Evidence map›Paper›PMID 23613359›Full record

ReviewInternational journal of cancer2014

Roles of Chk1 in cell biology and cancer therapy.

Youwei Zhang, Tony Hunter

Open access · bronzeAbstract readReview
In one paragraph

Review in International journal of cancer, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 253 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
253citing papers in PubMed, 1 pooled it
8.8field-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

253 citing papers in PubMed, 1 synthesis or guideline pooled it, 453 citations in OpenAlex.

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193 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.

Youwei ZhangDepartment of Pharmacology, Case Comprehensive Cancer Center, School of Medicine, Case Western Reserve University, Cleveland, OH.
Tony Hunter
Case Western Reserve University · USSalk Institute for Biological Studies · US

Funding

SOMATIC CELL CYCLE REGULATION BY PHOSPHORYLATIONR01CA080100 · NCI · SALK INSTITUTE FOR BIOLOGICAL STUDIES · PI HUNTER, TONY R. · 1999 to 2018
$13.1M
SIGNAL TRANSDUCTION BY TYROSINE PHOSPHORYLATIONR01CA082683 · NCI · SALK INSTITUTE FOR BIOLOGICAL STUDIES · PI HUNTER, TONY R. · 1999 to 2019
$12.2M
Spatiotemporal Regulation of Chk1 in Cell Biology, Cancer Etiology and TherapyR01CA163214 · NCI · CASE WESTERN RESERVE UNIVERSITY · PI ZHANG, YOU-WEI · 2012 to 2016
$1.6M
Roles of the Checkpoint Kinase Chk1 in Cancer Biology and TherapyR00CA126173 · NCI · CASE WESTERN RESERVE UNIVERSITY · PI ZHANG, YOU-WEI · 2009 to 2011
$740k
NCI NIH HHS CA80100NCI NIH HHS CA82683NCI NIH HHS R00 CA126173NCI NIH HHS R00CA126173NCI NIH HHS R01 CA080100NCI NIH HHS R01 CA082683NCI NIH HHS R01 CA163214
6 · The paper itself

Abstract

The evolutionally conserved DNA damage response (DDR) and cell cycle checkpoints preserve genome integrity. Central to these genome surveillance pathways is a protein kinase, Chk1. DNA damage induces activation of Chk1, which then transduces the checkpoint signal and facilitates cell cycle arrest and DNA damage repair. Significant progress has been made recently toward our understanding of Chk1 regulation and its implications in cancer etiology and therapy. Specifically, a model that involves both spatiotemporal and conformational changes of proteins has been proposed for Chk1 activation. Further, emerging evidence suggests that Chk1 does not appear to be a tumor suppressor; instead, it promotes tumor growth and may contribute to anticancer therapy resistance. Recent data from our laboratory suggest that activating, but not inhibiting, Chk1 in the absence of chemotherapy might represent an innovative approach to suppress tumor growth. These findings suggest unique regulation of Chk1 in cell biology and cancer etiology, pointing to novel strategies for targeting Chk1 in cancer therapy.

Indexed as

Cell CycleCheckpoint Kinase 1DNA ReplicationDrug Resistance, NeoplasmEnzyme ActivationHumansNeoplasmsPhosphorylationProtein ConformationProtein KinasesCheckpoint Kinase 1CHEK1 protein, humanProtein Kinasescancercancer therapycell cycle checkpointsChk1

Identifiers

PMID23613359
PMCPMC3852170
OpenAlexW1594035260

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.