Metabolic characterization of human IDH mutant and wild type gliomas using simultaneous pH- and oxygen-sensitive molecular MRI.


Journal

Neuro-oncology
ISSN: 1523-5866
Titre abrégé: Neuro Oncol
Pays: England
ID NLM: 100887420

Informations de publication

Date de publication:
06 09 2019
Historique:
pubmed: 9 5 2019
medline: 11 11 2020
entrez: 9 5 2019
Statut: ppublish

Résumé

Isocitrate dehydrogenase 1 (IDH1) mutant gliomas are thought to have distinct metabolic characteristics, including a blunted response to hypoxia and lower glycolytic flux. We hypothesized that non-invasive quantification of abnormal metabolic behavior in human IDH1 mutant gliomas could be performed using a new pH- and oxygen-sensitive molecular MRI technique. Simultaneous pH- and oxygen-sensitive MRI was obtained at 3T using amine CEST-SAGE-EPI. The pH-dependent measure of the magnetization transfer ratio asymmetry (MTRasym) at 3 ppm and oxygen-sensitive measure of R2' were quantified in 90 patients with gliomas. Additionally, stereotactic, image-guided biopsies were performed in 20 patients for a total of 52 samples. The association between imaging measurements and hypoxia-inducible factor 1 alpha (HIF1α) expression was identified using Pearson correlation analysis. IDH1 mutant gliomas exhibited significantly lower MTRasym at 3 ppm, R2', and MTRasymxR2' (P = 0.007, P = 0.003, and P = 0.001, respectively). MTRasymxR2' could identify IDH1 mutant gliomas with a high sensitivity (81.0%) and specificity (81.3%). HIF1α was positively correlated with MTRasym at 3 ppm, R2' and MTRasymxR2' in IDH1 wild type (r = 0.610, P = 0.003; r = 0.667, P = 0.008; r = 0.635, P = 0.006), but only MTRasymxR2' in IDH1 mutant gliomas (r = 0.727, P = 0.039). IDH1 mutant gliomas have distinct metabolic and microenvironment characteristics compared with wild type gliomas. An imaging biomarker combining tumor acidity and hypoxia (MTRasymxR2') can differentiate IDH1 mutation status and is correlated with tumor acidity and hypoxia.

Sections du résumé

BACKGROUND
Isocitrate dehydrogenase 1 (IDH1) mutant gliomas are thought to have distinct metabolic characteristics, including a blunted response to hypoxia and lower glycolytic flux. We hypothesized that non-invasive quantification of abnormal metabolic behavior in human IDH1 mutant gliomas could be performed using a new pH- and oxygen-sensitive molecular MRI technique.
METHODS
Simultaneous pH- and oxygen-sensitive MRI was obtained at 3T using amine CEST-SAGE-EPI. The pH-dependent measure of the magnetization transfer ratio asymmetry (MTRasym) at 3 ppm and oxygen-sensitive measure of R2' were quantified in 90 patients with gliomas. Additionally, stereotactic, image-guided biopsies were performed in 20 patients for a total of 52 samples. The association between imaging measurements and hypoxia-inducible factor 1 alpha (HIF1α) expression was identified using Pearson correlation analysis.
RESULTS
IDH1 mutant gliomas exhibited significantly lower MTRasym at 3 ppm, R2', and MTRasymxR2' (P = 0.007, P = 0.003, and P = 0.001, respectively). MTRasymxR2' could identify IDH1 mutant gliomas with a high sensitivity (81.0%) and specificity (81.3%). HIF1α was positively correlated with MTRasym at 3 ppm, R2' and MTRasymxR2' in IDH1 wild type (r = 0.610, P = 0.003; r = 0.667, P = 0.008; r = 0.635, P = 0.006), but only MTRasymxR2' in IDH1 mutant gliomas (r = 0.727, P = 0.039).
CONCLUSIONS
IDH1 mutant gliomas have distinct metabolic and microenvironment characteristics compared with wild type gliomas. An imaging biomarker combining tumor acidity and hypoxia (MTRasymxR2') can differentiate IDH1 mutation status and is correlated with tumor acidity and hypoxia.

Identifiants

pubmed: 31066901
pii: 5485508
doi: 10.1093/neuonc/noz078
pmc: PMC7594567
doi:

Substances chimiques

HIF1A protein, human 0
Hypoxia-Inducible Factor 1, alpha Subunit 0
Lactic Acid 33X04XA5AT
Isocitrate Dehydrogenase EC 1.1.1.41
IDH1 protein, human EC 1.1.1.42.

Types de publication

Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

1184-1196

Subventions

Organisme : NCI NIH HHS
ID : P50 CA211015
Pays : United States
Organisme : NCI NIH HHS
ID : R21 CA223757
Pays : United States

Commentaires et corrections

Type : CommentIn

Informations de copyright

© The Author(s) 2019. Published by Oxford University Press on behalf of the Society for Neuro-Oncology. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.

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Auteurs

Jingwen Yao (J)

UCLA Brain Tumor Imaging Laboratory, Center for Computer Vision and Imaging Biomarkers, University of California Los Angeles, Los Angeles, California.
Department of Radiological Sciences, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, California.
Department of Bioengineering, Henry Samueli School of Engineering and Applied Science, University of California Los Angeles, Los Angeles, California.

Ararat Chakhoyan (A)

UCLA Brain Tumor Imaging Laboratory, Center for Computer Vision and Imaging Biomarkers, University of California Los Angeles, Los Angeles, California.
Department of Radiological Sciences, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, California.

David A Nathanson (DA)

Department of Molecular and Medical Pharmacology, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, California.

William H Yong (WH)

Department of Pathology, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, California.

Noriko Salamon (N)

Department of Radiological Sciences, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, California.

Catalina Raymond (C)

UCLA Brain Tumor Imaging Laboratory, Center for Computer Vision and Imaging Biomarkers, University of California Los Angeles, Los Angeles, California.
Department of Radiological Sciences, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, California.

Sergey Mareninov (S)

Department of Pathology, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, California.

Albert Lai (A)

UCLA Neuro-Oncology Program, University of California Los Angeles, Los Angeles, California.
Department of Neurology, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, California.

Phioanh L Nghiemphu (PL)

UCLA Neuro-Oncology Program, University of California Los Angeles, Los Angeles, California.
Department of Neurology, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, California.

Robert M Prins (RM)

Department of Neurosurgery, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, California.

Whitney B Pope (WB)

Department of Radiological Sciences, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, California.

Richard G Everson (RG)

Department of Neurosurgery, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, California.

Linda M Liau (LM)

Department of Neurosurgery, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, California.

Timothy F Cloughesy (TF)

UCLA Neuro-Oncology Program, University of California Los Angeles, Los Angeles, California.
Department of Neurology, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, California.

Benjamin M Ellingson (BM)

UCLA Brain Tumor Imaging Laboratory, Center for Computer Vision and Imaging Biomarkers, University of California Los Angeles, Los Angeles, California.
Department of Radiological Sciences, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, California.
Department of Bioengineering, Henry Samueli School of Engineering and Applied Science, University of California Los Angeles, Los Angeles, California.
UCLA Neuro-Oncology Program, University of California Los Angeles, Los Angeles, California.

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Classifications MeSH