Evidence map›Paper›PMID 28938088›Full record

ReviewCell chemical biology2017

Small-Molecule Inhibitors Targeting DNA Repair and DNA Repair Deficiency in Research and Cancer Therapy.

Sarah R Hengel, M Ashley Spies, Maria Spies

Open access · bronzeAbstract readReview
In one paragraph

Review in Cell chemical biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 90 papers.

0numbers the graph read from it
0cells of the map it votes in
90citing papers in PubMed
6.6field-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

90 citing papers in PubMed, 138 citations in OpenAlex.

  1. Article
  2. Targeting IPNature communications · 2026
    Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Monomers and short oligomers of human RAD52 promote single-strand annealing.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. RAD52 prevents accumulation ofbioRxiv : the preprint server for biology · 2024
    Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Review
  19. Article
  20. Human DNA Mutations and their Impact on Genetic Disorders.Recent patents on biotechnology · 2024
    Review

30 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

3 authors at 1 institution in 1 country.

Sarah R HengelDepartment of Biochemistry, University of Iowa, Iowa City, IA 52242, USA.
M Ashley SpiesDepartment of Biochemistry, University of Iowa, Iowa City, IA 52242, USA; Department of Pharmaceutical Sciences and Experimental Therapeutics, Division of Medicinal and Natural Products Chemistry, University of Iowa, Iowa City, IA 52242, USA. Electronic address: m-ashley-spies@uiowa.edu.
Maria SpiesDepartment of Biochemistry, University of Iowa, Iowa City, IA 52242, USA. Electronic address: maria-spies@uiowa.edu.
University of Iowa · US

Funding

Viral VectorP30CA086862 · NCI · UNIVERSITY OF IOWA · PI Christopher K Laubenthal · 2000 to 2026
$70.0M
Exploiting Enzyme Plasticity in Drug Discovery: application to glutamate racemaseR01GM097373 · NIGMS · UNIVERSITY OF IOWA · PI SPIES, MICHAEL ASHLEY · 2012 to 2020
$2.7M
Regulation of unwinding and remodeling activities in FeS-DNA helicasesR01GM108617 · NIGMS · UNIVERSITY OF IOWA · PI SPIES, MARIA · 2014 to 2018
$1.6M
NCI NIH HHS P30 CA086862NIGMS NIH HHS R01 GM097373NIGMS NIH HHS R01 GM108617
6 · The paper itself

Abstract

To maintain stable genomes and to avoid cancer and aging, cells need to repair a multitude of deleterious DNA lesions, which arise constantly in every cell. Processes that support genome integrity in normal cells, however, allow cancer cells to develop resistance to radiation and DNA-damaging chemotherapeutics. Chemical inhibition of the key DNA repair proteins and pharmacologically induced synthetic lethality have become instrumental in both dissecting the complex DNA repair networks and as promising anticancer agents. The difficulty in capitalizing on synthetically lethal interactions in cancer cells is that many potential targets do not possess well-defined small-molecule binding determinates. In this review, we discuss several successful campaigns to identify and leverage small-molecule inhibitors of the DNA repair proteins, from PARP1, a paradigm case for clinically successful small-molecule inhibitors, to coveted new targets, such as RAD51 recombinase, RAD52 DNA repair protein, MRE11 nuclease, and WRN DNA helicase.

Indexed as

DNA RepairDNA-Binding ProteinsDNA HelicasesHumansMRE11 Homologue ProteinNeoplasmsPoly(ADP-ribose) Polymerase InhibitorsRad51 RecombinaseRad52 DNA Repair and Recombination ProteinSmall Molecule LibrariesDNA-Binding ProteinsDNA HelicasesMRE11 Homologue ProteinMRE11 protein, humanPoly(ADP-ribose) Polymerase InhibitorsRad51 RecombinaseRad52 DNA Repair and Recombination ProteinSmall Molecule LibrariesBLM DNA helicaseBRCA1BRCA2DNA repairhomologous recombinationMRE11PARP1 (poly(ADP-ribose)polymerase1)PARP inhibitorsRAD51RAD52RECQ1 DNA helicaseTOP1WRN DNA helicase

Identifiers

PMID28938088
PMCPMC5679738
OpenAlexW2757972128

What OpenQuestion holds

Textmetadata
LicenceTDM
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.