Evidence map›Paper›PMID 29123614›Full record

ReviewOxidative medicine and cellular longevity2017

The Roles of ROS in Cancer Heterogeneity and Therapy.

Paulo Luiz de Sá Junior, Diana Aparecida Dias Câmara, Allan Saj Porcacchia, Pâmela Maria Moreira Fonseca, Salomão Doria Jorge, Rodrigo Pinheiro Araldi, Adilson Kleber Ferreira

Open access · hybridAbstract readReview
In one paragraph

Review in Oxidative medicine and cellular longevity, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 139 papers.

0numbers the graph read from it
0cells of the map it votes in
139citing papers in PubMed
6.1field-weighted citation impact, top 2% 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

139 citing papers in PubMed, 288 citations in OpenAlex.

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79 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

7 authors at 4 institutions in 3 countries.

Paulo Luiz de Sá JuniorMogi das Cruzes University (UMC), Villa Lobos Campus, Sao Paulo, SP, Brazil.ORCID 0000-0002-7730-0859
Diana Aparecida Dias CâmaraLaboratory of Genetics, Butantan Institute, Sao Paulo, SP, Brazil.
Allan Saj PorcacchiaUniversity of Sao Paulo, Sao Paulo, SP, Brazil.
Pâmela Maria Moreira FonsecaMogi das Cruzes University (UMC), Villa Lobos Campus, Sao Paulo, SP, Brazil.
Salomão Doria JorgeDepartment of Immunology, Laboratory of Tumor Immunology, Institute of Biomedical Science, University of Sao Paulo, Sao Paulo, SP, Brazil.
Rodrigo Pinheiro AraldiLaboratory of Genetics, Butantan Institute, Sao Paulo, SP, Brazil.ORCID 0000-0001-8288-2577
Adilson Kleber FerreiraDepartment of Immunology, Laboratory of Tumor Immunology, Institute of Biomedical Science, University of Sao Paulo, Sao Paulo, SP, Brazil.ORCID 0000-0002-2605-1899
Universidade de São Paulo · BRUniversidade de Mogi das Cruzes · BRInstituto Butantan · BRMorpho (United States) · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cancer comprises a group of heterogeneous diseases encompassing high rates of morbidity and mortality. Heterogeneity, which is a hallmark of cancer, is one of the main factors related to resistance to chemotherapeutic agents leading to poor prognosis. Heterogeneity is profoundly affected by increasing levels of ROS. Under low concentrations, ROS may function as signaling molecules favoring tumorigenesis and heterogeneity, while under high ROS concentrations, these species may work as cancer modulators due to their deleterious, genotoxic or even proapoptotic effect on cancer cells. This double-edged sword effect represented by ROS relies on their ability to cause genetic and epigenetic modifications in DNA structure. Antitumor therapeutic approaches may use molecules that prevent the ROS formation precluding carcinogenesis or use chemical agents that promote a sudden increase of ROS causing considerable oxidative stress inside tumor mass. Therefore, herein, we review what ROS are and how they are produced in normal and in cancer cells while providing an argumentative discussion about their role in cancer pathophysiology. We also describe the various sources of ROS in cancer and their role in tumor heterogeneity. Further, we also discuss some therapeutic strategies from the current landscape of cancer heterogeneity, ROS modulation, or ROS production.

Indexed as

Epigenesis, GeneticGene Expression Regulation, NeoplasticSignal TransductionAnimalsDNA, NeoplasmHumansNeoplasmsReactive Oxygen SpeciesDNA, NeoplasmReactive Oxygen Species

Identifiers

PMID29123614
PMCPMC5662836
OpenAlexW2766112735

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.