Evidence map›Paper›PMID 38378898›Full record

ReviewNature reviews. Clinical oncology2024

Targeting ATR in patients with cancer.

Natalie Y L Ngoi, Patrick G Pilié, Daniel J McGrail, Michal Zimmermann, Katharina Schlacher, Timothy A Yap

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Clinical oncology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
65citing papers in PubMed, 1 pooled it
18.0field-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

65 citing papers in PubMed, 1 synthesis or guideline pooled it, 78 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Review
  4. Article
  5. A transcription factor regulates development of a bacteria-housing eukaryotic cell through DNA damage mitigation.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Pg-Induced ATR Activation Promotes ESCC Progression via M2 TAM Polarization.Journal of oral pathology & medicine : official publication of the International Association of Oral Pathologists and the American Academy of Oral Pathology · 2026
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article

5 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

6 authors at 3 institutions in 3 countries.

Natalie Y L NgoiDepartment of Investigational Cancer Therapeutics (Phase I Clinical Trials Program), Division of Cancer Medicine, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.ORCID http://orcid.org/0000-0003-2071-0715
Patrick G PiliéDepartment of Genitourinary Medical Oncology, Division of Cancer Medicine, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Daniel J McGrailCenter for Immunotherapy and Precision Immuno-Oncology, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, USA.
Michal ZimmermannRepare Therapeutics, St Laurent, Quebec, Canada.ORCID http://orcid.org/0000-0002-9955-1675
Katharina SchlacherDepartment of Cancer Biology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA. KSchlacher@mdanderson.org.
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
The University of Texas MD Anderson Cancer Center · USCleveland Clinic Lerner College of Medicine · USTelesta Therapeutics (Canada) · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pharmacological inhibition of the ataxia telangiectasia and Rad3-related protein serine/threonine kinase (ATR; also known as FRAP-related protein (FRP1)) has emerged as a promising strategy for cancer treatment that exploits synthetic lethal interactions with proteins involved in DNA damage repair, overcomes resistance to other therapies and enhances antitumour immunity. Multiple novel, potent ATR inhibitors are being tested in clinical trials using biomarker-directed approaches and involving patients across a broad range of solid cancer types; some of these inhibitors have now entered phase III trials. Further insight into the complex interactions of ATR with other DNA replication stress response pathway components and with the immune system is necessary in order to optimally harness the potential of ATR inhibitors in the clinic and achieve hypomorphic targeting of the various ATR functions. Furthermore, a deeper understanding of the diverse range of predictive biomarkers of response to ATR inhibitors and of the intraclass differences between these agents could help to refine trial design and patient selection strategies. Key challenges that remain in the clinical development of ATR inhibitors include the optimization of their therapeutic index and the development of rational combinations with these agents. In this Review, we detail the molecular mechanisms regulated by ATR and their clinical relevance, and discuss the challenges that must be addressed to extend the benefit of ATR inhibitors to a broad population of patients with cancer.

Indexed as

NeoplasmsAtaxia Telangiectasia Mutated ProteinsDNA DamageDNA RepairHumansProtein Kinase InhibitorsAtaxia Telangiectasia Mutated ProteinsATR protein, humanProtein Kinase Inhibitors

Identifiers

PMID38378898
OpenAlexW4391954183

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.