Evidence map›Paper›PMID 27418953›Full record

ReviewOxidative medicine and cellular longevity2016

Redox Homeostasis and Cellular Antioxidant Systems: Crucial Players in Cancer Growth and Therapy.

Barbara Marengo, Mariapaola Nitti, Anna Lisa Furfaro, Renata Colla, Chiara De Ciucis, Umberto Maria Marinari, Maria Adelaide Pronzato, Nicola Traverso, Cinzia Domenicotti

Open access · hybridAbstract readReview
In one paragraph

Review in Oxidative medicine and cellular longevity, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 162 papers.

0numbers the graph read from it
0cells of the map it votes in
162citing papers in PubMed
15.5field-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

162 citing papers in PubMed, 304 citations in OpenAlex.

  1. Deciphering the role of human peroxiredoxins for combating lead and zinc mediated cellular toxicity using a yeast model.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2026
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102 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

9 authors at 2 institutions in 1 country.

Barbara MarengoDepartment of Experimental Medicine, General Pathology Section, University of Genova, 16132 Genova, Italy.ORCID 0000-0003-3056-6569
Mariapaola NittiDepartment of Experimental Medicine, General Pathology Section, University of Genova, 16132 Genova, Italy.ORCID 0000-0002-1997-0678
Anna Lisa FurfaroGiannina Gaslini Institute, Genova, Italy.ORCID 0000-0003-3538-2056
Renata CollaDepartment of Experimental Medicine, General Pathology Section, University of Genova, 16132 Genova, Italy.ORCID 0000-0002-4644-4163
Chiara De CiucisDepartment of Experimental Medicine, General Pathology Section, University of Genova, 16132 Genova, Italy.
Umberto Maria MarinariDepartment of Experimental Medicine, General Pathology Section, University of Genova, 16132 Genova, Italy.ORCID 0000-0002-4843-2254
Maria Adelaide PronzatoDepartment of Experimental Medicine, General Pathology Section, University of Genova, 16132 Genova, Italy.ORCID 0000-0003-0487-1156
Nicola TraversoDepartment of Experimental Medicine, General Pathology Section, University of Genova, 16132 Genova, Italy.ORCID 0000-0002-0306-8647
Cinzia DomenicottiDepartment of Experimental Medicine, General Pathology Section, University of Genova, 16132 Genova, Italy.ORCID 0000-0002-5003-7333
University of Genoa · ITIstituto Giannina Gaslini · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Reactive oxygen species (ROS) and their products are components of cell signaling pathways and play important roles in cellular physiology and pathophysiology. Under physiological conditions, cells control ROS levels by the use of scavenging systems such as superoxide dismutases, peroxiredoxins, and glutathione that balance ROS generation and elimination. Under oxidative stress conditions, excessive ROS can damage cellular proteins, lipids, and DNA, leading to cell damage that may contribute to carcinogenesis. Several studies have shown that cancer cells display an adaptive response to oxidative stress by increasing expression of antioxidant enzymes and molecules. As a double-edged sword, ROS influence signaling pathways determining beneficial or detrimental outcomes in cancer therapy. In this review, we address the role of redox homeostasis in cancer growth and therapy and examine the current literature regarding the redox regulatory systems that become upregulated in cancer and their role in promoting tumor progression and resistance to chemotherapy.

Indexed as

HomeostasisAnimalsAntioxidantsCarcinogenesisClinical Trials as TopicHumansNeoplasmsOxidation-ReductionReactive Oxygen SpeciesAntioxidantsReactive Oxygen Species

Identifiers

PMID27418953
PMCPMC4932173
OpenAlexW2468344619

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.