Evidence map›Paper›PMID 30509603›Full record

ReviewRedox biology2019

Redox regulation of cell state and fate.

Bernice Woon Li Lee, Pramila Ghode, Derrick Sek Tong Ong

Open access · goldAbstract readReview
In one paragraph

Review in Redox biology, 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
4.6field-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, 117 citations in OpenAlex.

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  20. Mitochondria-derived HCell death & disease · 2023
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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

3 authors at 2 institutions in 1 country.

Bernice Woon Li LeeDepartment of Physiology, National University of Singapore, Singapore 117593, Singapore.
Pramila GhodeDepartment of Physiology, National University of Singapore, Singapore 117593, Singapore.
Derrick Sek Tong OngDepartment of Physiology, National University of Singapore, Singapore 117593, Singapore; Institute of Molecular and Cell Biology (IMCB), Agency for Science, Technology and Research (A⁎STAR), Singapore. Electronic address: phsostd@nus.edu.sg.
National University of Singapore · SGAgency for Science, Technology and Research · SG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The failure in effective cancer treatment is thought to be attributed to a subpopulation of tumor cells with stem cell-like properties. These cancer stem cells (CSCs) are intimately linked to tumor initiation, heterogeneity, maintenance, recurrence and metastasis. Increasing evidence supports the view that a tight redox regulation is crucial for CSC proliferation, tumorigenicity, therapy resistance and metastasis in many cancer types. Since the distinct metabolic and epigenetic states of CSCs may influence ROS levels, and hence their malignancy, ROS modulating agents hold promise in their utility as anti-CSC agents that may improve the durability of current cancer treatments. This review will focus on (i) how ROS levels are regulated for CSCs to elicit their hallmark features; (ii) the link between ROS and metabolic plasticity of CSCs; and (iii) how ROS may interface with epigenetics that would enable CSCs to thrive in a stressful tumor microenvironment and survive therapeutic insults.

Indexed as

Cell LineageCarcinogenesisEpigenesis, GeneticHumansNeoplastic Stem CellsOxidation-ReductionReactive Oxygen SpeciesReactive Oxygen SpeciesCancer stem cellsEpigeneticsMetabolismReactive oxygen speciesTherapeutics

Identifiers

PMID30509603
PMCPMC6859564
OpenAlexW2900847421

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.