Evidence map›Paper›PMID 26311249›Full record

ArticleJournal of neuro-oncology2015

Investigating a signature of temozolomide resistance in GBM cell lines using metabolomics.

Patrick-Denis St-Coeur, Julie J Poitras, Miroslava Cuperlovic-Culf, Mohamed Touaibia, Pier Morin

Abstract read
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In one paragraph

Article in Journal of neuro-oncology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.4field-weighted citation impact, top 12% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

26 citing papers in PubMed, 48 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 2 institutions in 1 country.

Patrick-Denis St-CoeurDepartment of Chemistry and Biochemistry, Université de Moncton, 18 Antonine-Maillet Avenue, Moncton, NB, E1A 3E9, Canada.
Julie J PoitrasDepartment of Chemistry and Biochemistry, Université de Moncton, 18 Antonine-Maillet Avenue, Moncton, NB, E1A 3E9, Canada.
Miroslava Cuperlovic-CulfNational Research Council of Canada, 100 des Aboiteaux Street, Moncton, NB, E1A 7R1, Canada.
Mohamed TouaibiaDepartment of Chemistry and Biochemistry, Université de Moncton, 18 Antonine-Maillet Avenue, Moncton, NB, E1A 3E9, Canada.
Pier MorinDepartment of Chemistry and Biochemistry, Université de Moncton, 18 Antonine-Maillet Avenue, Moncton, NB, E1A 3E9, Canada. pier.morin@umoncton.ca.
Université de Moncton · CANational Research Council Canada · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glioblastoma multiforme (GBM) is the most common form of malignant glioma. Current therapeutic approach to treat this malignancy involves a combination of surgery, radiotherapy and chemotherapy with temozolomide. Numerous mechanisms contributing to inherent and acquired resistance to this chemotherapeutic agent have been identified and can lead to treatment failure. This study undertook a metabolomics-based approach to characterize the metabolic profiles observed in temozolomide-sensitive and temozolomide-resistant GBM cell lines as well as in a small sub-set of primary GBM tumors. This approach was also utilized to explore the metabolic changes modulated upon cell treatment with temozolomide and lomeguatrib, an MGMT inhibitor with temozolomide-sensitizing potential. Metabolites previously explored for their potential role in chemoresistance including glucose, citrate and isocitrate demonstrated elevated levels in temozolomide-resistant GBM cells. In addition, a signature of metabolites comprising alanine, choline, creatine and phosphorylcholine was identified as up-regulated in sensitive GBM cell line across different treatments. These results present the metabolic profiles associated with temozolomide response in selected GBM models and propose interesting leads that could be leveraged for the development of therapeutic or diagnostic tools to impact temozolomide response in GBMs.

Indexed as

MetabolomicsAntineoplastic Agents, AlkylatingAntineoplastic Combined Chemotherapy ProtocolsBrain NeoplasmsCell Line, TumorDacarbazineDNA Modification MethylasesDNA Repair EnzymesDose-Response Relationship, DrugDrug Resistance, NeoplasmElectrophoresis, Gel, Two-DimensionalGlioblastomaHumansMagnetic Resonance SpectroscopyPurinesTemozolomideAntineoplastic Agents, AlkylatingDacarbazineDNA Modification MethylasesDNA Repair EnzymeslomeguatribMGMT protein, humanPurinesTemozolomideTritiumTumor Suppressor ProteinsCancer diagnosisCancer therapeuticsGlioblastoma multiformeLomeguatribMetabolomicsTemozolomide

Identifiers

PMID26311249
OpenAlexW1144254266

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.