first vaccine administration. Patients were imaged at regular time points thereafter. Imaging parameters were assessed for changes from baseline and for their association with overall survival (OS) and progression-free survival (PFS) using a Cox proportional hazards model.Results: Starting at 200 days after the completion of radiotherapy, significant increases from baseline were consistently seen in both 10th percentile of the normalized apparent diffusion coefficient (nADC) and the median nADC values in the T2 hyperintense lesion. At 250-350 days from baseline, significant associations were seen for nADC values with both PFS and OS.Conclusion: Multiparametric MR imaging provides a non-invasive method to elucidate more information about how the tumor is responding to combination therapies that include adding a novel immunotherapy vaccine to standard of care radiation and temozolomide.
Subjects/Keywords: Biomedical engineering; diffusion; GBM; glioblastoma multiforme; immunotherapy; MRI; perfusion
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Manager
APA (6th Edition):
Yeh, A. (2014). Serial MRI/MRSI of Patients with Gliomas Being Treated with Novel Therapies. (Thesis). University of California – San Francisco. Retrieved from http://www.escholarship.org/uc/item/5rd3r5pm
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Yeh, Alex. “Serial MRI/MRSI of Patients with Gliomas Being Treated with Novel Therapies.” 2014. Thesis, University of California – San Francisco. Accessed March 05, 2021.
http://www.escholarship.org/uc/item/5rd3r5pm.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Yeh, Alex. “Serial MRI/MRSI of Patients with Gliomas Being Treated with Novel Therapies.” 2014. Web. 05 Mar 2021.
Vancouver:
Yeh A. Serial MRI/MRSI of Patients with Gliomas Being Treated with Novel Therapies. [Internet] [Thesis]. University of California – San Francisco; 2014. [cited 2021 Mar 05].
Available from: http://www.escholarship.org/uc/item/5rd3r5pm.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Yeh A. Serial MRI/MRSI of Patients with Gliomas Being Treated with Novel Therapies. [Thesis]. University of California – San Francisco; 2014. Available from: http://www.escholarship.org/uc/item/5rd3r5pm
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Virginia Tech
13.
Varghese, Robin.
Novel Prognostic Markers and Therapeutic Targets for Glioblastoma.
Degree: PhD, Genetics, Bioinformatics, and Computational Biology, 2016, Virginia Tech
URL: http://hdl.handle.net/10919/71420
► Glioblastoma is the most common and lethal malignant brain tumor with a survival rate of 14.6 months and a tumor recurrence rate of ninety percent.…
(more)
▼ Glioblastoma is the most common and lethal malignant brain tumor with a survival rate of 14.6 months and a tumor recurrence rate of ninety percent. Two key causes for glioblastomas grim outcome derive from the lack of applicable prognostic markers and effective therapeutic targets. By employing a loss of function RNAi screen in
glioblastoma cells we found a list of 20 kinases that can be considered
glioblastoma survival kinases. These survival kinases which we term as survival kinase genes, (SKGs) were investigated to find prognostic markers as well as therapeutic targets for
glioblastoma. Analyzing these survival kinases in The Cancer Genome Atlas patient database, we found that CDCP1, CDKL5, CSNK1𝜀, IRAK3, LATS2, PRKAA1, STK3, TBRG4, and ULK4 genes could be used as prognostic markers for
glioblastoma with or without temozolomide chemotherapeutic treatment as a covariate. For the first time, we found that patients with increased levels of NEK9 and PIK3CB mRNA expression had a higher probability of recurrent tumors. We also discovered that expression of CDCP1, IGF2R, IRAK3, LATS2, PIK3CB, ULK4, or VRK1 in primary
glioblastoma tumors was associated with tumor recurrence prognosis. To note, of these recurrent prognostic candidates, PIK3CB expression in recurrent tumor tissue had much higher expression compared to primary tissue. Further investigation in the PI3K pathway showed a strong correlation with recurrence rate, days to recurrence and survival emphasizing the role of PIK3CB in tumor recurrence in
glioblastoma. In efforts to find effective therapeutic targets for
glioblastoma we used SKGs as potential candidates. We chose the serine/threonine kinase, Casein Kinase 1 Epsilon (CSNK1𝜀) as a target for
glioblastoma because multiple shRNAs targeted this gene in our loss of function screen and multiple commercially available inhibitors of this gene are available. Casein kinase 1 epsilon protein and mRNA expression were investigated using computational tools. It was revealed that CSNK1𝜀 expression has higher expression in
glioblastoma than normal tissue. To further examine this gene we knocked down (KD) or inhibited CSNK1𝜀 in
glioblastoma cells lines and noticed a significant increase in cell death without any significant effect on normal cell lines. KD and inhibition of CSNK1𝜀 in cancer stem cells, a culprit of tumor recurrence, also revealed limited self-renewal and proliferation in cancer stem cells and a significant decrease in cell survival without affecting normal stem cells. Further analysis of downstream effects of CSNK1𝜀 knockdown and inhibition indicate a significant increase in the protein expression of β-catenin (CTNNB1). We found that CSNK1𝜀 KD activated β-catenin, which increased
GBM cell death, but can be rescued using CTNNB1 shRNA. Our survival kinase screen, computational analyses, patient database analyses and experimental methods contributed to the discovery of novel prognostic markers and therapeutic targets for
glioblastoma.
Advisors/Committee Members: Sheng, Zhi (committeechair), Lamouille, Samy (committee member), Franck, Christopher T. (committee member), Michalak, Pawel (committee member).
Subjects/Keywords: Glioblastoma; Tumor Recurrence; GBM; Prognostic Markers; CSNK1E; PIK3CB
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APA (6th Edition):
Varghese, R. (2016). Novel Prognostic Markers and Therapeutic Targets for Glioblastoma. (Doctoral Dissertation). Virginia Tech. Retrieved from http://hdl.handle.net/10919/71420
Chicago Manual of Style (16th Edition):
Varghese, Robin. “Novel Prognostic Markers and Therapeutic Targets for Glioblastoma.” 2016. Doctoral Dissertation, Virginia Tech. Accessed March 05, 2021.
http://hdl.handle.net/10919/71420.
MLA Handbook (7th Edition):
Varghese, Robin. “Novel Prognostic Markers and Therapeutic Targets for Glioblastoma.” 2016. Web. 05 Mar 2021.
Vancouver:
Varghese R. Novel Prognostic Markers and Therapeutic Targets for Glioblastoma. [Internet] [Doctoral dissertation]. Virginia Tech; 2016. [cited 2021 Mar 05].
Available from: http://hdl.handle.net/10919/71420.
Council of Science Editors:
Varghese R. Novel Prognostic Markers and Therapeutic Targets for Glioblastoma. [Doctoral Dissertation]. Virginia Tech; 2016. Available from: http://hdl.handle.net/10919/71420
14.
Wigand, Amanda M.
ANALYSIS OF TUMOR SPECIFIC PROTEIN EXPRESSION IN GLIOBLASTOMA MULTIFORME (GBMs) TUMORS THROUGH IMMUNOHISTOCHEMISTRY.
Degree: MS, Biology, 2016, Northen Michigan University
URL: https://commons.nmu.edu/theses/92
► GBM tumors are the most aggressive and, unfortunately, the most fatal form of brain cancer. GBM tumors with isocitrate dehydrogenase-1 (IDH1) mutation being expressed,…
(more)
▼ GBM tumors are the most aggressive and, unfortunately, the most fatal form of brain cancer.
GBM tumors with isocitrate dehydrogenase-1 (IDH1) mutation being expressed, lead to higher survival rates in patients that also have full resection of the tumor and chemotherapy. Without this mutation, it is thought that tumors have a higher expression of the protein Basigin and O6-methylguanine-DNA-methyltrasnferase (MGMT) present, causing it to be more aggressive and less responsive to standard care. The objective of this study was to understand the correlation between IDH1 mutation presence and the expression of Basigin and MGMT. The expression of these proteins was observed in tissues sections from
GBM tumors. Proteins were labeled with a fluorescent antibody and imaged with a confocal microscope. The tissue images were then analyzed using Imaris software. It was shown that there was a significant difference between the presence of the IDH1 mutation and Basgin, and also MGMT among all of the tissue blocks.
Advisors/Committee Members: Robert Belton.
Subjects/Keywords: Glioblastoma Multiforme; GBM; immunohistochemistry; immunofluorescence; Medicine and Health Sciences
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APA (6th Edition):
Wigand, A. M. (2016). ANALYSIS OF TUMOR SPECIFIC PROTEIN EXPRESSION IN GLIOBLASTOMA MULTIFORME (GBMs) TUMORS THROUGH IMMUNOHISTOCHEMISTRY. (Thesis). Northen Michigan University. Retrieved from https://commons.nmu.edu/theses/92
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Wigand, Amanda M. “ANALYSIS OF TUMOR SPECIFIC PROTEIN EXPRESSION IN GLIOBLASTOMA MULTIFORME (GBMs) TUMORS THROUGH IMMUNOHISTOCHEMISTRY.” 2016. Thesis, Northen Michigan University. Accessed March 05, 2021.
https://commons.nmu.edu/theses/92.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Wigand, Amanda M. “ANALYSIS OF TUMOR SPECIFIC PROTEIN EXPRESSION IN GLIOBLASTOMA MULTIFORME (GBMs) TUMORS THROUGH IMMUNOHISTOCHEMISTRY.” 2016. Web. 05 Mar 2021.
Vancouver:
Wigand AM. ANALYSIS OF TUMOR SPECIFIC PROTEIN EXPRESSION IN GLIOBLASTOMA MULTIFORME (GBMs) TUMORS THROUGH IMMUNOHISTOCHEMISTRY. [Internet] [Thesis]. Northen Michigan University; 2016. [cited 2021 Mar 05].
Available from: https://commons.nmu.edu/theses/92.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Wigand AM. ANALYSIS OF TUMOR SPECIFIC PROTEIN EXPRESSION IN GLIOBLASTOMA MULTIFORME (GBMs) TUMORS THROUGH IMMUNOHISTOCHEMISTRY. [Thesis]. Northen Michigan University; 2016. Available from: https://commons.nmu.edu/theses/92
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
University of Illinois – Urbana-Champaign
15.
Sadeque, Ahmed.
Identification of alternative exon usage in cancer survival using hierarchical modeling.
Degree: MS, 4026, 2012, University of Illinois – Urbana-Champaign
URL: http://hdl.handle.net/2142/34549
► Background Alternative exon usage (AEU) is an important component of gene expression regulation. Exon expression platforms allow the detection of associations between AEU and phenotypes…
(more)
▼ Background
Alternative exon usage (AEU) is an important component of gene expression regulation. Exon expression platforms allow the detection of associations between AEU and phenotypes such as cancer. Numerous studies have identified associations between gene expression and the brain cancer
glioblastoma multiforme (
GBM). The few consistent gene expression biomarkers of
GBM that have been reported may be due to the limited consideration of AEU and the analytical approaches used. The objectives of this study were to develop a model that accounts for the
variations in expression present between the exons within a gene and to identify AEU biomarkers of
GBM survival.
Methods
The expression of exons corresponding to 25,403 genes was related to the survival of 250
individuals diagnosed with
GBM in a training data set. Genes exhibiting AEU in the training
data set were confirmed in an independent validation data set of 78 patients. A hierarchical
model allows the consideration of covariation between exons within a gene and of the effect of
the epidemiological characteristics of the patients was developed to identify associations
between exon expression and patient survival. The same model serves multi-exon models with
and without AEU and single-exon models.
Results
AEU associated with
GBM survival was identified on 2477 genes (P-value < 5.0E-04 (FDR adjusted P-value < 5.0E-04). G-protein coupled receptor 98 (Gpr98) and epidermal growth factor (Egf) were among the genes exhibiting AEU with 30 and 9 exons associated with
GBM survival, respectively. Pathways enriched among the AEU genes included focal adhesion, ECM-receptor interaction, ABC transporters and pathways in cancer. In addition, 24 multi-exon genes without AEU and 8 single-exon genes were associated with
GBM survival (P-value < 0.0005).
Conclusions
The inferred patterns of AEU were consistent with in silico AS models. The hierarchical model used offered a flexible and simple way to interpret and identify associations between survival that accommodates multi-exon genes with or without AEU and single exon genes.
Advisors/Committee Members: Rodriguez-Zas, Sandra L. (advisor).
Subjects/Keywords: Alternative Splicing (AS); Alternative Exon Usage (AEU); Glioblastoma (GBM)
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APA (6th Edition):
Sadeque, A. (2012). Identification of alternative exon usage in cancer survival using hierarchical modeling. (Thesis). University of Illinois – Urbana-Champaign. Retrieved from http://hdl.handle.net/2142/34549
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Sadeque, Ahmed. “Identification of alternative exon usage in cancer survival using hierarchical modeling.” 2012. Thesis, University of Illinois – Urbana-Champaign. Accessed March 05, 2021.
http://hdl.handle.net/2142/34549.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Sadeque, Ahmed. “Identification of alternative exon usage in cancer survival using hierarchical modeling.” 2012. Web. 05 Mar 2021.
Vancouver:
Sadeque A. Identification of alternative exon usage in cancer survival using hierarchical modeling. [Internet] [Thesis]. University of Illinois – Urbana-Champaign; 2012. [cited 2021 Mar 05].
Available from: http://hdl.handle.net/2142/34549.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Sadeque A. Identification of alternative exon usage in cancer survival using hierarchical modeling. [Thesis]. University of Illinois – Urbana-Champaign; 2012. Available from: http://hdl.handle.net/2142/34549
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
University of Sydney
16.
De Gzell, Cecelia Elizabeth.
OPTIMISING OUTCOMES IN PATIENTS WITH GLIOBLASTOMA RECEIVING RADIOTHERAPY
.
Degree: 2016, University of Sydney
URL: http://hdl.handle.net/2123/16549
► More than 1,400 new cases of malignant brain tumours are diagnosed each year in Australia. Glioblastoma, or GBM, remains the most common primary brain tumour…
(more)
▼ More than 1,400 new cases of malignant brain tumours are diagnosed each year in Australia. Glioblastoma, or GBM, remains the most common primary brain tumour in adults and the most devastating. The median age at diagnosis is 61 years and the median survival from diagnosis is only approximately 14 months. The aim of the work presented in this thesis is to optimise radiotherapy protocols in patients with glioblastoma to improve patient outcomes by targeting particular time points along the patients’ treatment journey. After describing the disease and epidemiology of GBM in Chapter 1, Chapter 2 explores the evolution of RT technique in treating this disease throughout the ages. In this disease patients >65 years are considered “elderly” and have a poorer prognosis compared with their younger cohorts. They also represent the majority of patients with GBM as the incidence for this tumour peaks in the sixth and seventh decades. There is currently no internationally accepted standard of care for treating this group. Chapter 3 analyses different RT protocols in this cohort of patients. The remaining chapters examine different aspects of the patient’s post-RT journey. Chapter 4 analyses the phenomenon of pseudoprogression (PsP), a radiological diagnosis of an increase in abnormality on post-RT magnetic resonance imaging (MRI) scan which subsequently improves over time with no change in treatment. This phenomenon is poorly understood and the pathological characteristics are explored. Directly expanding from the work on pseudoprogression, Chapter 5 introduces novel volumetric techniques to analyse post-RT MRI changes and explores whether these impact patients’ survival. Chapter 6 deals with the survivorship issue of a patient’s ability to return to work following RT. As patients are living longer with this disease, and a greater proportion are remaining functionally well until late in the course of the disease, more patients are being offered re-irradiation as part of their salvage treatment. Chapter 7 analyses the evolving role of re-irradiation. RT in addition to surgery remains the cornerstone of treatment of GBM. With ongoing improvements in the technical delivery of RT we expect there to be clinical benefit for patients with reduced short-and late toxicity, if not an improvement in survival. This thesis explores different aspects of the patients’ treatment journey on topics that have previously been poorly understood or novel areas of research.
Subjects/Keywords: Glioblastoma;
radiotherapy;
radiation oncology;
GBM;
neuro-oncology;
pseudoprogression
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APA ·
Chicago ·
MLA ·
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CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
De Gzell, C. E. (2016). OPTIMISING OUTCOMES IN PATIENTS WITH GLIOBLASTOMA RECEIVING RADIOTHERAPY
. (Thesis). University of Sydney. Retrieved from http://hdl.handle.net/2123/16549
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
De Gzell, Cecelia Elizabeth. “OPTIMISING OUTCOMES IN PATIENTS WITH GLIOBLASTOMA RECEIVING RADIOTHERAPY
.” 2016. Thesis, University of Sydney. Accessed March 05, 2021.
http://hdl.handle.net/2123/16549.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
De Gzell, Cecelia Elizabeth. “OPTIMISING OUTCOMES IN PATIENTS WITH GLIOBLASTOMA RECEIVING RADIOTHERAPY
.” 2016. Web. 05 Mar 2021.
Vancouver:
De Gzell CE. OPTIMISING OUTCOMES IN PATIENTS WITH GLIOBLASTOMA RECEIVING RADIOTHERAPY
. [Internet] [Thesis]. University of Sydney; 2016. [cited 2021 Mar 05].
Available from: http://hdl.handle.net/2123/16549.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
De Gzell CE. OPTIMISING OUTCOMES IN PATIENTS WITH GLIOBLASTOMA RECEIVING RADIOTHERAPY
. [Thesis]. University of Sydney; 2016. Available from: http://hdl.handle.net/2123/16549
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Indian Institute of Science
17.
Shukla, Sudhanshu Kumar.
Role of DNA Methylation in Glioblastoma Development.
Degree: PhD, Faculty of Science, 2018, Indian Institute of Science
URL: http://etd.iisc.ac.in/handle/2005/3378
► Glioblastoma (GBM) is the most common and malignant of the glial tumors. These tumors may develop from lower-grade astrocytomas (diffuse astrocytoma; grade II or anaplastic…
(more)
▼ Glioblastoma (
GBM) is the most common and malignant of the glial tumors. These tumors may develop from lower-grade astrocytomas (diffuse astrocytoma; grade II or anaplastic astrocytoma; grade III) through a progressive pathway, but, more frequently, they manifest de novo without any evidence of a pre-malignant lesion. The treatment of
GBM includes surgery, radiotherapy, and chemotherapy with temozolomide. Despite improvements in treatment protocols, the median survival of
GBM patients remains very low at 12-15 months.
The cause of glioma (either development or progression) can be genetic and epigenetic modification driven changes. In contrast to genetic modifications, where DNA sequence is changed, epigenetic modifications are those gene expression regulatory mechanisms which do not involve the change in the DNA sequence. It includes DNA methylation, chromatin modifications and miRNA mediated changes in gene expression. Aberrant DNA methylation is one of the common molecular lesions occurring in the cancer cell. The 5th position of cytosine (CpG) is the most preferred site of DNA methylation in mammalian cells. The methylated cytosines are prone to undergo oxidative deamination, and get mutated to thymine in DNA. Consequently, this led to decrease in CpG abundance in the genome. In normal conditions, promoters of majority of the genes escape methylation, because of which CpG of these regions remain same. This phenomenon led to the restriction of CpGs in the promoter regions of most of the genes. These CpG rich regions of the promoters are known as CpG islands, and the methylation status of these islands have a major role in regulating gene expression. The cancer genome is shown to undergo genome-wide hypomethylation whereas CpG islands undergo hypermethylation compared to normal tissue, resulting in net loss of total methylation, as the CpGs from non-island areas far exceed in number compared to the CpGs from islands.
The most studied change of DNA methylation in neoplasms is the silencing of the tumor suppressor genes by CpG island promoter hypermethylation. Apart from few studies, the role of DNA methylation in glioma development and progression is poorly known.
With this background, we have focused our study on DNA methylation changes in
GBM. To identify
GBM specific DNA methylation alterations, we have performed the genome wide methylation profile of 44
GBM and 8 normal samples using Infinium methylation array. Beta value, which is a measure of methylation, was calculated for all the CpG probes. Beta value ranges between 0-1 (from no methylation to complete methylation). We sought to understand the clinical importance, with particular importance to patient survival, of the DNA methylation pattern observed. We also undertook steps to understand the contribution of the differential DNA methylation and the associated gene expression changes in
GBM development.
This work has been divided into three parts:
Part I –Identification of
GBM specific methylome and development of a DNA methylation prognostic signature…
Advisors/Committee Members: Somasundaram, Kumaravel (advisor).
Subjects/Keywords: Glioblastoma (GBM); DNA Methylation; Glial Tumors; Astrocytoma; DNA Methylation and Cancer; DNA Methylation - Glioblastoma; Astrocytoma; Astrocyte Transformation; ULK2; Oncology
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APA (6th Edition):
Shukla, S. K. (2018). Role of DNA Methylation in Glioblastoma Development. (Doctoral Dissertation). Indian Institute of Science. Retrieved from http://etd.iisc.ac.in/handle/2005/3378
Chicago Manual of Style (16th Edition):
Shukla, Sudhanshu Kumar. “Role of DNA Methylation in Glioblastoma Development.” 2018. Doctoral Dissertation, Indian Institute of Science. Accessed March 05, 2021.
http://etd.iisc.ac.in/handle/2005/3378.
MLA Handbook (7th Edition):
Shukla, Sudhanshu Kumar. “Role of DNA Methylation in Glioblastoma Development.” 2018. Web. 05 Mar 2021.
Vancouver:
Shukla SK. Role of DNA Methylation in Glioblastoma Development. [Internet] [Doctoral dissertation]. Indian Institute of Science; 2018. [cited 2021 Mar 05].
Available from: http://etd.iisc.ac.in/handle/2005/3378.
Council of Science Editors:
Shukla SK. Role of DNA Methylation in Glioblastoma Development. [Doctoral Dissertation]. Indian Institute of Science; 2018. Available from: http://etd.iisc.ac.in/handle/2005/3378
Texas Medical Center
18.
Robinson, Frederick Scott.
Potential REST Targets in Neural Stem Cells and Glioblastoma-Derived Stem Cells.
Degree: MS, 2012, Texas Medical Center
URL: https://digitalcommons.library.tmc.edu/utgsbs_dissertations/288
► Glioblastoma multiforme (GBM) tumors are the most common malignant primary brain tumors in adults. The current theory is that these tumors are caused by…
(more)
▼ Glioblastoma multiforme (
GBM) tumors are the most common malignant primary brain tumors in adults. The current theory is that these tumors are caused by self-renewing
glioblastoma-derived stem cells (GSCs). At the current time, the mechanisms that regulate self-renewal and other oncogenic properties of GSCs remain unknown. Recently, we found transcriptional repressor REST maintains self-renewal in neural stem cells (NSCs) and in GSCs. REST also regulates other oncogenic properties, such as apoptosis, invasion and proliferation. However, the mechanisms by which REST regulates these oncogenic properties are unknown. In an attempt to determine these mechanisms, we performed loss and gain-of-function experiments and genome-wide mRNA expression analysis in GSCs, and we were able to identify REST-regulated genes in GSCs. This was accomplished, after screening concordantly regulated genes in NSCs and GSCs, utilizing two RE1 databases, and setting two-fold expression as filters on the resulting genes. These results received further validation by qRT-PCR. Ingenuity Pathway Analysis (IPA) analysis further revealed the top REST target genes in GSCs were downstream targets of REST and/or involved in other cancers in other cell lines. IPA also revealed that many of the differentially-regulated genes identified in this study are involved in oncogenic properties seen in
GBM, and which we believe are related to REST expression.
Advisors/Committee Members: Sadhan Majumder, Gregory Fuller, Gary Gallick.
Subjects/Keywords: REST; Neural Stem Cells; Glioblastoma Derived Stem Cells; Glioblastoma Multiforme; NSC; GSC; GBM; Cancer Biology; Computational Biology; Genetics
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Export
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APA (6th Edition):
Robinson, F. S. (2012). Potential REST Targets in Neural Stem Cells and Glioblastoma-Derived Stem Cells. (Thesis). Texas Medical Center. Retrieved from https://digitalcommons.library.tmc.edu/utgsbs_dissertations/288
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Robinson, Frederick Scott. “Potential REST Targets in Neural Stem Cells and Glioblastoma-Derived Stem Cells.” 2012. Thesis, Texas Medical Center. Accessed March 05, 2021.
https://digitalcommons.library.tmc.edu/utgsbs_dissertations/288.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Robinson, Frederick Scott. “Potential REST Targets in Neural Stem Cells and Glioblastoma-Derived Stem Cells.” 2012. Web. 05 Mar 2021.
Vancouver:
Robinson FS. Potential REST Targets in Neural Stem Cells and Glioblastoma-Derived Stem Cells. [Internet] [Thesis]. Texas Medical Center; 2012. [cited 2021 Mar 05].
Available from: https://digitalcommons.library.tmc.edu/utgsbs_dissertations/288.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Robinson FS. Potential REST Targets in Neural Stem Cells and Glioblastoma-Derived Stem Cells. [Thesis]. Texas Medical Center; 2012. Available from: https://digitalcommons.library.tmc.edu/utgsbs_dissertations/288
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
University of Southern California
19.
Vaikari, Vijaya Pooja.
Molecular targets for treatment of glioblastoma
multiforme.
Degree: MS, Molecular Microbiology and Immunology, 2016, University of Southern California
URL: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/506490/rec/4207
► In this study we have tried to understand mechanisms by which tumor suppression of glioblastoma mutliforme (GBM) can be enhanced. To do so we analyzed…
(more)
▼ In this study we have tried to understand mechanisms
by which tumor suppression of
glioblastoma mutliforme (
GBM) can be
enhanced. To do so we analyzed the effect of bevacizumab, an
inflammatory factor (IF), and the effect of serotonin on
GBM. ❧
Bevacizumab is a humanized monoclonal antibody derivated against
vascular endothelial growth factor (VEGF), a stimulator of
angiogenesis. Bevacizumab is the single most important therapeutic
agent for
glioblastoma since temozolomide. Bevacizumab has been
shown to increase the progression free survival by 4 months but is
known to have side effects like hypertension, renal failure and
deep venous thrombosis. In our study we determined whether there
are differences in angiogenesis and stem cell population when
bevacizumab is administered locally as compared to systemic
administration. Bevacizumab when administered locally improved
survival, and there were more cells secreting stromal derived
factor-1 (SDF-1) that plays a role in angiogenesis in the vehicle
and mice treated with bevacizumab systemically. Further, we found
no differences in the number of stem cells between the mice treated
with bevacizumab locally or systemically. ❧ We further analyzed the
effect of an inflammatory factor (IF) on the immune response in
GBM. We found that an increase in survival with absence or reduced
levels of IF occurred. This could be a result of increased number
of macrophages in IF knockout mice or mice treated with IF
inhibitors. ❧ Serotonin is a neurotransmitter present in the brain.
We found that serotonin can increase cell death in
GBM cells as
compared to serum-free medium.
Advisors/Committee Members: Hofman, Florence M. (Committee Chair), Schonthal, Axel H. (Committee Member), Schönthal, Axel H. (Committee Member), Shih, Jean C. (Committee Member), Landolph, Joseph R., Jr. (Committee Member).
Subjects/Keywords: glioblastoma multiforme; bevacizumab; temozolomide; angiogenesis; macrophages M1 and M2; dendritic cells; serotonin; glioblastoma multiforme (GBM) treatment
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APA ·
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Manager
APA (6th Edition):
Vaikari, V. P. (2016). Molecular targets for treatment of glioblastoma
multiforme. (Masters Thesis). University of Southern California. Retrieved from http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/506490/rec/4207
Chicago Manual of Style (16th Edition):
Vaikari, Vijaya Pooja. “Molecular targets for treatment of glioblastoma
multiforme.” 2016. Masters Thesis, University of Southern California. Accessed March 05, 2021.
http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/506490/rec/4207.
MLA Handbook (7th Edition):
Vaikari, Vijaya Pooja. “Molecular targets for treatment of glioblastoma
multiforme.” 2016. Web. 05 Mar 2021.
Vancouver:
Vaikari VP. Molecular targets for treatment of glioblastoma
multiforme. [Internet] [Masters thesis]. University of Southern California; 2016. [cited 2021 Mar 05].
Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/506490/rec/4207.
Council of Science Editors:
Vaikari VP. Molecular targets for treatment of glioblastoma
multiforme. [Masters Thesis]. University of Southern California; 2016. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/506490/rec/4207
University of New South Wales
20.
Mitic, Gorjana.
Investigation of the role of βIII-tubulin in glioblastoma multiforme tumourigenesis and response to therapy.
Degree: Women's & Children's Health, 2014, University of New South Wales
URL: http://handle.unsw.edu.au/1959.4/53648
;
https://unsworks.unsw.edu.au/fapi/datastream/unsworks:12343/SOURCE02?view=true
► Glioblastoma multiforme (GBM) is the most aggressive primary brain tumour with a very poor prognosis. Treatment usually involves surgical resection, radiotherapy and the chemotherapeutic agent…
(more)
▼ Glioblastoma multiforme (
GBM) is the most aggressive primary brain tumour with a very poor prognosis. Treatment usually involves surgical resection, radiotherapy and the chemotherapeutic agent temozolomide (TMZ). GBMs highly resistant nature frequently renders treatment ineffective. Understanding the mechanisms underlying the resistance phenotype could lead to improved therapeutic approaches. βIII-tubulin is a neuronal specific microtubule protein that is aberrantly expressed in
GBM. Glioma cells of origin do not express it. In contrast, in gliomas, its high histological expression correlates with increasing tumour grade, the functional significance of which is unknown. The aim was to investigate the role of βIII-tubulin in
GBM tumourigenesis and response to chemo- and radio-therapy. Immuno-histochemical staining for βIII-tubulin in patient samples of low and high grades of astrocytoma, including grade IV
GBM confirmed previously reported increasing levels of βIII-tubulin with increasing grades, signifying its potential role in the aggressiveness of
GBM. siRNA-mediated βIII-tubulin knockdown significantly reduced the formation of patient-derived primary
GBM neurospheres. The knockdown did not affect either organisation of a microtubule network or cell proliferation rates in
GBM cell lines. Furthermore,
GBM cells could be significantly sensitised to TMZ and epothilone B upon βIII-tubulin knockdown. The observed increase in cell death post TMZ treatment was associated with enhanced drug-induced senescence. A functional association between βIII-tubulin and p53 accumulation was found, specifically, an increase in transactivation of p53. Additionally, the relationship between βIII tubulin and
GBM response to radiotherapy was investigated. Silencing of βIII-tubulin in
GBM did not increase radio-sensitivity. On examination of other cancers, both non-small cell lung cancer (NSCLC) and pancreatic cancer were significantly radio-sensitised upon βIII-tubulin knockdown. This study also reports a novel phosphorylation on βIII-tubulin residue that is involved in the microtubule dynamic instability. Considering the highly chemo- and radio- resistant nature of
GBM, NSCLC and pancreatic cancer, this new data suggests that βIII tubulin knockdown could be used as a strategy to chemo- and radio-sensitise cancers, improve response to therapy and ultimately patient survival.
Advisors/Committee Members: Kavallaris, Maria, Women's & Children's Health, Faculty of Medicine, UNSW, Ziegler, David, Women's & Children's Health, Faculty of Medicine, UNSW.
Subjects/Keywords: β; III-tubulin; Glioblastoma multiforme tumourigenesis; Glioblastoma multiforme (GBM); Brain tumour; Temozolomide (TMZ); Non-small cell lung cancer (NSCLC); Pancreatic cancer
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APA (6th Edition):
Mitic, G. (2014). Investigation of the role of βIII-tubulin in glioblastoma multiforme tumourigenesis and response to therapy. (Doctoral Dissertation). University of New South Wales. Retrieved from http://handle.unsw.edu.au/1959.4/53648 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:12343/SOURCE02?view=true
Chicago Manual of Style (16th Edition):
Mitic, Gorjana. “Investigation of the role of βIII-tubulin in glioblastoma multiforme tumourigenesis and response to therapy.” 2014. Doctoral Dissertation, University of New South Wales. Accessed March 05, 2021.
http://handle.unsw.edu.au/1959.4/53648 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:12343/SOURCE02?view=true.
MLA Handbook (7th Edition):
Mitic, Gorjana. “Investigation of the role of βIII-tubulin in glioblastoma multiforme tumourigenesis and response to therapy.” 2014. Web. 05 Mar 2021.
Vancouver:
Mitic G. Investigation of the role of βIII-tubulin in glioblastoma multiforme tumourigenesis and response to therapy. [Internet] [Doctoral dissertation]. University of New South Wales; 2014. [cited 2021 Mar 05].
Available from: http://handle.unsw.edu.au/1959.4/53648 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:12343/SOURCE02?view=true.
Council of Science Editors:
Mitic G. Investigation of the role of βIII-tubulin in glioblastoma multiforme tumourigenesis and response to therapy. [Doctoral Dissertation]. University of New South Wales; 2014. Available from: http://handle.unsw.edu.au/1959.4/53648 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:12343/SOURCE02?view=true
UCLA
21.
Yu, Victoria YuiWen.
Improving Glioblastoma Multiforme (GBM) Radiotherapy Outcome through Personalized Biological Modeling and Optimization.
Degree: Biomedical Physics, 2017, UCLA
URL: http://www.escholarship.org/uc/item/9g41w0q6
► Purpose: To investigate the potential in substantially improving Glioblastoma Multiforme (GBM) radiotherapy outcome through personalized spatial dose distributions with 4π radiotherapy and temporal dose fractionation…
(more)
▼ Purpose: To investigate the potential in substantially improving Glioblastoma Multiforme (GBM) radiotherapy outcome through personalized spatial dose distributions with 4π radiotherapy and temporal dose fractionation schedule optimization with patient-specific biological models.Methods: An ordinary differential equation (ODE) model with consideration of cancer stem cell (CSC) dynamics that incorporates the distinct radiosensitivity between CSC and its non-stem counterpart, differentiated cancer cells (DCC) has been developed and shown to be capable of reflecting the definitive treatment failure of GBM was developed. Seven patient-specific models were fitted to match the known times to GBM recurrence of these patients. Recurrence volume of each patient was transferred to generate hypothetical subvolumes with higher tumor aggressiveness on the original clinical plan to receive simultaneous integrated boost (SIB) to study the compound effect in outcome improvement arising from spatial and temporal dose optimization. For each patient, the boost dose is maximized subject to the constraints maintaining acceptable dose to surrounding OARs and coverage to the original planning target volume. With the patient-specific biological models and boost dose, a dose fractionation schedule optimization (FSO) problem with the time interval between fractions and the dose to both the non-boost and boost volumes as variables was formulated and solved with a paired simulated annealing algorithm for boost volumes with a wide range of CSC concentrations. Results:Simultaneous integrated boost (SIB) dosage of up to 245 Gy within a 60 Gy PTV was shown to be feasible with the 4π SIB optimization formulation. Statistically significant OAR sparing was still achieved with 4π SIB compared with the originally delivered clinical plan with no boost. FSO resulted in high dose fractions in the beginning of the treatment course, followed by relatively constant dose fractions. Scenarios with lower CSC concentration within the boost volume resulted in fractionation schedules with dense once per day fractions in the beginning followed by a long time interval in the end with no treatment. With boost volume CSC concentration increased by 100 fold, maximum recurrence delay of up to 392 days was observed for a patient with the slowest growing disease. Conclusions: By combining the spatial dose sparing power of 4π radiotherapy and temporal dose fractionation optimization with a CSC dynamics biological model in a personalized manner, significant potential in GBM disease recurrence delay was demonstrated across a cohort with differing disease characteristics. Further investigation is needed to validate the proposed model and resultant dose fractionation schedules to fully realize and translate these substantial clinical benefits.
Subjects/Keywords: Biomedical engineering; Physics; Cancer Stem Cells; Fractionation schedule optimimization; Glioblastoma Multitforme (GBM); Raiotherapy Optimization
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APA ·
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CSE |
Export
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Manager
APA (6th Edition):
Yu, V. Y. (2017). Improving Glioblastoma Multiforme (GBM) Radiotherapy Outcome through Personalized Biological Modeling and Optimization. (Thesis). UCLA. Retrieved from http://www.escholarship.org/uc/item/9g41w0q6
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Yu, Victoria YuiWen. “Improving Glioblastoma Multiforme (GBM) Radiotherapy Outcome through Personalized Biological Modeling and Optimization.” 2017. Thesis, UCLA. Accessed March 05, 2021.
http://www.escholarship.org/uc/item/9g41w0q6.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Yu, Victoria YuiWen. “Improving Glioblastoma Multiforme (GBM) Radiotherapy Outcome through Personalized Biological Modeling and Optimization.” 2017. Web. 05 Mar 2021.
Vancouver:
Yu VY. Improving Glioblastoma Multiforme (GBM) Radiotherapy Outcome through Personalized Biological Modeling and Optimization. [Internet] [Thesis]. UCLA; 2017. [cited 2021 Mar 05].
Available from: http://www.escholarship.org/uc/item/9g41w0q6.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Yu VY. Improving Glioblastoma Multiforme (GBM) Radiotherapy Outcome through Personalized Biological Modeling and Optimization. [Thesis]. UCLA; 2017. Available from: http://www.escholarship.org/uc/item/9g41w0q6
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
22.
Le, Vinh Nguyen Du.
Evaluation of Diffuse Reflectance Spectroscopy and Fluorescence Spectroscopy for Detection of Glioma Brain Tumors.
Degree: PhD, 2016, McMaster University
URL: http://hdl.handle.net/11375/20739
► Imaging instruments are required for accurate tumor resection during neurosurgery, especially in the case of glioblastoma multiforme (GBM) - the most common and aggressive malignant…
(more)
▼ Imaging instruments are required for accurate tumor resection during neurosurgery, especially in the case of glioblastoma multiforme (GBM) - the most common and aggressive malignant glioma. However, current intraoperative imaging techniques for detection of glioma either suffer low sensitivity and low specificity or require a significant capital cost. Advances in diffuse reflectance spectroscopy and fluorescence spectroscopy have offered high sensitivity and high specificity in differentiating tumors from normal tissues with much lower capital cost. Whereas diffuse reflectance spectroscopy alone and fluorescence spectroscopy alone has been used in limited studies to differentiate normal brain tissues from brain tumors with moderate sensitivity and specificity, low specificity and sensitivity were usually observed when studying high grade glioma (HGG) such as GBM. Furthermore, optical properties and diffuse reflectance signal of HGG and low grade glioma (LGG) have not been observed separately, and thus a relation between optical properties and glioma progression has not been established. Intraoperative differentiation of GBM and LGG can be helpful in making treatment plan at the first surgery.
This thesis focuses on characterizing a previous integrated system of diffuse reflectance spectroscopy and fluorescence spectroscopy to extract optical properties and fluorescence properties of LGG and GBM. First, tissue-simulating phantom models were developed to calibrate the integrated system. The direct method and Mie theory were used to calculate optical scattering of the phantoms while Beer-Lambert’s law was used to calculate optical absorption. Second, an experimental method was introduced to recover intrinsic fluorescence because the measured fluorescence signal is likely distorted by the presence of scatterers and absorbers in tissue (i.e. hemoglobin). Third, an experimental method was developed to recover optical properties of both GBM and LGG. In addition, the sensitivity and specificity of the integrated system was optimized.
Thesis
Doctor of Philosophy (PhD)
Advisors/Committee Members: Fang, Qiyin, Medical Physics.
Subjects/Keywords: optical properties; diffuse reflectance spectroscopy (DRS); fluorescence spectroscopy; glioblastoma multiform (GBM); low grade glioma (LGG)
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APA (6th Edition):
Le, V. N. D. (2016). Evaluation of Diffuse Reflectance Spectroscopy and Fluorescence Spectroscopy for Detection of Glioma Brain Tumors. (Doctoral Dissertation). McMaster University. Retrieved from http://hdl.handle.net/11375/20739
Chicago Manual of Style (16th Edition):
Le, Vinh Nguyen Du. “Evaluation of Diffuse Reflectance Spectroscopy and Fluorescence Spectroscopy for Detection of Glioma Brain Tumors.” 2016. Doctoral Dissertation, McMaster University. Accessed March 05, 2021.
http://hdl.handle.net/11375/20739.
MLA Handbook (7th Edition):
Le, Vinh Nguyen Du. “Evaluation of Diffuse Reflectance Spectroscopy and Fluorescence Spectroscopy for Detection of Glioma Brain Tumors.” 2016. Web. 05 Mar 2021.
Vancouver:
Le VND. Evaluation of Diffuse Reflectance Spectroscopy and Fluorescence Spectroscopy for Detection of Glioma Brain Tumors. [Internet] [Doctoral dissertation]. McMaster University; 2016. [cited 2021 Mar 05].
Available from: http://hdl.handle.net/11375/20739.
Council of Science Editors:
Le VND. Evaluation of Diffuse Reflectance Spectroscopy and Fluorescence Spectroscopy for Detection of Glioma Brain Tumors. [Doctoral Dissertation]. McMaster University; 2016. Available from: http://hdl.handle.net/11375/20739
California State University – San Bernardino
23.
Baghdadchi, Negin.
CYTOKINE CONTROL OF GLIOMA ADHESION AND MIGRATION.
Degree: MSin Biology, Biology, 2014, California State University – San Bernardino
URL: https://scholarworks.lib.csusb.edu/etd/93
► Glioblastoma multiforme (GBM) is the most lethal primary central nervous system tumor, with median survival after diagnosis of less than 12 months because dissemination…
(more)
▼ Glioblastoma multiforme (
GBM) is the most lethal primary central nervous system tumor, with median survival after diagnosis of less than 12 months because dissemination into the brain parenchyma limits the long-term effectiveness of surgical resection, and because
GBM cells are resistant to radiation and chemotherapy. This sad dismal prognosis for patients with
GBM emphasizes the need for greater understand of the fundamental biology of the disease.
Invasion is one of the major causes of treatment failure and death from glioma, because disseminated tumor cells provide the seeds for tumor recurrence. Inflammation is increasingly recognized as an important component of invasion. In the brain, inflammation can occur by activation of microglia, the resident macrophages of the brain, or by tumor-associated blood macrophages. Therefore, we hypothesize that activity of the innate immune system in the brain can influence tumor progression by secreting cytokines such as Tumor Necrosis Factor alpha (TNF-α). In this study, we show that patient-derived glioma spheres undergo morphological changes in response to TNF‑α that are associated with changes in migration behavior in vitro. These morphological changes include appearance of tumor islands in site different from where the primary tumor cells were seeded. We further showed that TNF‑α treated cells significantly increased expression of cell adhesion molecules such as CD44 and VCAM-1. Furthermore, we demonstrate increased cell density also caused increased in expression of cell adhesion molecules. The extent to which these are recapitulated in vivo will be investigated.
Advisors/Committee Members: Nicole Bournias-Vardiabasis.
Subjects/Keywords: Glioblastoma multiforme (GBM); TNF-α; Microglia; Invasion; Biological Phenomena, Cell Phenomena, and Immunity
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APA (6th Edition):
Baghdadchi, N. (2014). CYTOKINE CONTROL OF GLIOMA ADHESION AND MIGRATION. (Thesis). California State University – San Bernardino. Retrieved from https://scholarworks.lib.csusb.edu/etd/93
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Baghdadchi, Negin. “CYTOKINE CONTROL OF GLIOMA ADHESION AND MIGRATION.” 2014. Thesis, California State University – San Bernardino. Accessed March 05, 2021.
https://scholarworks.lib.csusb.edu/etd/93.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Baghdadchi, Negin. “CYTOKINE CONTROL OF GLIOMA ADHESION AND MIGRATION.” 2014. Web. 05 Mar 2021.
Vancouver:
Baghdadchi N. CYTOKINE CONTROL OF GLIOMA ADHESION AND MIGRATION. [Internet] [Thesis]. California State University – San Bernardino; 2014. [cited 2021 Mar 05].
Available from: https://scholarworks.lib.csusb.edu/etd/93.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Baghdadchi N. CYTOKINE CONTROL OF GLIOMA ADHESION AND MIGRATION. [Thesis]. California State University – San Bernardino; 2014. Available from: https://scholarworks.lib.csusb.edu/etd/93
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
University of Western Ontario
24.
Albatany, Mohammed.
Acute Pharmacologic Modulation of Glioblastoma pH Monitored by Chemical Exchange Saturation Transfer Magnetic Resonance Imaging.
Degree: 2018, University of Western Ontario
URL: https://ir.lib.uwo.ca/etd/6056
► The response of tumor intracellular pH (pHi) to a pharmacological challenge could help identify aggressive cancer. In addition, tumor pHi may influence cell proliferation, apoptosis,…
(more)
▼ The response of tumor intracellular pH (pHi) to a pharmacological challenge could help identify aggressive cancer. In addition, tumor pHi may influence cell proliferation, apoptosis, chemotherapy resistance, and thermosensitivity. Chemical exchange saturation transfer (CEST) is a novel MRI contrast mechanism that is sensitive to cellular pH. More specifically, a CEST method called amine and amide concentration-independent detection (AACID) produces images weighted by intracellular pH (pHi) and can be used to study pharmacologic pH modulation in tumours.
The overall goal of this thesis was to maximize the magnitude of intracellular tumour acidification using pharmacologic agents. Several different drugs were studied, and we hypothesized that simulatenously blocking multiple pH regulatory mechanisms while also providing glucose as an energy substrate would increase the acute pH modulation effect. AACID CEST images were acquired in mice with glioblastoma using a 9.4T MRI scanner to measure acidification in tumours within the first two hours after treatment with dichloroacetate (DCA), cariporide, and five different drugs plus glucose.
Intravenous DCA injection produced a significant 0.04±0.01 increase in tumor AACID level corresponding to a 0.16 decrease in pHi. Intraperitoneal cariporide injection produced a significant 0.12±0.03 increase in tumor AACID value corresponding to a 0.48 decrease in pHi. Intraperitoneal injection of five drugs, plus glucose produced a 0.18±0.03 increase in AACID value corresponding to a 0.72 decrease in pHi.
Combination treatment produced the greatest tumour acidification. pH-weighted MRI in combination with a drug challenge represents a unique approach to cancer detection does not require injection of an imaging contrast agent.
Subjects/Keywords: Brain cancer; Glioblastoma multiforme(GBM); Apoptosis; pH; MRI; CEST; Medical Biophysics; Neoplasms; Oncology
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Export
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APA (6th Edition):
Albatany, M. (2018). Acute Pharmacologic Modulation of Glioblastoma pH Monitored by Chemical Exchange Saturation Transfer Magnetic Resonance Imaging. (Thesis). University of Western Ontario. Retrieved from https://ir.lib.uwo.ca/etd/6056
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Albatany, Mohammed. “Acute Pharmacologic Modulation of Glioblastoma pH Monitored by Chemical Exchange Saturation Transfer Magnetic Resonance Imaging.” 2018. Thesis, University of Western Ontario. Accessed March 05, 2021.
https://ir.lib.uwo.ca/etd/6056.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Albatany, Mohammed. “Acute Pharmacologic Modulation of Glioblastoma pH Monitored by Chemical Exchange Saturation Transfer Magnetic Resonance Imaging.” 2018. Web. 05 Mar 2021.
Vancouver:
Albatany M. Acute Pharmacologic Modulation of Glioblastoma pH Monitored by Chemical Exchange Saturation Transfer Magnetic Resonance Imaging. [Internet] [Thesis]. University of Western Ontario; 2018. [cited 2021 Mar 05].
Available from: https://ir.lib.uwo.ca/etd/6056.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Albatany M. Acute Pharmacologic Modulation of Glioblastoma pH Monitored by Chemical Exchange Saturation Transfer Magnetic Resonance Imaging. [Thesis]. University of Western Ontario; 2018. Available from: https://ir.lib.uwo.ca/etd/6056
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
25.
Duffy, Joseph.
EVALUATING THE EFFECTS OF FASTING CONDITIONS IN COMBINATION WITH TEMOZOLOMIDE FOR THE TREATMENT OF GLIOBLASTOMA MULTIFORME.
Degree: MS, Biology, 2020, Northen Michigan University
URL: https://commons.nmu.edu/theses/638
► Glioblastoma multiforme (GBM) is the most aggressive and lethal form of adult brain cancer. The standard of care for GBM is maximal surgical resection…
(more)
▼ Glioblastoma multiforme (
GBM) is the most aggressive and lethal form of adult brain cancer. The standard of care for
GBM is maximal surgical resection followed by adjuvant treatment with the chemotherapeutic agent temozolomide (TMZ) and radiotherapy. O-6-methylguanine-DNA methyltransferase (MGMT) is a DNA repair protein involved in TMZ resistance. Known as the Warburg effect, cancer cells will preferentially oxidize glucose to lactate in glycolysis. This less effective pathway of energy production means cancer cells must uptake significantly greater amounts of glucose to sustain physiological needs. One method that directly targets the bioavailability of glucose is fasting. Among other adaptations, fasting lowers systemic glucose levels and elevates ketone bodies like ß-hydroxybutyrate (ß-HB). This study sought to evaluate the effects of fasting in combination with TMZ on viability of
GBM cell lines LN229 and T98G, and normal astroglial cell line SVG p12. Glucose restriction significantly enhanced the cytotoxic effects of TMZ in LN229 and T98G cells, while having no effect in SVG p12 cells. ß-HB in combination with TMZ potentiated the cytotoxicity of TMZ in LN229 and T98G cells, while reducing the cytotoxicity of TMZ in SVG p12 cells. Furthermore, both glucose restriction and ß-HB supplementation in combination with TMZ significantly decreased the expression of MGMT levels in T98G cells. Together, this initial evidence suggests fasting may be a useful method to selectively sensitize
GBM cells to TMZ, while protecting normal cells. Future research is needed to further assess the efficacy of fasting as an adjuvant therapy in the treatment of
GBM.
Advisors/Committee Members: Robert Winn, Ph.D., Dean, College of Arts and Sciences.
Subjects/Keywords: Glioblastoma Multiforme; GBM; Temozolomide; MGMT; Fasting; Ketone Bodies; Hydroxybutyrate; UMBTC; Cancer Biology
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Export
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APA (6th Edition):
Duffy, J. (2020). EVALUATING THE EFFECTS OF FASTING CONDITIONS IN COMBINATION WITH TEMOZOLOMIDE FOR THE TREATMENT OF GLIOBLASTOMA MULTIFORME. (Thesis). Northen Michigan University. Retrieved from https://commons.nmu.edu/theses/638
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Duffy, Joseph. “EVALUATING THE EFFECTS OF FASTING CONDITIONS IN COMBINATION WITH TEMOZOLOMIDE FOR THE TREATMENT OF GLIOBLASTOMA MULTIFORME.” 2020. Thesis, Northen Michigan University. Accessed March 05, 2021.
https://commons.nmu.edu/theses/638.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Duffy, Joseph. “EVALUATING THE EFFECTS OF FASTING CONDITIONS IN COMBINATION WITH TEMOZOLOMIDE FOR THE TREATMENT OF GLIOBLASTOMA MULTIFORME.” 2020. Web. 05 Mar 2021.
Vancouver:
Duffy J. EVALUATING THE EFFECTS OF FASTING CONDITIONS IN COMBINATION WITH TEMOZOLOMIDE FOR THE TREATMENT OF GLIOBLASTOMA MULTIFORME. [Internet] [Thesis]. Northen Michigan University; 2020. [cited 2021 Mar 05].
Available from: https://commons.nmu.edu/theses/638.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Duffy J. EVALUATING THE EFFECTS OF FASTING CONDITIONS IN COMBINATION WITH TEMOZOLOMIDE FOR THE TREATMENT OF GLIOBLASTOMA MULTIFORME. [Thesis]. Northen Michigan University; 2020. Available from: https://commons.nmu.edu/theses/638
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
University of Melbourne
26.
Atkins, Ryan James.
The role of quiescence in treatment resistance and malignancy in glioblastoma multiforme.
Degree: 2018, University of Melbourne
URL: http://hdl.handle.net/11343/212465
► Glioblastoma multiforme (GBM) represents the most malignant incarnation of glial tumours – a World Health Organisation (WHO) grade IV brain malignancy. GBM is the most…
(more)
▼ Glioblastoma multiforme (GBM) represents the most malignant incarnation of glial tumours – a World Health Organisation (WHO) grade IV brain malignancy. GBM is the most common primary brain tumour in adults, accounting for 78% of all malignant central nervous system (CNS) tumours, and affecting 2-3 people per 100,000 in Europe and North America, with an average survival of only 14.6 months. Despite continued research and incremental advances in imaging, surgery, and chemoradiotherapy, patient survival has stagnated in the past decade, with several promising lines of investigation failing to fully deliver on their anticipated translational outcomes.
Recent advances in genetic sequencing and computational biology have allowed the simultaneous comparison of large numbers of patient cancer cell genomes and identified several GBM subtypes. It is hoped that such stratification will one day allow clinicians to tailor treatments specific to each GBM subtype as has already happened in cancers like medulloblastoma. However, despite best efforts, GBM remains highly aggressive, infiltrative, and treatment-resistant, rendering it incurable by current treatment modalities. Invasion of tumour cells into normal brain prohibits a surgical cure, while a high cancer stem cell (CSC) component resists treatment with radiation and temozolomide (TMZ) – both of which are more effective against rapidly dividing cells – and relapse remains the rule. Molecular mechanisms underlie GBM’s treatment resistance, and elucidating the key drivers that garner inherent resistance to the quiescent, stem-like fraction of cells that lead to treatment failure therefore presents as an exciting area of research that may uncover new potential drug targets that improve patient outcomes.
This study has shown that the proliferation rate of GBM cells is spectral, approximating a positively skewed normal distribution, with highly proliferative cells at one end and quiescent cells at the other. The quiescent cell fraction was subsequently shown to be inherently more resistant to chemoradiotherapy than the proliferative fraction. The quiescent fraction also displayed increased size, complexity, rates of migration and invasion, secretion of extracellular matrix-degrading enzymes, and invadopodia activity than their proliferative counterparts. Similarly, quiescent cells proliferated slower as intracranial tumours but displayed significantly greater invasive properties than a subset of proliferative cells grown in vivo.
mRNA expression analysis revealed the genetic signature that underpins the disparity in proliferation rate between quiescent and proliferative cells, and the putative genes that are responsible for the malignant properties identified in both populations.
This body of work has uncovered the inherently dichotomous treatment response of quiescent and rapidly dividing GBM cells, as well as the difference in their abilities to migrate and invade. This study has also shed light on the fundamental molecular mechanisms that are at the root of…
Subjects/Keywords: GBM; glioma; glioblastoma; quiescence; invasion; migration; proliferation; temozolomide; radiation; chemoradiotherapy; treatment; resistance; TMZ; XRT
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APA ·
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Export
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APA (6th Edition):
Atkins, R. J. (2018). The role of quiescence in treatment resistance and malignancy in glioblastoma multiforme. (Doctoral Dissertation). University of Melbourne. Retrieved from http://hdl.handle.net/11343/212465
Chicago Manual of Style (16th Edition):
Atkins, Ryan James. “The role of quiescence in treatment resistance and malignancy in glioblastoma multiforme.” 2018. Doctoral Dissertation, University of Melbourne. Accessed March 05, 2021.
http://hdl.handle.net/11343/212465.
MLA Handbook (7th Edition):
Atkins, Ryan James. “The role of quiescence in treatment resistance and malignancy in glioblastoma multiforme.” 2018. Web. 05 Mar 2021.
Vancouver:
Atkins RJ. The role of quiescence in treatment resistance and malignancy in glioblastoma multiforme. [Internet] [Doctoral dissertation]. University of Melbourne; 2018. [cited 2021 Mar 05].
Available from: http://hdl.handle.net/11343/212465.
Council of Science Editors:
Atkins RJ. The role of quiescence in treatment resistance and malignancy in glioblastoma multiforme. [Doctoral Dissertation]. University of Melbourne; 2018. Available from: http://hdl.handle.net/11343/212465
University of New South Wales
27.
Abuhusain , Hazem Jasim.
Investigating Sphingolipid Metabolism in Glioblastoma.
Degree: Clinical School - Prince of Wales Hospital, 2013, University of New South Wales
URL: http://handle.unsw.edu.au/1959.4/53729
;
https://unsworks.unsw.edu.au/fapi/datastream/unsworks:12424/SOURCE02?view=true
► Glioblastoma (GBM), a genetically heterogeneous disease, has a significant burden onour society. Currently, the standard treatment for newly diagnosed GBM patientsconsists of surgery followed by…
(more)
▼ Glioblastoma (
GBM), a genetically heterogeneous disease, has a significant burden onour society. Currently, the standard treatment for newly diagnosed
GBM patientsconsists of surgery followed by concomitant radiotherapy and temozolomidechemotherapy, resulting in a median survival of 12-15 months. Targeted therapies arebeing developed to inhibit oncogenes based upon
GBM molecular profiling, thoughhave not been as successful as expected. Our understanding of DNA and RNAalterations in
GBM has grown considerably over the past few years. However, ourunderstanding of the lipid biology, specifically sphingolipids, in
GBM is lagging andmay prove useful in the arsenal of targeted therapies. The sphingolipid pathwaycontains lipid signalling molecules, which modulate cellular survival through thebalance of ceramide, a pro-apoptotic metabolite, and Sphingosine-1-Phosphate (S1P), apro-survival metabolite.Herein, I characterise for the first time the sphingolipid profile of normal grey matter(NGM), diffuse astrocytomas (AII), anaplastic astrocytomas (AIII), and
GBM usingliquid chromatography tandem mass spectrometry. The lipid profile is supported by anenzyme expression profile favouring ceramide catabolism and S1P formation, includingupregulation of acid ceramidase (ASAH1) and sphingosine kinase 1 (SPHK1), and adown regulation of S1P phosphatase 2 (SGPP2). Significantly, C18 ceramide wasreduced 5-fold in
GBM compared to NGM, while S1P was increased in
GBM byapproximately 9-fold compared to NGM. Based on the sphingolipid profiles, ASAH1and SPHK1 were assessed for functional relevance in vitro. Using gene silencing andpharmacological inhibition, I found SPHK1 to be critical for U87MG-inducedangiogenesis through S1P paracrine signalling, which was independent of VEGF levels.EGFR mutations were associated with increased C16 and C22 ceramide levels. For thefirst time, I measured sphingolipid metabolites in plasma extracted from
GBM patientsand healthy controls. Elevated levels of S1P were found in
GBM plasma and togetherwith tumour S1P levels, were associated with a poor survival outcome. In contrast lowS1P levels in tissue combined with MGMT methylation was associated with a goodsurvival outcome.Overall, the data presented in this thesis reaffirm the importance of sphingolipidmetabolism in
GBM biology, reflected by a shift in the ceramide-S1P balance,favouring the pro-angiogenic S1P. Additionally, sphingolipid interactions with alteredgenetic pathways and potential biomarker capacity are novel findings that requirefurther validation, with the hope of informing and monitoring therapeutic responses forGBM patients.
Advisors/Committee Members: McDonald, Kerrie, Clinical School - Prince of Wales Hospital, Faculty of Medicine, UNSW, Don, Anthony, Clinical School - Prince of Wales Hospital, Faculty of Medicine, UNSW.
Subjects/Keywords: Glioblastoma; Sphingosine-1-phosphate; Ceramide; Gliomas; Sphingolipids; Angiogenesis; Sphingosine kinase 1; GBM; S1P; SPHK1; SPHK2
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APA ·
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Export
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APA (6th Edition):
Abuhusain , H. J. (2013). Investigating Sphingolipid Metabolism in Glioblastoma. (Doctoral Dissertation). University of New South Wales. Retrieved from http://handle.unsw.edu.au/1959.4/53729 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:12424/SOURCE02?view=true
Chicago Manual of Style (16th Edition):
Abuhusain , Hazem Jasim. “Investigating Sphingolipid Metabolism in Glioblastoma.” 2013. Doctoral Dissertation, University of New South Wales. Accessed March 05, 2021.
http://handle.unsw.edu.au/1959.4/53729 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:12424/SOURCE02?view=true.
MLA Handbook (7th Edition):
Abuhusain , Hazem Jasim. “Investigating Sphingolipid Metabolism in Glioblastoma.” 2013. Web. 05 Mar 2021.
Vancouver:
Abuhusain HJ. Investigating Sphingolipid Metabolism in Glioblastoma. [Internet] [Doctoral dissertation]. University of New South Wales; 2013. [cited 2021 Mar 05].
Available from: http://handle.unsw.edu.au/1959.4/53729 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:12424/SOURCE02?view=true.
Council of Science Editors:
Abuhusain HJ. Investigating Sphingolipid Metabolism in Glioblastoma. [Doctoral Dissertation]. University of New South Wales; 2013. Available from: http://handle.unsw.edu.au/1959.4/53729 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:12424/SOURCE02?view=true
University of Cincinnati
28.
Aljohani, Hashim M., B.S.
Signaling Pathways Associated with Gefitinib Resistance in
Glioblastoma Multiforme (GBM).
Degree: MS, Medicine: Molecular Genetics, Biochemistry, and
Microbiology, 2014, University of Cincinnati
URL: http://rave.ohiolink.edu/etdc/view?acc_num=ucin1406900804
► Glioblastoma multiforme (GBM) is the most aggressive brain tumor in adults and remains incurable despite multimodal intensive treatment regimens. The majority of GBM tumors show…
(more)
▼ Glioblastoma multiforme (
GBM) is the most aggressive
brain tumor in adults and remains incurable despite multimodal
intensive treatment regimens. The majority of
GBM tumors show a
mutated or overexpressed EGFR. However, the kinase domain mutations
that usually correlate with response to the tyrosine kinase
inhibitors in other cancers are infrequent in glioblastomas and
phase II trials of the tyrosine kinase inhibitor (TKI), gefitinib
showed no survival benefit in
glioblastoma. Furthermore, tumors
treated with the TKIs will inevitably recur highlighting the need
to identify signaling pathways involved in
GBM resistance to TKIs.
To this end, we treated
GBM cells that over express EGFR with
increasing concentrations of Gefitinib and isolated resistant
clones. These resistant clones were
subject to RNAseq and the
expression of several genes was found to be upregulated in these
clones. These genes are all tyrosine kinase receptors and include
ROS1, DDR1 and PDGFRA. The upregulation of these genes was
confirmed at the protein level by western blot. Treatment with ROS1
inhibitors in ROS1 overexpressing clones led to sensitization of
these clones to gefitinib. Our current study led to the discovery
of alternative pathways used by
GBM cells to evade cell death
following treatment with gefitinib and identifies new therapeutic
targets to prevent
GBM cell resistance to the drug.
Advisors/Committee Members: Bahassi, El Mustapha (Committee Chair).
Subjects/Keywords: Surgery; Glioblastoma multiforme; EGFR; tyrosine kinase inhibitor; GBM resistance to TKIs; Gefitinib; ROS1
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APA (6th Edition):
Aljohani, Hashim M., B. S. (2014). Signaling Pathways Associated with Gefitinib Resistance in
Glioblastoma Multiforme (GBM). (Masters Thesis). University of Cincinnati. Retrieved from http://rave.ohiolink.edu/etdc/view?acc_num=ucin1406900804
Chicago Manual of Style (16th Edition):
Aljohani, Hashim M., B S. “Signaling Pathways Associated with Gefitinib Resistance in
Glioblastoma Multiforme (GBM).” 2014. Masters Thesis, University of Cincinnati. Accessed March 05, 2021.
http://rave.ohiolink.edu/etdc/view?acc_num=ucin1406900804.
MLA Handbook (7th Edition):
Aljohani, Hashim M., B S. “Signaling Pathways Associated with Gefitinib Resistance in
Glioblastoma Multiforme (GBM).” 2014. Web. 05 Mar 2021.
Vancouver:
Aljohani, Hashim M. BS. Signaling Pathways Associated with Gefitinib Resistance in
Glioblastoma Multiforme (GBM). [Internet] [Masters thesis]. University of Cincinnati; 2014. [cited 2021 Mar 05].
Available from: http://rave.ohiolink.edu/etdc/view?acc_num=ucin1406900804.
Council of Science Editors:
Aljohani, Hashim M. BS. Signaling Pathways Associated with Gefitinib Resistance in
Glioblastoma Multiforme (GBM). [Masters Thesis]. University of Cincinnati; 2014. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=ucin1406900804
University of Lund
29.
Enriquez Perez, Julio.
Immunological aspects of intratumoral chemotherapy and
immunotherapy in malignant brain tumors.
Degree: 2020, University of Lund
URL: https://lup.lub.lu.se/record/6f107ade-24c0-4ad0-8075-477884ac1f84
;
https://portal.research.lu.se/ws/files/77393474/Julio_Enriquez_Avhandling.pdf
► Advances in surgery, chemo- and radiotherapy have only modestly improved survival rates of malignant brain tumor patients during the last decades. Emerging evidence suggests that…
(more)
▼ Advances in surgery, chemo- and radiotherapy have
only modestly improved survival rates of malignant brain tumor
patients during the last decades. Emerging evidence suggests that
an efficient treatment of malignant brain tumors will likely
require the management of multiple aspects of tumor pathobiology in
order to manipulate features as tumor heterogeneity and tumor
immunosuppression. Immunotherapy based on peripheral vaccination of
autologous tumor cells target both dividing and non-dividing tumor
cells and lead to immunological memory. Moreover, intratumoral
administration of chemotherapeutic drugs, also referred to as
convection-enhanced delivery (CED), is a technique used to
circumvent the blood-brain barrier (BBB) and increase the drug
distribution within the tumor, while reducing the systemic side
effects associated with systemically delivered chemotherapeutic
drugs.In this doctoral thesis, I propose intratumoral delivery of
cytostatic drugs and immunotherapy as combined tools to treat
malignant brain tumors. Thus, the treatment efficacy and the
immune-related mechanisms of CED of clinically relevant cytostatic
drugs and immunotherapy were investigated in glioma mouse models.
CED of temozolomide (CED-TMZ) cured GL261-bearing mice and acted
synergistically with wildtype cell immunizations. In addition, CED-
TMZ was more effective and less toxic than single intratumoral
injections of TMZ in the GL261 model. CED-TMZ prolonged survival in
KR158-bearing mice but cure was only achieved with immunotherapy as
a monotherapy and in combination with CED-TMZ. The immune
dependence of the therapeutic effect of CED-TMZ was confirmed in
immunocompromised mice bearing GL261. Infiltration of CD8+ and CD4+
T cells was increased in both models after CED-TMZ and
immunization. CED of cisplatin (CED-CIS) induced cure in the GL261
model. As for CED-TMZ, the effect of CED-CIS was abrogated in
immunocompromised mice. However, cell immunizations did not have
any additive effect with CED-CIS. CED of mitoxantrone cured both
GL261- and SB28-bearing mice. In addition, plasma samples from
pediatric brain tumor patients were immune-profiled using cytokine
multiplex arrays. We identified two patient groups with distinct
preoperative inflammatory cytokine profiles that could be used as
peripheral biomarkers to help design, predict or monitor the
response of immunotherapy.Altogether, these results have important
implications for the future development and implementation of
locally administered cytostatic drugs and immunotherapy against
malignant brain tumors.
Subjects/Keywords: Cancer and Oncology; Glioblastoma (GBM); Immunotherapy; Mouse glioma; Convection-enhanced delivery; Intratumoral chemotherapy; Glioblastom; Immuneterapi
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APA (6th Edition):
Enriquez Perez, J. (2020). Immunological aspects of intratumoral chemotherapy and
immunotherapy in malignant brain tumors. (Doctoral Dissertation). University of Lund. Retrieved from https://lup.lub.lu.se/record/6f107ade-24c0-4ad0-8075-477884ac1f84 ; https://portal.research.lu.se/ws/files/77393474/Julio_Enriquez_Avhandling.pdf
Chicago Manual of Style (16th Edition):
Enriquez Perez, Julio. “Immunological aspects of intratumoral chemotherapy and
immunotherapy in malignant brain tumors.” 2020. Doctoral Dissertation, University of Lund. Accessed March 05, 2021.
https://lup.lub.lu.se/record/6f107ade-24c0-4ad0-8075-477884ac1f84 ; https://portal.research.lu.se/ws/files/77393474/Julio_Enriquez_Avhandling.pdf.
MLA Handbook (7th Edition):
Enriquez Perez, Julio. “Immunological aspects of intratumoral chemotherapy and
immunotherapy in malignant brain tumors.” 2020. Web. 05 Mar 2021.
Vancouver:
Enriquez Perez J. Immunological aspects of intratumoral chemotherapy and
immunotherapy in malignant brain tumors. [Internet] [Doctoral dissertation]. University of Lund; 2020. [cited 2021 Mar 05].
Available from: https://lup.lub.lu.se/record/6f107ade-24c0-4ad0-8075-477884ac1f84 ; https://portal.research.lu.se/ws/files/77393474/Julio_Enriquez_Avhandling.pdf.
Council of Science Editors:
Enriquez Perez J. Immunological aspects of intratumoral chemotherapy and
immunotherapy in malignant brain tumors. [Doctoral Dissertation]. University of Lund; 2020. Available from: https://lup.lub.lu.se/record/6f107ade-24c0-4ad0-8075-477884ac1f84 ; https://portal.research.lu.se/ws/files/77393474/Julio_Enriquez_Avhandling.pdf
University of Vienna
30.
van Schoonhoven, Sushilla Tamara.
Characterization of fibroblast growth factor receptor 4 as contributor to oncogenesis in Glioblastoma multiforme.
Degree: 2018, University of Vienna
URL: http://othes.univie.ac.at/50626/
► Mit 45-55% aller malignen Gliomen ist das Glioblastom (GBM) der häufigste Tumor des zentralen Nervensystems (ZNS) in Erwachsenen. Das GBM ist der aggressivste primäre Gehirntumor…
(more)
▼ Mit 45-55% aller malignen Gliomen ist das Glioblastom (GBM) der häufigste Tumor des zentralen Nervensystems (ZNS) in Erwachsenen. Das GBM ist der aggressivste primäre Gehirntumor und gehört zur Gruppe der hochgradigen Astrozytome, welche sich durch eine besonders niedrige Überlebenszeit von 14 Monaten auszeichnet. Besonders charakteristisch für das GBM sind seine heterogene Zellpopulation, starke Vaskularisierung und strichförmige Nekrosen, welche die wichtigsten histo- pathologischen Merkmale des Tumors darstellen. In Bezug auf die molekular-diagnostischen Eigenschaften dieser Entität sind besonders Mutationen in den Genen der Isozitrat-Dehydrogenase 1/2 (IDH1/2), des Telomerase reverse Transkriptase (TERT) Promoters, des O6-Methylguanin Methyltransferase (MGMT) Promoters und Amplifikationen des epidermalen Wachstumsfakor-Rezeptor (EGFR) Gens nennenswert. Trotz intensiver Forschung im Bereich der zielgerichteten Krebstherapie, wurden bisher keine GBM-spezifischen Biomarker identifiziert und auch die zuvor genannten molekularen Marker konnten nicht dafür genutzt werden. Frühere Beobachtungen in unsere Arbeitsgruppe ergaben gesteigerte Zellproliferation und Tumorwachstum in vivo welche stark von fibroblastischen Wachstumsfaktoren (FGFs) beeinflusst wurden. Basierend auf diesen vorherigen Ergebnissen konzentriert sich diese Studie auf FGF Rezeptor 4 (FGFR4), die Unterschiede zwischen seinen Varianten (Arg388 und Gly388), und dessen Rolle in GBM -Wachstum, -Aggressivität, -migration und 3D-Wachstum in vitro. Um FGFR4 in FGFR4 niedrig exprimierende GBM Zelllinien über zu exprimieren, wurden U251MG und HU-MI mit FGFR4 Arg388 oder Gly388 Expressionsvektoren transfiziert. Klonformation, 3D-Wachstum, und Migrationspotential wurden in den transfizierten Zellmodellen untersucht. FGFR4 Arg388 und Gly388 Überexprimierung hat induzierte Migration in U251MG zur Folge. Dieser Effekt konnte jedoch nicht in transfizierten HU-MI Zellen nachgewiesen werden. Bemerkenswerterweise zeigen alle transfizierten Zellmodelle außer HU-MI FGFR4 Gly388 gesteigertes Klon- und 3D-wachstum. Zusammenfassend ist wichtig zu erwähnen, dass induzierte FGFR4 (Arg388 und Gly388) Expression in U251MG zu verstärkter Migration, Klon- und 3D-Wachstum führt. Weiterführend wird die Funktion von FGFR4 noch in vivo untersucht werden.
Glioblastoma multiforme (GBM) is a high-grade astrocytoma and accounts for 45-55% of all malignant gliomas in adults. GBM represents the most aggressive primary brain tumor and survival rates are very low with a median overall survival of 14 months under treatment and a 5-year survival of only 5.5%. A heterogenous cell population, high vascularization and pseudopalisading necrosis are the main histopathological characteristics typifying GBM tumor tissue. Molecular features such as isocitrate dehydrogenase 1/2 (IDH 1/2) mutations, telomerase reverse transcriptase (TERT) promoter mutations, O6-methylguanine DNA methyltransferase (MGMT) promoter methylation and epidermal growth factor receptor (EGFR) amplification are parameters used…
Subjects/Keywords: 42.13 Molekularbiologie; 42.20 Genetik; Gliomen / Glioblastom / GBM / FGFR4 / Gly388Arg / Klonierung / Migration / 3D-Wachstum / Klonformation; Gliomas / Glioblastoma / GBM / FGFR4 / Gly388Arg / Cloning / Migration / 3D-Growth / Colony formation
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APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
van Schoonhoven, S. T. (2018). Characterization of fibroblast growth factor receptor 4 as contributor to oncogenesis in Glioblastoma multiforme. (Thesis). University of Vienna. Retrieved from http://othes.univie.ac.at/50626/
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
van Schoonhoven, Sushilla Tamara. “Characterization of fibroblast growth factor receptor 4 as contributor to oncogenesis in Glioblastoma multiforme.” 2018. Thesis, University of Vienna. Accessed March 05, 2021.
http://othes.univie.ac.at/50626/.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
van Schoonhoven, Sushilla Tamara. “Characterization of fibroblast growth factor receptor 4 as contributor to oncogenesis in Glioblastoma multiforme.” 2018. Web. 05 Mar 2021.
Vancouver:
van Schoonhoven ST. Characterization of fibroblast growth factor receptor 4 as contributor to oncogenesis in Glioblastoma multiforme. [Internet] [Thesis]. University of Vienna; 2018. [cited 2021 Mar 05].
Available from: http://othes.univie.ac.at/50626/.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
van Schoonhoven ST. Characterization of fibroblast growth factor receptor 4 as contributor to oncogenesis in Glioblastoma multiforme. [Thesis]. University of Vienna; 2018. Available from: http://othes.univie.ac.at/50626/
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
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