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11 results on '"Philip, Beatrice"'

3. Mutant IDH1 Promotes Glioma Formation In Vivo

Author

Philip, Beatrice, primary, Yu, Diana X., additional, Silvis, Mark R., additional, Shin, Clifford H., additional, Robinson, James P., additional, Robinson, Gemma L., additional, Welker, Adam E., additional, Angel, Stephanie N., additional, Tripp, Sheryl R., additional, Sonnen, Joshua A., additional, VanBrocklin, Matthew W., additional, Gibbons, Richard J., additional, Looper, Ryan E., additional, Colman, Howard, additional, and Holmen, Sheri L., additional

Published
2018
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4. TMOD-45. DEFINING THE ROLE OF MUTANT IDH IN GLIOMA INITIATION

Author

Philip, Beatrice, primary, Silvis, Mark, additional, Yu, Diana, additional, Shin, Clifford, additional, Robinson, James, additional, Sonnen, Joshua, additional, Welker, Adam, additional, VanBrocklin, Matthew, additional, Colman, Howard, additional, and Holmen, Sheri, additional

Published
2017
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5. Association of cytotoxic T lymphocyte-associated antigen 4 gene single nucleotide polymorphism with type 1 diabetes mellitus in Madurai population of Southern India

Author

Philip, Beatrice and Isabel, W.

Subjects
South India -- Health aspects, T cells -- Genetic aspects -- Health aspects, Type 1 diabetes -- Diagnosis -- Care and treatment -- Demographic aspects -- Genetic aspects, Single nucleotide polymorphisms -- Identification and classification -- Genetic aspects -- Health aspects, Health, Science and technology
Abstract

Byline: Beatrice. Philip, W. Isabel Type 1 diabetes mellitus formerly called juvenile diabetes, is an organ specific T-cell mediated autoimmune disease characterized by the progressive loss of function of the [...]

Published
2011

6. An Investigation Into the Molecular Mechanisms and Genes Involved in Hypoxic Signalling Pathways in Neural Crest Derived Tumours

Author

Philip, Beatrice

Subjects
Cancer cells, Prolyl hydroxylases (PHDs), Hypoxia-inducing factors (HIF’s)
Abstract

Hypoxia-inducing factors (HIF’s) are master regulators of metastasis in most solid tumours because of their ability to cause rapid cell proliferation, glycolytic metabolism, angiogenesis, and tumour invasiveness. Considerable progress has been made in defining HIF function in many hallmarks of carcinogenesis, including primary and metastatic tumour aggressiveness, poor prognosis, radio and chemotherapeutic resistance, vascular remodelling, inflammation, and hypoxia/ischemia induced cell damage. Hypoxic activation of HIF’s is gaining prominence in many cancer types as an essential mediator of malignant progression to metastasis. However, in neuroendocrine tumours of neural crest origin, hypoxia is often associated with dysfunction in genes encoding key enzymes of the TCA cycle leading to abnormally high levels of particular metabolites such as succinate that cause HIF stabilization.

Published
2014
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8. An Investigation Into the Molecular Mechanisms and Genes Involved in Hypoxic Signalling Pathways in Neural Crest Derived Tumours

Author

Ralph, Steve, McMillan, Nigel, Philip, Beatrice, Ralph, Steve, McMillan, Nigel, and Philip, Beatrice

Abstract

Full Text, Thesis (PhD Doctorate), Doctor of Philosophy (PhD), School of Medical Science, Griffith Health, Hypoxia-inducing factors (HIF’s) are master regulators of metastasis in most solid tumours because of their ability to cause rapid cell proliferation, glycolytic metabolism, angiogenesis, and tumour invasiveness. Considerable progress has been made in defining HIF function in many hallmarks of carcinogenesis, including primary and metastatic tumour aggressiveness, poor prognosis, radio and chemotherapeutic resistance, vascular remodelling, inflammation, and hypoxia/ischemia induced cell damage. Hypoxic activation of HIF’s is gaining prominence in many cancer types as an essential mediator of malignant progression to metastasis. However, in neuroendocrine tumours of neural crest origin, hypoxia is often associated with dysfunction in genes encoding key enzymes of the TCA cycle leading to abnormally high levels of particular metabolites such as succinate that cause HIF stabilization.

Published
2014

9. Mutant IDH1Promotes Glioma Formation In Vivo

Author

Philip, Beatrice, Yu, Diana X., Silvis, Mark R., Shin, Clifford H., Robinson, James P., Robinson, Gemma L., Welker, Adam E., Angel, Stephanie N., Tripp, Sheryl R., Sonnen, Joshua A., VanBrocklin, Matthew W., Gibbons, Richard J., Looper, Ryan E., Colman, Howard, and Holmen, Sheri L.

Abstract

Isocitrate dehydrogenase 1 (IDH1) is the most commonly mutated gene in grade II–III glioma and secondary glioblastoma (GBM). A causal role for IDH1R132Hin gliomagenesis has been proposed, but functional validation in vivohas not been demonstrated. In this study, we assessed the role of IDH1R132Hin glioma development in the context of clinically relevant cooperating genetic alterations in vitroand in vivo. Immortal astrocytes expressing IDH1R132Hexhibited elevated (R)-2-hydroxyglutarate levels, reduced NADPH, increased proliferation, and anchorage-independent growth. Although not sufficient on its own, IDH1R132Hcooperated with PDGFA and loss of Cdkn2a, Atrx, and Ptento promote glioma development in vivo. These tumors resembled proneural human mutant IDH1 GBM genetically, histologically, and functionally. Our findings support the hypothesis that IDH1R132Hpromotes glioma development. This model enhances our understanding of the biology of IDH1R132H-driven gliomas and facilitates testing of therapeutic strategies designed to combat this deadly disease.

Published
2018
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11. In vitro visualization and characterization of wild type and mutant IDH homo- and heterodimers using Bimolecular Fluorescence Complementation.

Author

Robinson GL, Philip B, Guthrie MR, Cox JE, Robinson JP, VanBrocklin MW, and Holmen SL

Abstract

Mutations in the metabolic enzyme isocitrate dehydrogenase (IDH) were recently found in ~80% of WHO grade II-III gliomas and secondary glioblastomas. These mutations reduce the enzyme's ability to convert isocitrate to α-ketoglutarate and, instead, confer a novel gain-of-function resulting in the conversion of α-ketoglutarate to 2-hydroxglutarate (2-HG). However, IDH mutations exist in a heterozygous state such that a functional wild type allele is retained. Recent data suggest that the ability of mutant IDH1, but not mutant IDH2, to produce 2-HG is dependent on the activity of the retained wild type allele. In this study, we aimed to further our understanding of the interaction and function of wild type and mutant IDH heterodimers utilizing Bimolecular Fluorescence Complementation (BiFC). Dimerization of wild type and mutant IDH monomers conjugated to the N- and C-terminus of Venus protein, respectively, is directly proportional to the amount of fluorescence emitted and can be used as an approach to visualize and assess IDH dimerization. Thus, we utilized this method to visualize IDH homo- and heterodimers and to examine their cellular physiology based on subcellular localization, NADPH production, and 2-HG levels. Our results demonstrate that wild type and mutant IDH1 or IDH2 heterodimers display similar physiological characteristics to that of mutant IDH1 or IDH2 homodimers with the exception of their ability to generate NADPH. IDH1 heterodimers consistently generate NADPH whereas IDH2 heterodimers do not. However, the presence of mutant IDH1 or IDH2 in homo- or heterodimer configurations consistently generates equivalent levels of 2-HG. Our data suggest that the wild type protein is not required for the generation of 2-HG., Competing Interests: Competing Interests: The authors declare no competing financial interests.

Published
2016
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