Evidence map›Paper›PMID 26501110›Full record

ArticleEBioMedicine2015

Successful Treatment of Intracranial Glioblastoma Xenografts With a Monoamine Oxidase B-Activated Pro-Drug.

Martyn A Sharpe, Andrew D Livingston, Taylor L Gist, Pardip Ghosh, Junyan Han, David S Baskin

Open access · goldAbstract read
In one paragraph

Article in EBioMedicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

17 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Review
  6. Article
  7. Review
  8. Review
  9. Mitochondrial Dysfunction, Macrophage, and Microglia in Brain Cancer.Frontiers in cell and developmental biology · 2020
    Article
  10. Monoamine oxidase isoenzymes: genes, functions and targets for behavior and cancer therapy.Journal of neural transmission (Vienna, Austria : 1996) · 2018
    Review
  11. Monoamine Oxidase B in Renal Cell Carcinoma.Medical science monitor : international medical journal of experimental and clinical research · 2018
    Article
  12. Article
  13. Current trends in mouse models of glioblastoma.Journal of neuro-oncology · 2017
    Review
  14. Article
  15. Article
  16. Article
  17. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 1 country.

Martyn A SharpeDepartment of Neurosurgery, Kenneth R. Peak Brain and Pituitary Tumor Center, Houston Methodist Hospital, 6565 Fannin, Suite 944, Houston, TX 77030, United States.
Andrew D LivingstonDepartment of Neurosurgery, Kenneth R. Peak Brain and Pituitary Tumor Center, Houston Methodist Hospital, 6565 Fannin, Suite 944, Houston, TX 77030, United States.
Taylor L GistDepartment of Neurosurgery, Kenneth R. Peak Brain and Pituitary Tumor Center, Houston Methodist Hospital, 6565 Fannin, Suite 944, Houston, TX 77030, United States.
Pardip GhoshCenter for Molecular Imaging, Institute of Molecular Medicine, UT Health Science Center-Houston, Houston, TX 77030, United States.
Junyan HanDepartment of Neurosurgery, Kenneth R. Peak Brain and Pituitary Tumor Center, Houston Methodist Hospital, 6565 Fannin, Suite 944, Houston, TX 77030, United States.
David S BaskinDepartment of Neurosurgery, Kenneth R. Peak Brain and Pituitary Tumor Center, Houston Methodist Hospital, 6565 Fannin, Suite 944, Houston, TX 77030, United States.
Houston Methodist · USThe University of Texas Health Science Center at Houston · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The last major advance in the treatment of glioblastoma multiforme (GBM) was the introduction of temozolomide in 1999. Treatment with temozolomide following surgical debulking extends survival rate compared to radiotherapy and debulking alone. However, virtually all glioblastoma patients experience disease progression within 7 to 10 months. Although many salvage treatments, including bevacizumab, rechallenge with temozolomide, and other alkylating agents, have been evaluated, none of these clearly improves survival. Monoamine oxidase B (MAOB) is highly expressed in glioblastoma cell mitochondria, and mitochondrial function is intimately tied to treatment-resistant glioblastoma progression. These glioblastoma properties provide a strong rationale for pursuing a MAOB-selective pro-drug treatment approach that, upon drug activation, targets glioblastoma mitochondria, especially mitochondrial DNA. MP-MUS is the lead compound in a family of pro-drugs designed to treat GBM that is converted into the mature, mitochondria-targeting drug, P(+)-MUS, by MAOB. We show that MP-MUS can successfully kill primary gliomas in vitro and in vivo mouse xenograft models.

Indexed as

AnimalsBrain NeoplasmsCell Line, TumorDNA, MitochondrialGlioblastomaHumansL-Lactate DehydrogenaseMembrane Potential, MitochondrialMice, NudeMonoamine OxidaseParkinson DiseasePhenotypeProdrugsReactive Oxygen SpeciesTreatment OutcomeTumor BurdenDNA, MitochondrialL-Lactate DehydrogenaseMonoamine OxidaseProdrugsReactive Oxygen SpeciesChemotherapyGlioblastoma multiformeMonoamine oxidase BMP-MUSPro-drugXenograft

Identifiers

PMID26501110
PMCPMC4588367
OpenAlexW2138288043

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.