ReviewFrontiers in pharmacology2014
Glutathione S-conjugates as prodrugs to target drug-resistant tumors.
Review in Frontiers in pharmacology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 1 of them a synthesis that pooled 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.
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.
Who cites it
40 citing papers in PubMed, 1 synthesis or guideline pooled it, 117 citations in OpenAlex.
- Association of GSTM1, GSTT1, GSTM3, and GSTP1 Genes Polymorphisms with Susceptibility to Osteosarcoma: a Case- Control Study and Meta-AnalysisAsian Pacific journal of cancer prevention : APJCP · 2019Pooled it
- Unveiling the Role of GlutathioneACS pharmacology & translational science · 2026Review
- Article
- The arsenic proteome in cancer: Unravelling molecular mechanisms of anticancer drugs.Journal of biological inorganic chemistry : JBIC : a publication of the Society of Biological Inorganic Chemistry · 2026Review
- The role of glutathione S-transferases in human disease pathogenesis and their current inhibitors.Genes & diseases · 2025Review
- Article
- Advances in nephroprotection: the therapeutic role of selenium, silver, and gold nanoparticles in renal health.International urology and nephrology · 2025Review
- CHAC1 in urological tumors: contextual dualism and therapeutic implications.Frontiers in oncology · 2025Review
- Review
- Glutathione‑degrading enzymes in the complex landscape of tumors (Review).International journal of oncology · 2024Review
- Sedanolide Activates KEAP1-NRF2 Pathway and Ameliorates Hydrogen Peroxide-Induced Apoptotic Cell Death.International journal of molecular sciences · 2023Article
- Antioxidants of Non-Enzymatic Nature: Their Function in Higher Plant Cells and the Ways of Boosting Their Biosynthesis.Antioxidants (Basel, Switzerland) · 2023Review
- Review
- The Effects of BSA-Stabilized Selenium Nanoparticles and Sodium Selenite Supplementation on the Structure, Oxidative Stress Parameters and Selenium Redox Biology in Rat Placenta.International journal of molecular sciences · 2022Article
- Glutathione-Mediated Conjugation of Anticancer Drugs: An Overview of Reaction Mechanisms and Biological Significance for Drug Detoxification and Bioactivation.Molecules (Basel, Switzerland) · 2022Review
- Response ofJournal of fungi (Basel, Switzerland) · 2022Article
- The role of polyphenols in overcoming cancer drug resistance: a comprehensive review.Cellular & molecular biology letters · 2022Review
- Redox and Thiols in Archaea.Antioxidants (Basel, Switzerland) · 2020Review
- Mechanisms of Multidrug Resistance in Cancer Chemotherapy.International journal of molecular sciences · 2020Review
- Secondary Metabolites from the Culture of the Marine-derived FungusMarine drugs · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Living organisms are continuously exposed to xenobiotics. The major phase of enzymatic detoxification in many species is the conjugation of activated xenobiotics to reduced glutathione (GSH) catalyzed by the glutathione-S-transferase (GST). It has been reported that some compounds, once transformed into glutathione S-conjugates, enter the mercapturic acid pathway whose end products are highly reactive and toxic for the cell responsible for their production. The cytotoxicity of these GSH conjugates depends essentially on GST and gamma-glutamyl transferases (γGT), the enzymes which initiate the mercapturic acid synthesis pathway. Numerous studies support the view that the expression of GST and γGT in cancer cells represents an important factor in the appearance of a more aggressive and resistant phenotype. High levels of tumor GST and γGT expression were employed to selectively target tumor with GST- or γGT-activated drugs. This strategy, explored over the last two decades, has recently been successful using GST-activated nitrogen mustard (TLK286) and γGT-activated arsenic-based (GSAO and Darinaparsin) prodrugs confirming the potential of GSH-conjugates as anticancer drugs.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.