ArticleNature2025
Comprehensive interrogation of synthetic lethality in the DNA damage response.
Abstract read
In one paragraph
Article in Nature, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
–field-weighted citation impact
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.
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.
Who cites it
41 citing papers in PubMed.
- CRISPR in clinical oncology: translational advances from molecular diagnostics to therapeutics.Nature reviews. Clinical oncology · 2026Review
- Article
- Chemogenomic maps reveal a PRDX1-dependent iron-damage axis in the DNA damage response.Nature chemical biology · 2026Article
- Twisting the End Game: How Telomere Chromatin Modifications Shape Telomere Maintenance.Aging cell · 2026Review
- Nuclear localization of the glutaminyl-tRNA synthetase QARS reveals its role in DNA damage response in ovarian cancer.Nature communications · 2026Article
- SMARCAL1 is a candidate therapeutic target for ALT-positive tumors.Genes & development · 2026Article
- The role of the WD40-repeat protein family in cancer.Molecular cancer · 2026Review
- CME-KGDTI: integrating clustered mutations into knowledge graph embedding for drug-target interaction prediction.BioData mining · 2026Article
- A RHNO1-ATR/Chk1 positive feedback loop sustains the DNA replication stress response.bioRxiv : the preprint server for biology · 2026Article
- Zfp36l1 Inhibits DNA Damage by Regulating p21-E2F1-Rad51 Signaling During Myogenic Differentiation.International journal of molecular sciences · 2026Article
- Article
- CRISPRi-mediatedAntimicrobial agents and chemotherapy · 2026Article
- SLX4IP limits replication stress globally and at ALT telomeres.The EMBO journal · 2026Article
- FET Fusion Oncoproteins Disrupt Physiologic DNA Repair and Create a Targetable Opportunity for ATR Inhibitor Therapy.Cancer research · 2026Article
- Polyadenylation of insulin mRNA by Tent5a regulates pancreatic beta cells.Nature communications · 2026Article
- USP1 inhibition promotes RAD18-dependent PCNA degradation and BRCA1 synthetic lethality.bioRxiv : the preprint server for biology · 2026Article
- Parallel Activation and Interference CRISPR (PAIR) with Sequencing Uncovers DNA Repair Networks Guiding Precision Cell Engineering.bioRxiv : the preprint server for biology · 2026Article
- Secoemestrin C exerts rapid and prominent anti-breast cancer effect in triple-negative breast cancer by inducing SLX4 and YAP degradation.Acta pharmacologica Sinica · 2026Article
- Pancancer Fine-Mapping of Mutational Intolerance Identifies CHEK1 as an Immunosuppressive Driver in Lung Adenocarcinoma.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- SMARCAL1 is a targetable synthetic lethal therapeutic vulnerability in ATRX-deficient gliomas that use alternative lengthening of telomeres.Neuro-oncology · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors.
John Fielden *Institute of Molecular Health Sciences, Department of Biology, Swiss Federal Institute of Technology (ETH) Zurich, Zurich, Switzerland.
Sebastian M Siegner *Institute of Molecular Health Sciences, Department of Biology, Swiss Federal Institute of Technology (ETH) Zurich, Zurich, Switzerland.
Danielle N GallagherInstitute of Molecular Health Sciences, Department of Biology, Swiss Federal Institute of Technology (ETH) Zurich, Zurich, Switzerland.ORCID 0000-0001-5832-652X
Markus S SchröderInstitute of Molecular Health Sciences, Department of Biology, Swiss Federal Institute of Technology (ETH) Zurich, Zurich, Switzerland.ORCID 0000-0001-5942-1254
Maria Rosaria Dello StrittoInstitute for Research in Biomedicine, Faculty of Biomedical Sciences, Università della Svizzera italiana (USI), Bellinzona, Switzerland.ORCID 0000-0002-3899-8051
Simon LamCancer Research UK Cambridge Institute, University of Cambridge, Cambridge, UK.ORCID 0000-0002-4476-0971
Lena KobelInstitute of Molecular Health Sciences, Department of Biology, Swiss Federal Institute of Technology (ETH) Zurich, Zurich, Switzerland.ORCID 0000-0001-7949-141X
Moritz F SchlapanskyInstitute of Molecular Health Sciences, Department of Biology, Swiss Federal Institute of Technology (ETH) Zurich, Zurich, Switzerland.ORCID 0000-0001-6072-7840
Stephen P JacksonCancer Research UK Cambridge Institute, University of Cambridge, Cambridge, UK.ORCID 0000-0001-9317-7937
Petr CejkaInstitute for Research in Biomedicine, Faculty of Biomedical Sciences, Università della Svizzera italiana (USI), Bellinzona, Switzerland.ORCID 0000-0002-9087-032X
Marco JostDepartment of Microbiology, Harvard Medical School, Boston, MA, USA.ORCID 0000-0002-1369-4908
Jacob E CornInstitute of Molecular Health Sciences, Department of Biology, Swiss Federal Institute of Technology (ETH) Zurich, Zurich, Switzerland. jacob.corn@biol.ethz.ch.ORCID 0000-0002-7798-5309
Funding
Capturing, quantifying, and understanding combinatorial effects in small molecule signalingDP2GM154152 · NIGMS · HARVARD MEDICAL SCHOOL · PI Marco Jost · 2023 to 2026
$2.5MDeciphering the logic of glycolipid signaling at the host-microbiome interfaceR00GM130964 · NIGMS · HARVARD MEDICAL SCHOOL · PI JOST, MARCO · 2021 to 2023
$747kNIGMS NIH HHS DP2 GM154152NIGMS NIH HHS R00 GM130964
Abstract
The DNA damage response (DDR) is a multifaceted network of pathways that preserves genome stability
Indexed as
DNA RepairSynthetic Lethal MutationsChromosome BreakageCRISPR-Cas SystemsDNA-Binding ProteinsDNA DamageDNA HelicasesDNA ReplicationEndonucleasesFlap EndonucleasesGenomic InstabilityHeLa CellsHomeostasisHumansIntracellular Signaling Peptides and ProteinsK562 CellsDNA-Binding ProteinsDNA HelicasesEndonucleasesERCC1 protein, humanFANCM protein, humanFlap EndonucleasesIntracellular Signaling Peptides and ProteinsNuclear ProteinsProliferating Cell Nuclear AntigenSMARCAL1 protein, humanUbiquitin-Specific ProteasesUSP1 protein, humanWDR48 protein, human
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Read underepoch 390
Registered trials
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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.