Evidence map›Paper›PMID 40024979›Full record

ReviewTargeted oncology2025

The Development of ATM Inhibitors in Cancer Therapy.

Elizabeth A Ampolini, Judit Jimenez-Sainz, David T Long

Abstract readReview
In one paragraph

Review in Targeted oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing 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

10 citing papers in PubMed.

  1. Review
  2. Review
  3. Review
  4. Review
  5. Review
  6. Review
  7. Review
  8. Article
  9. Article
  10. Therapeutic Targeting of DNA Damage Response Pathways inBrain tumor research and treatment · 2025
    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

3 authors.

Elizabeth A AmpoliniDepartment of Biochemistry and Molecular Biology, Hollings Cancer Center, Medical University of South Carolina, Charleston, SC, 29425, USA.
Judit Jimenez-SainzDepartment of Biochemistry and Molecular Biology, Hollings Cancer Center, Medical University of South Carolina, Charleston, SC, 29425, USA.
David T LongDepartment of Biochemistry and Molecular Biology, Hollings Cancer Center, Medical University of South Carolina, Charleston, SC, 29425, USA. longdt@musc.edu.ORCID http://orcid.org/0000-0001-9232-0316

Funding

Connecting BRCA1 functions with DNA crosslink sensitivityR35GM119512 · NIGMS · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI LONG, DAVID THOMAS · 2016 to 2025
$3.9M
Cellular, Biochemical and Molecular Sciences Training Program: Developing the skills and expertise needed for a changing biomedical landscapeT32GM132055 · NIGMS · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI Amy D Bradshaw, John P O'Bryan · 2019 to 2026
$3.9M
DNA repair dysfunction in cancer induced by altered BRCA2 localizationK22CA273681 · NCI · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI JIMENEZ SAINZ, JUDIT · 2023 to 2025
$618k
American Cancer Society CAT-24-1410062-01-CATHollings Cancer Center, Medical University of South Carolina Dr. Mark Green Young Investigator AwardHollings Cancer Center, Medical University of South Carolina Marti's Wish AwardNational Science Foundation Graduate Research Fellowship Program 2024372992NCI NIH HHS K22 CA273681NIGMS NIH HHS R35 GM119512NIGMS NIH HHS T32 GM132055
6 · The paper itself

Abstract

The ataxia-telangiectasia mutated (ATM) protein kinase plays a critical role in activating the cellular response to DNA double-strand breaks and promoting homology-directed repair. ATM is frequently mutated in cancer, contributing to an accumulation of DNA damage that drives genomic instability. To exploit cancer cells' inherent vulnerability to DNA damage, various small molecule inhibitors have been developed that target ATM. ATM inhibitors have shown great versatility in preclinical studies and increasing use in the clinic. Here, we review the development of ATM inhibitors and their role in cancer therapy. We describe their limitations and the advances that have led to increases in both the number and diversity of active clinical trials targeting ATM. We also discuss ATM's role in personalized medicine and the current challenges to more widespread use of ATM inhibitors in the clinic.

Indexed as

Ataxia Telangiectasia Mutated ProteinsNeoplasmsProtein Kinase InhibitorsHumansAtaxia Telangiectasia Mutated ProteinsATM protein, humanProtein Kinase Inhibitors

Identifiers

PMID40024979
PMCPMC11933189

What OpenQuestion holds

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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.