Evidence map›Paper›PMID 34861994›Full record

ReviewSeminars in radiation oncology2022

Targeting the ATM Kinase to Enhance the Efficacy of Radiotherapy and Outcomes for Cancer Patients.

María E Guerra García, David G Kirsch, Zachary J Reitman

Open access · greenAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Seminars in radiation oncology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 1 pooled it
2.8field-weighted citation impact, top 8% 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

22 citing papers in PubMed, 1 synthesis or guideline pooled it, 43 citations in OpenAlex.

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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 at 1 institution in 1 country.

María E Guerra GarcíaDepartment of Radiation Oncology, Duke University School of Medicine, Durham NC.
David G KirschDepartment of Radiation Oncology, Duke University School of Medicine, Durham NC; Department of Pharmacology & Cancer Biology, Duke University School of Medicine, Durham NC.
Zachary J ReitmanDepartment of Radiation Oncology, Duke University School of Medicine, Durham NC; The Preston Robert Tisch Brain Tumor Center at Duke University Medical Center, Durham NC. Electronic address: zjr@duke.edu.
Duke University · US

Funding

Advancing Cancer Therapy through Ground Breaking Research in Radiation BiologyR35CA197616 · NCI · ROSWELL PARK CANCER INSTITUTE CORP · PI David Guy Kirsch · 2016 to 2026
$10.7M
NCI NIH HHS R35 CA197616
6 · The paper itself

Abstract

Targeting the DNA damage response represents a promising approach to improve the efficacy of radiation therapy. One appealing target for this approach is the serine/threonine kinase ataxia telangiectasia mutated (ATM), which is activated by DNA double strand breaks to orchestrate the cellular response to ionizing radiation. Small-molecule inhibitors targeting ATM have entered clinical trials testing their safety in combination with radiation therapy or in combination with other DNA damaging agents. Here, we review biochemical, genetic, and cellular functional studies of ATM, phenotypes associated with germline and somatic cancer mutations in ATM in humans, and experiments in genetically engineered mouse models that support a rationale for investigating ATM inhibitors as radiosensitizers for cancer therapy. These data identify important synthetic lethal relationships, which suggest that ATM inhibitors may be particularly effective in tumors with defects in other nodes of the DNA damage response. The potential for ATM inhibition to improve immunotherapy responses in preclinical models represents another emerging area of research. We summarize ongoing clinical trials of ATM inhibitors with radiotherapy. We also discuss critical ongoing areas of investigation that include discovery of biomarkers that predict for radiosensitization by ATM inhibitors and identification of effective combinations of ATM inhibitors, radiation therapy, other DNA damage response-directed therapies, and/or immunotherapies.

Indexed as

Ataxia Telangiectasia Mutated ProteinsNeoplasmsAnimalsCell Cycle ProteinsDNADNA-Binding ProteinsDNA DamageDNA RepairHumansMiceTumor Suppressor ProteinsAtaxia Telangiectasia Mutated ProteinsATM protein, humanCell Cycle ProteinsDNADNA-Binding ProteinsTumor Suppressor Proteins

Identifiers

PMID34861994
PMCPMC8647772
OpenAlexW3217332990

What OpenQuestion holds

Textmetadata
LicenceTDM
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.