Evidence map›Paper›PMID 29054375›Full record

ReviewRadiotherapy and oncology : journal of the European Society for Therapeutic Radiology and Oncology2018

ATR/CHK1 inhibitors and cancer therapy.

Zhaojun Qiu, Nancy L Oleinick, Junran Zhang

Open access · greenAbstract readReview
In one paragraph

Review in Radiotherapy and oncology : journal of the European Society for Therapeutic Radiology and Oncology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 219 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
219citing papers in PubMed, 1 pooled it
7.8field-weighted citation impact, top 2% 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

219 citing papers in PubMed, 1 synthesis or guideline pooled it, 372 citations in OpenAlex.

  1. Pooled it
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  14. Targeting IPNature communications · 2026
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  18. Pro-ATO/Allicin Liposomes for Dual-Pathway Targeting of p53-Mutant Tumors.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
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  20. Article

159 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

3 authors at 1 institution in 1 country.

Zhaojun QiuDepartment of Radiation Oncology, School of Medicine, Case Western Reserve University, Cleveland, USA.
Nancy L OleinickDepartment of Radiation Oncology, School of Medicine, Case Western Reserve University, Cleveland, USA; Case Comprehensive Cancer Center, Case Western Reserve University, Cleveland, USA.
Junran ZhangDepartment of Radiation Oncology, School of Medicine, Case Western Reserve University, Cleveland, USA; Case Comprehensive Cancer Center, Case Western Reserve University, Cleveland, USA. Electronic address: Junran.zhang@case.edu.
Case Western Reserve University · US

Funding

TUMOR METABOLISM PROGRAMP30CA043703 · NCI · CASE WESTERN RESERVE UNIVERSITY · PI Amar Desai · 1987 to 2026
$142.3M
THE ROLE OF NEDD4-1 IN IGF-1R SIGNALINGR01CA154625 · NCI · WASHINGTON UNIVERSITY · PI ZHANG, JUNRAN · 2011 to 2016
$1.6M
NCI NIH HHS P30 CA043703NCI NIH HHS R01 CA154625
6 · The paper itself

Abstract

The cell cycle checkpoint proteins ataxia-telangiectasia-mutated-and-Rad3-related kinase (ATR) and its major downstream effector checkpoint kinase 1 (CHK1) prevent the entry of cells with damaged or incompletely replicated DNA into mitosis when the cells are challenged by DNA damaging agents, such as radiation therapy (RT) or chemotherapeutic drugs, that are the major modalities to treat cancer. This regulation is particularly evident in cells with a defective G1 checkpoint, a common feature of cancer cells, due to p53 mutations. In addition, ATR and/or CHK1 suppress replication stress (RS) by inhibiting excess origin firing, particularly in cells with activated oncogenes. Those functions of ATR/CHK1 make them ideal therapeutic targets. ATR/CHK1 inhibitors have been developed and are currently used either as single agents or paired with radiotherapy or a variety of genotoxic chemotherapies in preclinical and clinical studies. Here, we review the status of the development of ATR and CHK1 inhibitors. We also discuss the potential mechanisms by which ATR and CHK1 inhibition induces cell killing in the presence or absence of exogenous DNA damaging agents, such as RT and chemotherapeutic agents. Lastly, we discuss synthetic lethality interactions between the inhibition of ATR/CHK1 and defects in other DNA damage response (DDR) pathways/genes.

Indexed as

Ataxia Telangiectasia Mutated ProteinsCheckpoint Kinase 1DNA DamageHumansMolecular Targeted TherapyNeoplasmsPoly(ADP-ribose) Polymerase InhibitorsProtein Kinase InhibitorsRadiation ToleranceAtaxia Telangiectasia Mutated ProteinsATR protein, humanCheckpoint Kinase 1CHEK1 protein, humanPoly(ADP-ribose) Polymerase InhibitorsProtein Kinase InhibitorsATRCell cycle checkpointsCHK1DNA damage responseDNA replication stressSynthetic lethality

Identifiers

PMID29054375
PMCPMC5856582
OpenAlexW2766300480

What OpenQuestion holds

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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.