Evidence map›Paper›PMID 29899559›Full record

ReviewNature reviews. Cancer2018

Targeting ATR in cancer.

Emilio Lecona, Oscar Fernandez-Capetillo

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Cancer, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 219 papers.

0numbers the graph read from it
0cells of the map it votes in
219citing papers in PubMed
14.1field-weighted citation impact, top 1% 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

219 citing papers in PubMed, 341 citations in OpenAlex.

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  3. Design, synthesis and anti-breast cancer activity evaluation of 6,7-dihydro-5Journal of enzyme inhibition and medicinal chemistry · 2026
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159 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

2 authors at 1 institution in 1 country.

Emilio LeconaGenomic Instability Group, Spanish National Cancer Research Centre (CNIO), Madrid, Spain.
Oscar Fernandez-CapetilloGenomic Instability Group, Spanish National Cancer Research Centre (CNIO), Madrid, Spain. ofernandez@cnio.es.
Spanish National Cancer Research Centre · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The chemical treatment of cancer started with the realization that DNA damaging agents such as mustard gas present notable antitumoural properties. Consequently, early drug development focused on genotoxic chemicals, some of which are still widely used in the clinic. However, the efficacy of such therapies is often limited by the side effects of these drugs on healthy cells. A refinement to this approach is to use compounds that can exploit the presence of DNA damage in cancer cells. Given that replication stress (RS) is a major source of genomic instability in cancer, targeting the RS-response kinase ataxia telangiectasia and Rad3-related protein (ATR) has emerged as a promising alternative. With ATR inhibitors now entering clinical trials, we here revisit the biology behind this strategy and discuss potential biomarkers that could be used for a better selection of patients who respond to therapy.

Indexed as

Ataxia Telangiectasia Mutated ProteinsDNA DamageDrug DevelopmentGenomic InstabilityHumansIndolesIsoxazolesMolecular Targeted TherapyMorpholinesNeoplasmsNitroso CompoundsOxazinesProtein Kinase InhibitorsPyrazinesPyrimidinesQuinolines4-cyclohexylmethoxy-5-nitrosopyrimidine-2,6-diamineAtaxia Telangiectasia Mutated ProteinsATR protein, humanberzosertibceralasertibETP-46464IndolesIsoxazolesMorpholinesNitroso CompoundsOxazinesProtein Kinase InhibitorsPyrazinesPyrimidinesQuinolinesSulfonamidesSulfoxides

Identifiers

PMID29899559
OpenAlexW2808161922

What OpenQuestion holds

Textmetadata
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.