Evidence map›Paper›PMID 26988419›Full record

ArticleGenes & development2016

Coordination of stress signals by the lysine methyltransferase SMYD2 promotes pancreatic cancer.

Nicolas Reynoird, Pawel K Mazur, Timo Stellfeld, Natasha M Flores, Shane M Lofgren, Scott M Carlson, Elisabeth Brambilla, Pierre Hainaut, Ewa B Kaznowska, Cheryl H Arrowsmith and 4 more

Open access · diamondAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Genes & development, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed
–field-weighted citation impact
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

52 citing papers in PubMed, 86 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

14 authors at 6 institutions in 5 countries.

Nicolas ReynoirdDepartment of Biology, Stanford University, Stanford, California 94305, USA; Institut Albert Bonniot, U1209, Institut National de la Santé et de la Recherche Médicale, UMR5309, Centre National de la Recherche Scientifique, Université Grenoble-Alpes, F-38700 Grenoble, France;
Pawel K MazurDepartment of Pediatrics, Stanford University School of Medicine, Stanford, California 94305, USA; Department of Genetics, Stanford University School of Medicine, Stanford, California 94305, USA;
Timo StellfeldGlobal Drug Discovery, Bayer Pharma AG, 13353 Berlin, Germany;
Natasha M FloresDepartment of Pediatrics, Stanford University School of Medicine, Stanford, California 94305, USA; Department of Genetics, Stanford University School of Medicine, Stanford, California 94305, USA;
Shane M LofgrenDepartment of Medicine, Stanford University School of Medicine, Stanford, California 94305, USA; Institute for Immunity, Transplantation, and Infection, Stanford University School of Medicine, Stanford, California 94305, USA;
Scott M CarlsonDepartment of Biology, Stanford University, Stanford, California 94305, USA;
Elisabeth BrambillaInstitut Albert Bonniot, U1209, Institut National de la Santé et de la Recherche Médicale, UMR5309, Centre National de la Recherche Scientifique, Université Grenoble-Alpes, F-38700 Grenoble, France;
Pierre HainautInstitut Albert Bonniot, U1209, Institut National de la Santé et de la Recherche Médicale, UMR5309, Centre National de la Recherche Scientifique, Université Grenoble-Alpes, F-38700 Grenoble, France;
Ewa B KaznowskaFaculty of Medicine, Centre for Innovative Research in Medical and Natural Sciences, University of Rzeszów, 35959 Rzeszów, Poland;
Cheryl H ArrowsmithStructural Genomics Consortium, Princess Margaret Cancer Centre, University of Toronto, Toronto, Ontario M5G 2M9, Canada; Department of Medical Biophysics, University of Toronto, Toronto, Ontario M5G 2M9, Canada.
Purvesh KhatriDepartment of Medicine, Stanford University School of Medicine, Stanford, California 94305, USA; Institute for Immunity, Transplantation, and Infection, Stanford University School of Medicine, Stanford, California 94305, USA;
Carlo StresemannGlobal Drug Discovery, Bayer Pharma AG, 13353 Berlin, Germany;
Or GozaniDepartment of Biology, Stanford University, Stanford, California 94305, USA;
Julien SageDepartment of Pediatrics, Stanford University School of Medicine, Stanford, California 94305, USA; Department of Genetics, Stanford University School of Medicine, Stanford, California 94305, USA;
Stanford University · USBayer (Germany) · DEUniversité Grenoble Alpes · FRCentre National de la Recherche Scientifique · FRPrincess Margaret Cancer Centre · CARzeszów University · PL

Funding

Leveraging innovative technologies in basic and clinical cancer researchT32CA009302 · NCI · STANFORD UNIVERSITY · PI LAURA D ATTARDI, Aaron M Newman · 1985 to 2026
$19.1M
Mechanisms of action of the Smyd3 methyltransferase in cancer cellsR01CA172560 · NCI · STANFORD UNIVERSITY · PI GOZANI, OR P., SAGE, JULIEN · 2013 to 2017
$2.3M
The SMYD3-ERK5 signaling module in pancreatic cancerR00CA197816 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI MAZUR, PAWEL K. · 2017 to 2019
$732k
The SMYD3-ERK5 signaling module in pancreatic cancerK99CA197816 · NCI · STANFORD UNIVERSITY · PI MAZUR, PAWEL K. · 2015 to 2016
$294k
The role of PRDM1 in epigenetic regulation and tumor suppressionK99CA190803 · NCI · STANFORD UNIVERSITY · PI CARLSON, SCOTT MOORE · 2015 to 2016
$225k
NCI NIH HHS K99 CA190803NCI NIH HHS K99CA190803NCI NIH HHS K99 CA197816NCI NIH HHS K99CA19781601NCI NIH HHS R00 CA197816NCI NIH HHS R01 CA172560NCI NIH HHS T32 CA009302Wellcome Trust
6 · The paper itself

Abstract

Pancreatic ductal adenocarcinoma (PDAC) is a lethal form of cancer with few therapeutic options. We found that levels of the lysine methyltransferase SMYD2 (SET and MYND domain 2) are elevated in PDAC and that genetic and pharmacological inhibition of SMYD2 restricts PDAC growth. We further identified the stress response kinase MAPKAPK3 (MK3) as a new physiologic substrate of SMYD2 in PDAC cells. Inhibition of MAPKAPK3 impedes PDAC growth, identifying a potential new kinase target in PDAC. Finally, we show that inhibition of SMYD2 cooperates with standard chemotherapy to treat PDAC cells and tumors. These findings uncover a pivotal role for SMYD2 in promoting pancreatic cancer.

Indexed as

AnimalsCarcinoma, Pancreatic DuctalCell ProliferationDisease Models, AnimalEnzyme ActivationEnzyme InhibitorsHEK293 CellsHistone-Lysine N-MethyltransferaseHumansIntracellular Signaling Peptides and ProteinsMiceMice, Inbred C57BLPancreatic NeoplasmsProtein Serine-Threonine KinasesSignal TransductionStress, PhysiologicalEnzyme InhibitorsHistone-Lysine N-MethyltransferaseIntracellular Signaling Peptides and ProteinsMAP-kinase-activated kinase 3Protein Serine-Threonine KinasesSmyd2 protein, mouselung adenocarcinomalysine methylationMAPKAPK3pancreatic cancerRasSMYD2

Identifiers

PMID26988419
PMCPMC4826394
OpenAlexW2301007008

What OpenQuestion holds

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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.