Evidence map›Paper›PMID 23132408›Full record

ArticleNeuro-oncology2012

Aldehyde dehydrogenase 1A1--a new mediator of resistance to temozolomide in glioblastoma.

Andrea Schäfer, Julian Teufel, Florian Ringel, Marcus Bettstetter, Ingrid Hoepner, Michael Rasper, Jens Gempt, Julia Koeritzer, Friederike Schmidt-Graf, Bernhard Meyer and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in Neuro-oncology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.

0numbers the graph read from it
0cells of the map it votes in
63citing papers in PubMed
3.9field-weighted citation impact, top 6% 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

63 citing papers in PubMed, 101 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. Review
  13. Review
  14. A Sequential Targeting Strategy Interrupts AKT-Driven Subclone-Mediated Progression in Glioblastoma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2023
    Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Tumour-associated CD204Neuropathology and applied neurobiology · 2022
    Article
  20. Article

3 more citing papers are in PubMed but not listed here.

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

12 authors at 6 institutions in 1 country.

Andrea SchäferDivision of Neuropathology, Institute of Pathology, Technische Universität München, München, Germany.
Julian Teufel
Florian Ringel
Marcus Bettstetter
Ingrid Hoepner
Michael Rasper
Jens Gempt
Julia Koeritzer
Friederike Schmidt-Graf
Bernhard Meyer
Christoph P Beier
Jürgen Schlegel
Max Planck Institute for Extraterrestrial Physics · DETechnical University of Munich · DEPraxis für Humangenetik · DERWTH Aachen University · DEHelmholtz Zentrum München · DEMax Planck Institute of Psychiatry · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Implementation of chemotherapy with the drug temozolomide increased the overall survival of patients with glioblastoma multiforme (GBM; WHO grade IV), in particular when the O(6)-methylguanine DNA methyltransferase (MGMT) promoter is epigenetically silenced. Nevertheless, the prognosis remains poor, and relapse in GBM occurs regularly. This clinical behavior seems to be due to the existence of a therapy-resistant subpopulation of cells that induce tumor regrowth. The objective of this work was to analyze the role of aldehyde dehydrogenase (ALDH) 1A1 in mediating temozolomide resistance and its value as a predictor of clinical outcome in GBM patients. Nine GBM cell lines were treated with temozolomide alone or in combination with 4-diethylaminobenzaldehyde (DEAB), an inhibitor of ALDH1A1, or with ALDH1A1 short hairpin (sh)RNA. ALDH1A1 expression and MGMT status of 70 primary GBM patients were correlated with median survival. ALDH1A1 overexpression predicted temozolomide resistance in vitro. Sensitivity of ALDH1A1 positive/MGMT-positive cells to temozolomide could be restored by inhibition of ALDH1A1 by DEAB or by knockdown with shRNA, as indicated by increased cytotoxicity, reduced clonogenicity, and accumulation in the G2/M cell-cycle phase. The prognosis of patients with a high level of ALDH1A1 expression was poor compared with that of patients with low levels (P < .0001). ALDH1A1 is a new mediator for resistance of GBM to temozolomide and a reliable predictor of clinical outcome and may serve as a potential target to improve treatment of human GBM.

Indexed as

AgedAldehyde DehydrogenaseAldehyde Dehydrogenase 1 FamilyAntineoplastic AgentsBiomarkers, TumorBlotting, WesternBrain NeoplasmsCell Line, TumorDacarbazineDNA Modification MethylasesDNA Repair EnzymesDrug Resistance, NeoplasmFemaleGene Knockdown TechniquesGlioblastomaHumansAldehyde DehydrogenaseAldehyde Dehydrogenase 1 FamilyALDH1A1 protein, humanAntineoplastic AgentsBiomarkers, TumorDacarbazineDNA Modification MethylasesDNA Repair EnzymesMGMT protein, humanRetinal DehydrogenaseTemozolomideTumor Suppressor Proteins

Identifiers

PMID23132408
PMCPMC3499020
OpenAlexW2165244997

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.