Evidence map›Paper›PMID 20068082›Full record

ReviewClinical cancer research : an official journal of the American Association for Cancer Research2010

New insights into checkpoint kinase 1 in the DNA damage response signaling network.

Yun Dai, Steven Grant

Registry-linked trialOpen access · bronzeAbstract readReview
In one paragraph

Review in Clinical cancer research : an official journal of the American Association for Cancer Research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT01748825 (A Phase I Study of Single-agent AZD1775), which is not on this map. Cited by 233 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
233citing papers in PubMed, 1 pooled it
18.1field-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.

NCT01748825 phase1completednot on this mapstarted 2012, after this paper: background citation

A Phase I Study of Single-agent AZD1775 (MK-1775), a Wee1 Inhibitor, in Patients With Advanced Refractory Solid Tumors

TypeinterventionalSponsorNational Cancer Institute (NCI)Ran2012 to 2020Enrolled67ConditionsSolid TumorsArmsMK-1775 (AZD1775)
3 · Its place in the literature

Who cites it

233 citing papers in PubMed, 1 synthesis or guideline pooled it, 435 citations in OpenAlex.

  1. Pooled it
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  13. Molecular therapy. Oncology · 2025
    Article
  14. Article
  15. Targeting WEE1 Kinase for Breast Cancer Therapeutics: An Update.International journal of molecular sciences · 2025
    Review
  16. Article
  17. Article
  18. Review
  19. Article
  20. Article

173 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

2 authors at 2 institutions in 1 country.

Yun DaiDepartment of Medicine, Institute for Molecular Medicine, and Division of Hematology/Oncology, Department of Medicine, Virginia Commonwealth University Massey Cancer Center, Richmond, Virginia 23298, USA.
Steven Grant
Institute for Molecular Medicine · USVirginia Commonwealth University · US

Funding

SPORE in LymphomaP50CA130805 · NCI · UNIVERSITY OF ROCHESTER · PI FISHER, RICHARD I · 2008 to 2012
$11.7M
NF-kappaB Inhibitors and Differentiation-Inducers in LeukemiaR01CA093738 · NCI · VIRGINIA COMMONWEALTH UNIVERSITY · PI GRANT, STEVEN · 2002 to 2011
$2.4M
Checkpoint Abrogation and MEK 1/2 Inhibition in MyelomaR01CA100866 · NCI · VIRGINIA COMMONWEALTH UNIVERSITY · PI GRANT, STEVEN · 2003 to 2013
$2.2M
Promotion of Nucleoside Analog Induced Apoptosis by HDIsR01CA063753 · NCI · VIRGINIA COMMONWEALTH UNIVERSITY · PI GRANT, STEVEN · 1994 to 2008
$2.2M
Phase I Trial of Bortezomib and Romidepsin in CLL and Small Cell LymphomaR21CA137823 · NCI · VIRGINIA COMMONWEALTH UNIVERSITY · PI GRANT, STEVEN · 2009 to 2010
$537k
CDK/histone deacetylase inhibition in acute leukemiaR21CA115260 · NCI · VIRGINIA COMMONWEALTH UNIVERSITY · PI GRANT, STEVEN · 2005 to 2006
$529k
NCI NIH HHS 1P50 CA130805NCI NIH HHS CA100866NCI NIH HHS CA63753NCI NIH HHS CA93738NCI NIH HHS P50 CA130805NCI NIH HHS R01 CA063753NCI NIH HHS R01 CA093738NCI NIH HHS R01 CA100866NCI NIH HHS R21 CA115260NCI NIH HHS R21 CA137823
6 · The paper itself

Abstract

The DNA damage response (DDR) represents a complex network of multiple signaling pathways involving cell cycle checkpoints, DNA repair, transcriptional programs, and apoptosis, through which cells maintain genomic integrity following various endogenous (metabolic) or environmental stresses. In cancer treatment, the DDR occurs in response to various genotoxic insults by diverse cytotoxic agents and radiation, representing an important mechanism limiting chemotherapeutic and radiotherapeutic efficacy. This has prompted the development of agents targeting DDR signaling pathways, particularly checkpoint kinase 1 (Chk1), which contributes to all currently defined cell cycle checkpoints, including G1/S, intra-S-phase, G2/M, and the mitotic spindle checkpoint. Although numerous agents have been developed with the primary goal of enhancing the activity of DNA-damaging agents or radiation, the therapeutic outcome of this strategy remains to be determined. Recently, new insights into DDR signaling pathways support the notion that Chk1 represents a core component central to the entire DDR, including direct involvement in DNA repair and apoptotic events in addition to checkpoint regulation. Together, these new insights into the role of Chk1 in the DDR machinery could provide an opportunity for novel approaches to the development of Chk1 inhibitor strategies.

Indexed as

DNA DamageAntineoplastic AgentsCheckpoint Kinase 1DNA RepairEnzyme ActivationHumansModels, BiologicalNeoplasmsProtein Kinase InhibitorsProtein KinasesSignal TransductionAntineoplastic AgentsCheckpoint Kinase 1CHEK1 protein, humanProtein Kinase InhibitorsProtein Kinases

Identifiers

PMID20068082
PMCPMC2939735
OpenAlexW2140990686

What OpenQuestion holds

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Registered trials

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.