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3 results on '"Kyle Hurth"'

1. Medulloblastoma uses GABA transaminase to survive in the cerebrospinal fluid microenvironment and promote leptomeningeal dissemination

Author

Vahan Martirosian, Krutika Deshpande, Hao Zhou, Keyue Shen, Kyle Smith, Paul Northcott, Michelle Lin, Vazgen Stepanosyan, Diganta Das, Jan Remsik, Danielle Isakov, Adrienne Boire, Henk De Feyter, Kyle Hurth, Shaobo Li, Joseph Wiemels, Brooke Nakamura, Ling Shao, Camelia Danilov, Thomas Chen, and Josh Neman

Subjects
Biology (General), QH301-705.5
Published
2021
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2. Fatal refractory cardiac arrest as presentation of systemic amyloidosis

Author

Peter Chung, Sarah Wheeler, Andrew Fong, Kyle Hurth, and Bassam Yaghmour

Subjects
Amyloidosis, Cardiac arrest, Diseases of the respiratory system, RC705-779
Abstract

Amyloidosis is a challenging diagnosis in the absence of clinical suspicion. The two patients reported here lacked any symptoms suggestive of amyloidosis. Instead, they presented with sudden, unexplained cardiac arrests that were persistent, treatment refractory, and ultimately fatal. Post-mortem examination unexpectedly revealed evidence of diffuse, systemic amyloidosis throughout multiple organ systems. We bring awareness to this unusual presentation of systemic amyloidosis that portends to poor outcome.

Published
2020
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3. Medulloblastoma uses GABA transaminase to survive in the cerebrospinal fluid microenvironment and promote leptomeningeal dissemination

Author

Joseph L. Wiemels, Paul A. Northcott, Diganta Das, Shaobo Li, Josh Neman, Camelia A. Danilov, Hao Zhou, Henk M. De Feyter, Vahan Martirosian, Brooke N. Nakamura, Kyle Hurth, Michelle Lin, Keyue Shen, Vazgen Stepanosyan, Krutika Deshpande, Danielle Isakov, Thomas C. Chen, Adrienne Boire, Ling Shao, Kyle S. Smith, and Ján Remšík

Subjects
0301 basic medicine, Cerebellum, Nude, Medical Physiology, Oxidative Phosphorylation, Histones, Mice, GABA transaminase, Meninges, 0302 clinical medicine, Cerebrospinal fluid, GABA shunt, Tumor Microenvironment, Meningeal Neoplasms, 2.1 Biological and endogenous factors, Aetiology, Biology (General), gamma-Aminobutyric Acid, Cancer, Pediatric, Neurons, Tumor, leptomeningeal disease, Wnt signaling pathway, Acetylation, Cell Differentiation, Mitochondria, Phenotype, medicine.anatomical_structure, GABAergic, Female, Energy source, tumor dormancy, Pediatric Cancer, Cell Survival, QH301-705.5, oxidative phosphorylation, Mice, Nude, Biology, medulloblastoma, Histone Deacetylases, General Biochemistry, Genetics and Molecular Biology, cerebrospinal fluid, Cell Line, 03 medical and health sciences, Rare Diseases, Cell Line, Tumor, medicine, Animals, tumor microenvironment, Cerebellar Neoplasms, Cell Proliferation, Medulloblastoma, Tumor microenvironment, Lysine, Neurosciences, medicine.disease, ABAT, Brain Disorders, Rats, Brain Cancer, 030104 developmental biology, 4-Aminobutyrate Transaminase, Cancer research, Biochemistry and Cell Biology, 030217 neurology & neurosurgery
Abstract

Summary: Medulloblastoma (MB) is a malignant pediatric brain tumor arising in the cerebellum. Although abnormal GABAergic receptor activation has been described in MB, studies have not yet elucidated the contribution of receptor-independent GABA metabolism to MB pathogenesis. We find primary MB tumors globally display decreased expression of GABA transaminase (ABAT), the protein responsible for GABA metabolism, compared with normal cerebellum. However, less aggressive WNT and SHH subtypes express higher ABAT levels compared with metastatic G3 and G4 tumors. We show that elevated ABAT expression results in increased GABA catabolism, decreased tumor cell proliferation, and induction of metabolic and histone characteristics mirroring GABAergic neurons. Our studies suggest ABAT expression fluctuates depending on metabolite changes in the tumor microenvironment, with nutrient-poor conditions upregulating ABAT expression. We find metastatic MB cells require ABAT to maintain viability in the metabolite-scarce cerebrospinal fluid by using GABA as an energy source substitute, thereby facilitating leptomeningeal metastasis formation.

Published
2021

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