Evidence map›Paper›PMID 42909385›Full record

ArticleNAR cancer2026

EXO1 inhibition selectively kills replication repair-deficient cancer cells.

Marija Maric, Sarah E McClelland, Simon J Boulton

Abstract read
In one paragraph

Article in NAR cancer, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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.

Marija MaricDSB Repair Metabolism Lab, The Francis Crick Institute, London NW1 1AT, United Kingdom.
Sarah E McClellandThe Chromosomal Instability Lab, Centre for Cancer Evolution, Barts Cancer Institute, Queen Mary University of London, London EC1M 6BQ, United Kingdom.
Simon J BoultonDSB Repair Metabolism Lab, The Francis Crick Institute, London NW1 1AT, United Kingdom.ORCID https://orcid.org/0000-0001-6936-6834

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Deficiencies in DNA repair pathways create context-specific vulnerabilities that may be exploited therapeutically. Recent studies have established EXO1 as a druggable nuclease, but the genetic contexts that confer sensitivity to EXO1 inhibition remain incompletely defined. Here, we assessed whether pharmacological inhibition of EXO1 selectively targets repair-deficient cancer cells across multiple DNA repair backgrounds. Using potent and selective EXO1 inhibitors, we demonstrate impaired viability in cells deficient for Fanconi Anaemia pathway components (FANCG and APITD1/MHF1), BRCA1-A complex factor BRCC36, and the spliceosome factor ZRSR2. EXO1 inhibition in

Indexed as

DNA RepairDNA Repair EnzymesDNA ReplicationEnzyme InhibitorsExodeoxyribonucleasesCell Line, TumorCell SurvivalHistonesHumansPhosphorylationPoly(ADP-ribose) Polymerase InhibitorsDNA Repair EnzymesEnzyme InhibitorsEXO1 protein, humanExodeoxyribonucleasesHistonesPoly(ADP-ribose) Polymerase Inhibitors

Identifiers

PMID42909385
PMCPMC13684273

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.