Summary of Study ST000276

This data is available at the NIH Common Fund's National Metabolomics Data Repository (NMDR) website, the Metabolomics Workbench, https://www.metabolomicsworkbench.org, where it has been assigned Project ID PR000154. The data can be accessed directly via it's Project DOI: 10.21228/M8688J This work is supported by NIH grant, U2C- DK119886.

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Study IDST000276
Study TitleIDH1 and Glioma knockdown idh1
Study SummaryThis study is a part of series performed for the same researcher through pilot/feasibility grant program, so the publication is relevant reference for other studies (ST000199) This specific experiment is a pilot study to compare the metabolism of cells transformed using empty vector against cells transformed with vector carrying short hairpin RNA (shRNA) targeted to silence isocitrate dehydrogenase-1 (IDH1) gene.
Institute
University of Michigan
DepartmentNeurology
LaboratoryStegh Lab (Northwestern University)
Last NameCalvert
First NameAndrea
AddressEvanston, IL
Emaila-calvert@u.northwestern.edu
Phone312-503-3134
Submit Date2014-06-11
Num Groups2
Total Subjects10
Study CommentsSubject IDs are updated to correcly show before/after exercise samples taken from the same person
Raw Data File Type(s)d
Analysis Type DetailGC-MS/LC-MS
Release Date2016-01-13
Release Version1
Andrea Calvert Andrea Calvert
https://dx.doi.org/10.21228/M8688J
ftp://www.metabolomicsworkbench.org/Studies/ application/zip

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Project:

Project ID:PR000154
Project DOI:doi: 10.21228/M8688J
Project Title:Isocitrate dehydrogenase-1 and Glioma Studies
Project Summary:Dr. Stegh will define the role of a novel glioma oncoprotein, termed isocitrate dehydrogenase-1 (IDH1), in driving progression and therapy resistance of glioblastoma (GBM). Understanding the molecular basis of the therapy refractoriness of GBM is one of the most important areas of glioma research.IDH1 is a critical enzyme of the citric acid cycle (CAC) and is a master regulator of metabolism. Building on his preliminary studies, Dr. Stegh will molecularly characterize the precise mechanism, by which IDH1 protects glioma cells from therapy-induced cell death using glioma cell and mouse models. To target IDH1 signaling in GBM, he will leverage these model systems and mechanistical knowledge to develop and preclinically characterize RNA interference RNAi-based nanomaterials. He will generate RNAi-functionalized spherical nucleic acids (SNAs) that neutralize IDH1 expression in established gliomas. Due to the negative charge of the RNA backbone, however, siRNA oligonucleotides have many downsides, such as they trigger auto-immune responses, and cannot cross the blood-brain-barrier (BBB). In contrast, SNAs are able to transverse cellular membranes, do not require the use of toxic auxiliary reagents, and accumulate in cells and intracranial tumors very effectively. They also exhibit extraordinary stability in physiological environments, cross the BBB, are highly resistant to nuclease degradation, and thus, can move through biological fluids and avoid being destroyed as “foreign materials.” Dr. Stegh proposes to preclinically evaluate these IDH1-targeting nanoconjugates to provide a fundamentally novel treatment option of patients diagnosed with GBM, and will aid in successfully implementing RNAi-based therapies into neuro-oncological practice.
Institute:Northwestern University
Department:Neurology
Laboratory:Stegh Lab
Last Name:Stegh
First Name:Alexander
Address:Evanston, IL
Email:a-stegh@northwestern.edu
Phone:312-503-2879
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