Evidence map›Paper›PMID 29770165›Full record

ReviewOxidative medicine and cellular longevity2018

Targeting Oxidatively Induced DNA Damage Response in Cancer: Opportunities for Novel Cancer Therapies.

Pierpaola Davalli, Gaetano Marverti, Angela Lauriola, Domenico D'Arca

Open access · hybridAbstract readReview
In one paragraph

Review in Oxidative medicine and cellular longevity, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
80citing papers in PubMed, 1 pooled it
5.3field-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

80 citing papers in PubMed, 1 synthesis or guideline pooled it, 135 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Review
  5. Microbial medicines: Unlocking the therapeutic potential of the microbiome in cancer treatment.Journal of controlled release : official journal of the Controlled Release Society · 2026
    Review
  6. Review
  7. Review
  8. Article
  9. The therapeutic potential ofFrontiers in microbiology · 2026
    Review
  10. Review
  11. Article
  12. Article
  13. Review
  14. Food science & nutrition · 2025
    Article
  15. Review
  16. Article
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  18. Article
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  20. Article

20 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

4 authors at 1 institution in 1 country.

Pierpaola DavalliDepartment of Biomedical, Metabolic and Neural Sciences, University of Modena and Reggio Emilia, 41125 Modena, Italy.ORCID 0000-0002-3867-8621
Gaetano MarvertiDepartment of Biomedical, Metabolic and Neural Sciences, University of Modena and Reggio Emilia, 41125 Modena, Italy.ORCID 0000-0002-9074-0795
Angela LauriolaDepartment of Life Sciences, University of Modena and Reggio Emilia, 41125 Modena, Italy.ORCID 0000-0001-5286-8627
Domenico D'ArcaDepartment of Biomedical, Metabolic and Neural Sciences, University of Modena and Reggio Emilia, 41125 Modena, Italy.ORCID 0000-0002-7240-6005
University of Modena and Reggio Emilia · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cancer is a death cause in economically developed countries that results growing also in developing countries. Improved outcome through targeted interventions faces the scarce selectivity of the therapies and the development of resistance to them that compromise the therapeutic effects. Genomic instability is a typical cancer hallmark due to DNA damage by genetic mutations, reactive oxygen and nitrogen species, ionizing radiation, and chemotherapeutic agents. DNA lesions can induce and/or support various diseases, including cancer. The DNA damage response (DDR) is a crucial signaling-transduction network that promotes cell cycle arrest or cell death to repair DNA lesions. DDR dysregulation favors tumor growth as downregulated or defective DDR generates genomic instability, while upregulated DDR may confer treatment resistance. Redox homeostasis deeply and capillary affects DDR as ROS activate/inhibit proteins and enzymes integral to DDR both in healthy and cancer cells, although by different routes. DDR regulation through modulating ROS homeostasis is under investigation as anticancer opportunity, also in combination with other treatments since ROS affect DDR differently in the patients during cancer development and treatment. Here, we highlight ROS-sensitive proteins whose regulation in oxidatively induced DDR might allow for selective strategies against cancer that are better tailored to the patients.

Indexed as

Antineoplastic AgentsAtaxia Telangiectasia Mutated ProteinsCyclin-Dependent KinasesDNA DamageDNA RepairHumansNeoplasmsReactive Nitrogen SpeciesReactive Oxygen SpeciesTumor Suppressor ProteinsAntineoplastic AgentsAtaxia Telangiectasia Mutated ProteinsCyclin-Dependent KinasesReactive Nitrogen SpeciesReactive Oxygen SpeciesTumor Suppressor Proteins

Identifiers

PMID29770165
PMCPMC5892224
OpenAlexW2794532094

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.