Evidence map›Paper›PMID 35583750›Full record

ReviewMolecular oncology2022

Targeting the DNA damage response and repair in cancer through nucleotide metabolism.

Thomas Helleday, Sean G Rudd

Open access · goldAbstract readReview
In one paragraph

Review in Molecular oncology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
3.4field-weighted citation impact, top 6% 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

34 citing papers in PubMed, 43 citations in OpenAlex.

  1. Review
  2. Structural and cellular insights into DCTPP1 antagonists and their synergistic action with DNMT inhibitors.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  3. Purine metabolic adaptation protects the endothelium from disturbed flow-induced DNA damage and atherosclerosis.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  4. MTHFD2: a promising metabolic checkpoint for diseases.Journal of translational medicine · 2026
    Review
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  8. Review
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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

2 authors at 1 institution in 2 countries.

Thomas HelledayScience for Life Laboratory, Department of Oncology-Pathology, Karolinska Institutet, Stockholm, Sweden.ORCID 0000-0002-7384-092X
Sean G RuddScience for Life Laboratory, Department of Oncology-Pathology, Karolinska Institutet, Stockholm, Sweden.ORCID 0000-0002-4368-3855
Science for Life Laboratory · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The exploitation of the DNA damage response and DNA repair proficiency of cancer cells is an important anticancer strategy. The replication and repair of DNA are dependent upon the supply of deoxynucleoside triphosphate (dNTP) building blocks, which are produced and maintained by nucleotide metabolic pathways. Enzymes within these pathways can be promising targets to selectively induce toxic DNA lesions in cancer cells. These same pathways also activate antimetabolites, an important group of chemotherapies that disrupt both nucleotide and DNA metabolism to induce DNA damage in cancer cells. Thus, dNTP metabolic enzymes can also be targeted to refine the use of these chemotherapeutics, many of which remain standard of care in common cancers. In this review article, we will discuss both these approaches exemplified by the enzymes MTH1, MTHFD2 and SAMHD1. © 2022 The Authors. Molecular Oncology published by John Wiley & Sons Ltd on behalf of Federation of European Biochemical Societies.

Indexed as

NeoplasmsDNA DamageDNA RepairHumansNucleotidesNucleotidescancerDNA damage responsedNTP metabolismMTH1MTHFD2SAMHD1

Identifiers

PMID35583750
PMCPMC9627788
OpenAlexW4280539627

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.