Evidence map›Paper›PMID 33287345›Full record

ReviewInternational journal of molecular sciences2020

Focus on DNA Glycosylases-A Set of Tightly Regulated Enzymes with a High Potential as Anticancer Drug Targets.

Fabienne Hans, Muge Senarisoy, Chandini Bhaskar Naidu, Joanna Timmins

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.4field-weighted citation impact, top 39% 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

9 citing papers in PubMed, 15 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. Recognition of DNA Lesions.International journal of molecular sciences · 2023
    Article
  7. Article
  8. Article
  9. Article
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.

Fabienne HansInstitut de Biologie Structurale (IBS), University Grenoble Alpes, CEA, CNRS, F-38000 Grenoble, France.
Muge SenarisoyInstitut de Biologie Structurale (IBS), University Grenoble Alpes, CEA, CNRS, F-38000 Grenoble, France.
Chandini Bhaskar NaiduInstitut de Biologie Structurale (IBS), University Grenoble Alpes, CEA, CNRS, F-38000 Grenoble, France.
Joanna TimminsInstitut de Biologie Structurale (IBS), University Grenoble Alpes, CEA, CNRS, F-38000 Grenoble, France.ORCID 0000-0002-9066-9095
Centre National de la Recherche Scientifique · FR

Funding

Commissariat à l'Énergie Atomique et aux Énergies Alternatives Radiobiology grant
6 · The paper itself

Abstract

Cancer is the second leading cause of death with tens of millions of people diagnosed with cancer every year around the world. Most radio- and chemotherapies aim to eliminate cancer cells, notably by causing severe damage to the DNA. However, efficient repair of such damage represents a common mechanism of resistance to initially effective cytotoxic agents. Thus, development of new generation anticancer drugs that target DNA repair pathways, and more particularly the base excision repair (BER) pathway that is responsible for removal of damaged bases, is of growing interest. The BER pathway is initiated by a set of enzymes known as DNA glycosylases. Unlike several downstream BER enzymes, DNA glycosylases have so far received little attention and the development of specific inhibitors of these enzymes has been lagging. Yet, dysregulation of DNA glycosylases is also known to play a central role in numerous cancers and at different stages of the disease, and thus inhibiting DNA glycosylases is now considered a valid strategy to eliminate cancer cells. This review provides a detailed overview of the activities of DNA glycosylases in normal and cancer cells, their modes of regulation, and their potential as anticancer drug targets.

Indexed as

AnimalsAntineoplastic AgentsDisease SusceptibilityDNA DamageDNA GlycosylasesDNA RepairEnzyme ActivationGene Expression Regulation, EnzymologicHumansMolecular Targeted TherapyNeoplasmsStructure-Activity RelationshipAntineoplastic AgentsDNA Glycosylasesbase excision repaircancerDNA glycosylasesdrug resistanceinhibitors

Identifiers

PMID33287345
PMCPMC7730500
OpenAlexW3108873487

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.