Evidence map›Paper›PMID 36420962›Full record

ArticleBioscience reports2022

Evolving DNA repair synthetic lethality targets in cancer.

Sanat Kulkarni, Juliette Brownlie, Jennie N Jeyapalan, Nigel P Mongan, Emad A Rakha, Srinivasan Madhusudan

Open access · goldAbstract read
In one paragraph

Article in Bioscience reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.3field-weighted citation impact, top 9% 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

17 citing papers in PubMed, 23 citations in OpenAlex.

  1. Review
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  4. SGSS05-NS3, a covalent SETD8 inhibitor that activates p53 pathway in neuroblastoma.Journal of experimental & clinical cancer research : CR · 2025
    Article
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  13. Targeting chromosomal instability in patients with cancer.Nature reviews. Clinical oncology · 2024
    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

6 authors at 3 institutions in 1 country.

Sanat KulkarniDepartment of Medicine, Sandwell and West Birmingham Hospitals, Lyndon, West Bromwich B71 4HJ, U.K.
Juliette BrownlieAcademic Unit of Translational Medical Sciences, Nottingham Biodiscovery Institute, School of Medicine, University of Nottingham, University Park, Nottingham NG7 3RD, U.K.
Jennie N JeyapalanAcademic Unit of Translational Medical Sciences, Nottingham Biodiscovery Institute, School of Medicine, University of Nottingham, University Park, Nottingham NG7 3RD, U.K.
Nigel P MonganAcademic Unit of Translational Medical Sciences, Nottingham Biodiscovery Institute, School of Medicine, University of Nottingham, University Park, Nottingham NG7 3RD, U.K.
Emad A RakhaAcademic Unit of Translational Medical Sciences, Nottingham Biodiscovery Institute, School of Medicine, University of Nottingham, University Park, Nottingham NG7 3RD, U.K.
Srinivasan MadhusudanAcademic Unit of Translational Medical Sciences, Nottingham Biodiscovery Institute, School of Medicine, University of Nottingham, University Park, Nottingham NG7 3RD, U.K.ORCID 0000-0002-5354-5480
University of Nottingham · GBNottingham University Hospitals NHS Trust · GBSandwell & West Birmingham Hospitals NHS Trust · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

DNA damage signaling response and repair (DDR) is a critical defense mechanism against genomic instability. Impaired DNA repair capacity is an important risk factor for cancer development. On the other hand, up-regulation of DDR mechanisms is a feature of cancer chemotherapy and radiotherapy resistance. Advances in our understanding of DDR and its complex role in cancer has led to several translational DNA repair-targeted investigations culminating in clinically viable precision oncology strategy using poly(ADP-ribose) polymerase (PARP) inhibitors in breast, ovarian, pancreatic, and prostate cancers. While PARP directed synthetic lethality has improved outcomes for many patients, the lack of sustained clinical response and the development of resistance pose significant clinical challenges. Therefore, the search for additional DDR-directed drug targets and novel synthetic lethality approaches is highly desirable and is an area of intense preclinical and clinical investigation. Here, we provide an overview of the mammalian DNA repair pathways and then focus on current state of PARP inhibitors (PARPi) and other emerging DNA repair inhibitors for synthetic lethality in cancer.

Indexed as

NeoplasmsSynthetic Lethal MutationsAnimalsDNA DamageDNA RepairHumansPoly(ADP-ribose) Polymerase InhibitorsPoly(ADP-ribose) PolymerasesPrecision MedicinePoly(ADP-ribose) Polymerase InhibitorsPoly(ADP-ribose) PolymerasesATM inhibitorsATR inhibitorsDNA synthesis and repairPARPPARP inhibitorsSynthetic lethality

Identifiers

PMID36420962
PMCPMC9760629
OpenAlexW4309859277

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.