Evidence map›Paper›PMID 31357507›Full record

ReviewInternational journal of molecular sciences2019

Glutathione Metabolism in Renal Cell Carcinoma Progression and Implications for Therapies.

Yi Xiao, David Meierhofer

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed
6.0field-weighted citation impact, top 3% 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

58 citing papers in PubMed, 114 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

2 authors at 1 institution in 1 country.

Yi XiaoMax Planck Institute for Molecular Genetics, Ihnestraße 63-73, 14195 Berlin, Germany.
David MeierhoferMax Planck Institute for Molecular Genetics, Ihnestraße 63-73, 14195 Berlin, Germany. meierhof@molgen.mpg.de.
Max Planck Institute for Molecular Genetics · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A significantly increased level of the reactive oxygen species (ROS) scavenger glutathione (GSH) has been identified as a hallmark of renal cell carcinoma (RCC). The proposed mechanism for increased GSH levels is to counteract damaging ROS to sustain the viability and growth of the malignancy. Here, we review the current knowledge about the three main RCC subtypes, namely clear cell RCC (ccRCC), papillary RCC (pRCC), and chromophobe RCC (chRCC), at the genetic, transcript, protein, and metabolite level and highlight their mutual influence on GSH metabolism. A further discussion addresses the question of how the manipulation of GSH levels can be exploited as a potential treatment strategy for RCC.

Indexed as

AnimalsBiomarkers, TumorCarcinoma, Renal CellDisease Models, AnimalDisease ProgressionGlutathioneHumansKidney NeoplasmsMetabolic Networks and PathwaysMolecular Targeted TherapyOxidative StressReactive Oxygen SpeciesTumor MicroenvironmentBiomarkers, TumorGlutathioneReactive Oxygen Speciescancer therapychromophobe RCCclear cell RCCglutathione (GSH) metabolismpapillary RCCreactive oxygen species (ROS)Renal cell carcinoma (RCC)

Identifiers

PMID31357507
PMCPMC6696504
OpenAlexW2963487588

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.