Summary of Study ST002806

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 PR001753. The data can be accessed directly via it's Project DOI: 10.21228/M8413M This work is supported by NIH grant, U2C- DK119886.

See: https://www.metabolomicsworkbench.org/about/howtocite.php

This study contains a large results data set and is not available in the mwTab file. It is only available for download via FTP as data file(s) here.

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Study IDST002806
Study TitleComprehensive Metabolic Profiling of MYC-Amplified Medulloblastoma Tumors Reveals Key Dependencies on Amino Acid, Tricarboxylic Acid and Hexosamine Pathways
Study SummaryReprogramming of cellular metabolism is a hallmark of cancer. Altering metabolism allows cancer cells to overcome unfavorable microenvironment conditions and to increase and invade. Medulloblastoma is the most common malignant brain tumor in children. Genomic amplification of MYC defines a subset of poor-prognosis medulloblastoma. We performed comprehensive metabolic studies of human MYC-amplified medulloblastoma by comparing the metabolic profiles of tumor cells in three different conditions—in vitro, in flank xenografts, and orthotopic xenografts in the cerebellum. Principal component analysis showed that the metabolic profiles of brain and flank high-MYC medulloblastoma tumors clustered closely together and separated away from the normal brain and in vitro MYC-amplified cells. Compared to typical brains, MYC-amplified medulloblastoma orthotopic xenograft tumors showed upregulation of the TCA cycle and the synthesis of nucleotides, hexosamines, amino acids, and glutathione. There was significantly higher glucose uptake and usage in orthotopic xenograft tumors compared to flank xenograft tumors and cells in culture. In orthotopic tumors, glucose was the primary carbon source for the de novo synthesis of glutamate, glutamine, and glutathione through the TCA cycle. In vivo, the glutaminase II pathway was the main pathway utilizing glutamine. Glutathione was the most abundant upregulated metabolite in orthotopic tumors compared to normal brains. Glutamine-derived glutathione was synthesized through the glutamine transaminase K (GTK) enzyme in vivo. In conclusion, high MYC medulloblastoma cells have different metabolic profiles in vitro compared to in vivo; critical vulnerabilities may be missed by not performing in vivo metabolic analyses.
Institute
Johns Hopkins University
Last NamePham
First NameKhoa
Address600 N. Wolfe Street, Pathology Bldg., Rm. 401, Baltimore, Maryland, 21287, USA
Emailkpham8@jhmi.edu
Phone4109553439
Submit Date2023-07-29
Raw Data AvailableYes
Raw Data File Type(s)mzXML
Analysis Type DetailLC-MS
Release Date2023-08-20
Release Version1
Khoa Pham Khoa Pham
https://dx.doi.org/10.21228/M8413M
ftp://www.metabolomicsworkbench.org/Studies/ application/zip

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Factors:

Subject type: Human; Subject species: Homo sapiens (Factor headings shown in green)

mb_sample_id local_sample_id Treatment
SA30085357Flank Tumor
SA30085456Flank Tumor
SA30085558Flank Tumor
SA30085660Flank Tumor
SA30085761Flank Tumor
SA30085855Flank Tumor
SA30085959Flank Tumor
SA30086053Flank Tumor
SA30086148Flank Tumor
SA30086247Flank Tumor
SA30086349Flank Tumor
SA30086451Flank Tumor
SA30086562Flank Tumor
SA30086652Flank Tumor
SA30086754Flank Tumor
SA30086864Flank Tumor
SA30086973Flank Tumor
SA30087072Flank Tumor
SA30087174Flank Tumor
SA30087275Flank Tumor
SA30087377Flank Tumor
SA30087476Flank Tumor
SA30087571Flank Tumor
SA30087670Flank Tumor
SA30087765Flank Tumor
SA30087846Flank Tumor
SA30087966Flank Tumor
SA30088067Flank Tumor
SA30088169Flank Tumor
SA30088268Flank Tumor
SA30088363Flank Tumor
SA30088450Flank Tumor
SA30088585Invitro
SA30088686Invitro
SA30088787Invitro
SA30088888Invitro
SA30088983Invitro
SA30089082Invitro
SA30089178Invitro
SA30089279Invitro
SA30089380Invitro
SA30089481Invitro
SA30089589Invitro
SA30089684Invitro
SA30089794Invitro
SA30089890Invitro
SA30089993Invitro
SA30090095Invitro
SA30090191Invitro
SA30090292Invitro
SA3009038Orthotopic
SA3009047Orthotopic
SA3009059Orthotopic
SA30090610Orthotopic
SA3009076Orthotopic
SA30090811Orthotopic
SA30090912Orthotopic
SA3009102Orthotopic
SA30091196Orthotopic
SA30091213Orthotopic
SA30091397Orthotopic
SA30091498Orthotopic
SA3009154Orthotopic
SA3009163Orthotopic
SA3009175Orthotopic
SA30091814Orthotopic
SA30091945Orthotopic
SA30092044Orthotopic
SA30092143Orthotopic
SA30092233Orthotopic
SA30092332Orthotopic
SA30092430Orthotopic
SA30092531Orthotopic
SA30092642Orthotopic
SA30092741Orthotopic
SA30092836Orthotopic
SA30092935Orthotopic
SA30093037Orthotopic
SA30093138Orthotopic
SA30093240Orthotopic
SA30093339Orthotopic
SA3009341Orthotopic
SA30093529Orthotopic
SA30093619Orthotopic
SA30093720Orthotopic
SA30093818Orthotopic
SA30093917Orthotopic
SA30094015Orthotopic
SA30094116Orthotopic
SA30094221Orthotopic
SA30094322Orthotopic
SA30094427Orthotopic
SA30094528Orthotopic
SA30094626Orthotopic
SA30094725Orthotopic
SA30094823Orthotopic
SA30094924Orthotopic
SA30095034Orthotopic
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