Evidence map›Paper›PMID 39627502›Full record

ReviewNature reviews. Clinical oncology2025

Synthetic lethal strategies for the development of cancer therapeutics.

Natalie Y L Ngoi, David Gallo, Carlos Torrado, Mirella Nardo, Daniel Durocher, Timothy A Yap

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Clinical oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing 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

39 citing papers in PubMed.

  1. Review
  2. Review
  3. Review
  4. Target identification and assessment in the era of AI.Nature reviews. Drug discovery · 2026
    Review
  5. Review
  6. Review
  7. Review
  8. Review
  9. Article
  10. Current oncology (Toronto, Ont.) · 2026
    Review
  11. Article
  12. VEXAS syndrome.Nature reviews. Disease primers · 2026
    Review
  13. Review
  14. Review
  15. Review
  16. Review
  17. Article
  18. Usnic Acid Derivatives as Inhibitors ofInternational journal of molecular sciences · 2026
    Article
  19. Article
  20. Review
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.

Natalie Y L Ngoi *Department of Investigational Cancer Therapeutics (Phase I Clinical Trials Program), Division of Cancer Medicine, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
David Gallo *Repare Therapeutics, Inc., Montreal, Quebec, Canada.
Carlos TorradoDepartment of Investigational Cancer Therapeutics (Phase I Clinical Trials Program), Division of Cancer Medicine, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Mirella NardoDepartment of Investigational Cancer Therapeutics (Phase I Clinical Trials Program), Division of Cancer Medicine, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Daniel DurocherLunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital, Toronto, Ontario, Canada.
Timothy A YapDepartment of Investigational Cancer Therapeutics (Phase I Clinical Trials Program), Division of Cancer Medicine, The University of Texas MD Anderson Cancer Center, Houston, TX, USA. tyap@mdanderson.org.ORCID http://orcid.org/0000-0002-2154-3309

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Synthetic lethality is a genetic phenomenon whereby the simultaneous presence of two different genetic alterations impairs cellular viability. Importantly, targeting synthetic lethal interactions offers potential therapeutic strategies for cancers with alterations in pathways that might otherwise be considered undruggable. High-throughput screening methods based on modern CRISPR-Cas9 technologies have emerged and become crucial for identifying novel synthetic lethal interactions with the potential for translation into biologically rational cancer therapeutic strategies as well as associated predictive biomarkers of response capable of guiding patient selection. Spurred by the clinical success of PARP inhibitors in patients with BRCA-mutant cancers, novel agents targeting multiple synthetic lethal interactions within DNA damage response pathways are in clinical development, and rational strategies targeting synthetic lethal interactions spanning alterations in epigenetic, metabolic and proliferative pathways have also emerged and are in late preclinical and/or early clinical testing. In this Review, we provide a comprehensive overview of established and emerging technologies for synthetic lethal drug discovery and development and discuss promising therapeutic strategies targeting such interactions.

Indexed as

NeoplasmsSynthetic Lethal MutationsAntineoplastic AgentsCRISPR-Cas SystemsDNA DamageDrug DiscoveryHumansPoly(ADP-ribose) Polymerase InhibitorsAntineoplastic AgentsPoly(ADP-ribose) Polymerase Inhibitors

Identifiers

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.