Evidence map›Paper›PMID 31659152›Full record

ArticleCell death & disease2019

Truncated PPM1D impairs stem cell response to genotoxic stress and promotes growth of APC-deficient tumors in the mouse colon.

Monika Burocziova, Kamila Burdova, Andra S Martinikova, Petr Kasparek, Petra Kleiblova, Stine A Danielsen, Marianna Borecka, Gabriela Jenikova, Lucie Janečková, Jozef Pavel and 14 more

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

17 citing papers in PubMed, 20 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

24 authors at 6 institutions in 4 countries.

Monika BurocziovaCancer Cell Biology, Institute of Molecular Genetics of the Czech Academy of Sciences, Prague, Czech Republic.
Kamila BurdovaCancer Cell Biology, Institute of Molecular Genetics of the Czech Academy of Sciences, Prague, Czech Republic.
Andra S MartinikovaCancer Cell Biology, Institute of Molecular Genetics of the Czech Academy of Sciences, Prague, Czech Republic.
Petr KasparekCzech Centre for Phenogenomics, Institute of Molecular Genetics of the Czech Academy of Sciences, Prague, Czech Republic.
Petra KleiblovaInstitute of Biochemistry and Experimental Oncology, First Faculty of Medicine, Charles University, Prague, Czech Republic.
Stine A DanielsenDepartment Molecular Oncology, Institute for Cancer Research, & K.G. Jebsen Colorectal Cancer Research Centre, Oslo University Hospital, Oslo, Norway.
Marianna BoreckaInstitute of Biochemistry and Experimental Oncology, First Faculty of Medicine, Charles University, Prague, Czech Republic.ORCID http://orcid.org/0000-0001-6413-222X
Gabriela JenikovaCancer Cell Biology, Institute of Molecular Genetics of the Czech Academy of Sciences, Prague, Czech Republic.
Lucie JanečkováCell and Developmental Biology, Institute of Molecular Genetics of the Czech Academy of Sciences, Prague, Czech Republic.ORCID http://orcid.org/0000-0003-0139-7065
Jozef PavelCancer Cell Biology, Institute of Molecular Genetics of the Czech Academy of Sciences, Prague, Czech Republic.
Petra ZemankovaInstitute of Biochemistry and Experimental Oncology, First Faculty of Medicine, Charles University, Prague, Czech Republic.
Michaela SchneiderovaDepartment of Abdominal, Thoracic Surgery and Traumatology, First Faculty of Medicine, Charles University and General Faculty Hospital in Prague, Prague, Czech Republic.
Lucie SchwarzovaDepartment of Endocrinology and Metabolism, First Faculty of Medicine, Charles University and General Faculty Hospital in Prague, Prague, Czech Republic.
Ivana TichaDepartment of Oncology and Department of Clinical and Experimental Medicine, Linköping University, Linköping, Sweden.
Xiao-Feng SunDepartment of Oncology and Department of Clinical and Experimental Medicine, Linköping University, Linköping, Sweden.
Katerina JiraskovaMolecular Biology of Cancer, Institute of Experimental Medicine, ASCR, Prague, Czech Republic.
Vaclav LiskaBiomedical Centre, Faculty of Medicine in Pilsen, Charles University, Prague, Czech Republic.
Ludmila VodickovaMolecular Biology of Cancer, Institute of Experimental Medicine, ASCR, Prague, Czech Republic.
Pavel VodickaMolecular Biology of Cancer, Institute of Experimental Medicine, ASCR, Prague, Czech Republic.
Radislav SedlacekCzech Centre for Phenogenomics, Institute of Molecular Genetics of the Czech Academy of Sciences, Prague, Czech Republic.
Zdenek KleiblInstitute of Biochemistry and Experimental Oncology, First Faculty of Medicine, Charles University, Prague, Czech Republic.ORCID http://orcid.org/0000-0003-2050-9667
Ragnhild A LotheDepartment Molecular Oncology, Institute for Cancer Research, & K.G. Jebsen Colorectal Cancer Research Centre, Oslo University Hospital, Oslo, Norway.
Vladimír KorinekCell and Developmental Biology, Institute of Molecular Genetics of the Czech Academy of Sciences, Prague, Czech Republic.
Libor MacurekCancer Cell Biology, Institute of Molecular Genetics of the Czech Academy of Sciences, Prague, Czech Republic. libor.macurek@img.cas.cz.
Charles University · CZCzech Academy of Sciences, Institute of Molecular Genetics · CZLinköping University · SEOslo University Hospital · NOCzech Academy of Sciences · CZCzech Academy of Sciences, Institute of Experimental Medicine · CZ

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Protein phosphatase magnesium-dependent 1 delta (PPM1D) terminates cell response to genotoxic stress by negatively regulating the tumor suppressor p53 and other targets at chromatin. Mutations in the exon 6 of the PPM1D result in production of a highly stable, C-terminally truncated PPM1D. These gain-of-function PPM1D mutations are present in various human cancers but their role in tumorigenesis remains unresolved. Here we show that truncated PPM1D impairs activation of the cell cycle checkpoints in human non-transformed RPE cells and allows proliferation in the presence of DNA damage. Next, we developed a mouse model by introducing a truncating mutation in the PPM1D locus and tested contribution of the oncogenic PPM1D

Indexed as

Adenomatous Polyposis Coli ProteinAnimalsCarcinogenesisCell Cycle CheckpointsCell ProliferationChromatinColonic NeoplasmsDNA DamageDNA RepairExonsFluorouracilGene Expression Regulation, NeoplasticHumansMiceMutationProtein Phosphatase 2CAdenomatous Polyposis Coli Proteinadenomatous polyposis coli protein, mouseChromatinFluorouracilPPM1D protein, humanProtein Phosphatase 2CTrp53 protein, mouseTumor Suppressor Protein p53

Identifiers

PMID31659152
PMCPMC6817818
OpenAlexW2981655495

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.