Evidence map›Paper›PMID 29915025›Full record

ReviewThe Journal of cell biology2018

Glutathione metabolism in cancer progression and treatment resistance.

Ankita Bansal, M Celeste Simon

Open access · bronzeAbstract readReview
In one paragraph

Review in The Journal of cell biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 521 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
521citing papers in PubMed, 2 pooled it
34.2field-weighted citation impact, top 1% 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

521 citing papers in PubMed, 2 syntheses or guidelines pooled it, 1,214 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Physiological Significance and Functions of AA.Reviews of physiology, biochemistry and pharmacology · 2027
    Review
  4. Circadian rhythms in health and disease.Molecular biomedicine · 2026
    Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Review
  13. Targeting glutathione metabolism for tumor radiosensitization (Review).International journal of molecular medicine · 2026
    Review
  14. Article
  15. Article
  16. Review
  17. Review
  18. Review
  19. Article
  20. Article

461 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

2 authors at 1 institution in 1 country.

Ankita BansalAbramson Family Cancer Research Institute, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA.ORCID 0000-0002-6668-1676
M Celeste SimonAbramson Family Cancer Research Institute, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA celeste2@pennmedicine.upenn.edu.ORCID 0000-0001-9106-447X
Cancer Research Institute · US

Funding

TRANSLATIONAL CONTROL IN ADAPTATION TO HYPOXIAP01CA104838 · NCI · UNIVERSITY OF PENNSYLVANIA · PI DIEHL, JOHN ALAN · 2004 to 2018
$17.6M
Metabolic Tumor Suppressors in Renal Cancer: Unprecedented Roles in Disease ProgressionR35CA220483 · NCI · UNIVERSITY OF PENNSYLVANIA · PI M. CELESTE SIMON · 2017 to 2026
$9.4M
NCI NIH HHS P01 CA104838NCI NIH HHS R35 CA220483
6 · The paper itself

Abstract

Glutathione (GSH) is the most abundant antioxidant found in living organisms and has multiple functions, most of which maintain cellular redox homeostasis. GSH preserves sufficient levels of cysteine and detoxifies xenobiotics while also conferring therapeutic resistance to cancer cells. However, GSH metabolism plays both beneficial and pathogenic roles in a variety of malignancies. It is crucial to the removal and detoxification of carcinogens, and alterations in this pathway can have a profound effect on cell survival. Excess GSH promotes tumor progression, where elevated levels correlate with increased metastasis. In this review, we discuss recent studies that focus on deciphering the role of GSH in tumor initiation and progression as well as mechanisms underlying how GSH imparts treatment resistance to growing cancers. Targeting GSH synthesis/utilization therefore represents a potential means of rendering tumor cells more susceptible to different treatment options such as chemotherapy and radiotherapy.

Indexed as

AntioxidantsCysteineDrug Resistance, NeoplasmGlutathioneHomeostasisHumansNeoplasmsSignal TransductionXenobioticsAntioxidantsCysteineGlutathioneXenobiotics

Identifiers

PMID29915025
PMCPMC6028537
OpenAlexW2809388839

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.