Evidence map›Paper›PMID 29167438›Full record

ArticleNature communications2017

Checkpoint kinase 1 is essential for normal B cell development and lymphomagenesis.

Fabian Schuler, Johannes G Weiss, Silke E Lindner, Michael Lohmüller, Sebastian Herzog, Simon F Spiegl, Philipp Menke, Stephan Geley, Verena Labi, Andreas Villunger

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.7field-weighted citation impact, top 9% 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

20 citing papers in PubMed, 45 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

10 authors at 1 institution in 1 country.

Fabian SchulerDivision of Developmental Immunology, Biocenter, Medical University of Innsbruck, Innrain 80, A-6020, Innsbruck, Austria.
Johannes G WeissDivision of Developmental Immunology, Biocenter, Medical University of Innsbruck, Innrain 80, A-6020, Innsbruck, Austria.
Silke E LindnerDivision of Developmental Immunology, Biocenter, Medical University of Innsbruck, Innrain 80, A-6020, Innsbruck, Austria.
Michael LohmüllerDivision of Developmental Immunology, Biocenter, Medical University of Innsbruck, Innrain 80, A-6020, Innsbruck, Austria.
Sebastian HerzogDivision of Developmental Immunology, Biocenter, Medical University of Innsbruck, Innrain 80, A-6020, Innsbruck, Austria.
Simon F SpieglDivision of Molecular Pathophysiology, Biocenter, Medical University of Innsbruck, Innrain 80, A-6020, Innsbruck, Austria.ORCID http://orcid.org/0000-0001-6445-1087
Philipp MenkeDivision of Molecular Pathophysiology, Biocenter, Medical University of Innsbruck, Innrain 80, A-6020, Innsbruck, Austria.ORCID http://orcid.org/0000-0002-9795-4470
Stephan GeleyDivision of Molecular Pathophysiology, Biocenter, Medical University of Innsbruck, Innrain 80, A-6020, Innsbruck, Austria.
Verena LabiDivision of Developmental Immunology, Biocenter, Medical University of Innsbruck, Innrain 80, A-6020, Innsbruck, Austria.
Andreas VillungerDivision of Developmental Immunology, Biocenter, Medical University of Innsbruck, Innrain 80, A-6020, Innsbruck, Austria. andreas.villunger@i-med.ac.at.
Innsbruck Medical University · AT

Funding

Austrian Science Fund FWF I 3271
6 · The paper itself

Abstract

Checkpoint kinase 1 (CHK1) is critical for intrinsic cell cycle control and coordination of cell cycle progression in response to DNA damage. Despite its essential function, CHK1 has been identified as a target to kill cancer cells and studies using Chk1 haploinsufficient mice initially suggested a role as tumor suppressor. Here, we report on the key role of CHK1 in normal B-cell development, lymphomagenesis and cell survival. Chemical CHK1 inhibition induces BCL2-regulated apoptosis in primary as well as malignant B-cells and CHK1 expression levels control the timing of lymphomagenesis in mice. Moreover, total ablation of Chk1 in B-cells arrests their development at the pro-B cell stage, a block that, surprisingly, cannot be overcome by inhibition of mitochondrial apoptosis, as cell cycle arrest is initiated as an alternative fate to limit the spread of damaged DNA. Our findings define CHK1 as essential in B-cell development and potent target to treat blood cancer.

Indexed as

AnimalsApoptosisB-LymphocytesBurkitt LymphomaCarcinogenesisCell DifferentiationCell Line, TumorCell SurvivalCheckpoint Kinase 1DNA DamageGenes, mycHaploinsufficiencyHumansLymphomaLymphopoiesisMiceCheckpoint Kinase 1CHEK1 protein, humanChek1 protein, mouse

Identifiers

PMID29167438
PMCPMC5700047
OpenAlexW2770695743

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.