Evidence map›Paper›PMID 35418690›Full record

ArticleOncogene2022

Suppression of mutant Kirsten-RAS (KRAS

Andrew M Kidger, Mark K Saville, Linda K Rushworth, Jane Davidson, Julia Stellzig, Motoharu Ono, Ludwig A Kuebelsbeck, Klaus-Peter Janssen, Bernhard Holzmann, Jennifer P Morton and 3 more

Open access · hybridAbstract read
In one paragraph

Article in Oncogene, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
5.7field-weighted citation impact, top 3% 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

15 citing papers in PubMed, 52 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

13 authors at 4 institutions in 2 countries.

Andrew M KidgerStress Response Laboratory, Jacqui Wood Cancer Centre, Division of Cellular and Systems Medicine, School of Medicine, University of Dundee, Dundee, DD1 9SY, UK.
Mark K SavilleStress Response Laboratory, Jacqui Wood Cancer Centre, Division of Cellular and Systems Medicine, School of Medicine, University of Dundee, Dundee, DD1 9SY, UK.
Linda K RushworthStress Response Laboratory, Jacqui Wood Cancer Centre, Division of Cellular and Systems Medicine, School of Medicine, University of Dundee, Dundee, DD1 9SY, UK.
Jane DavidsonStress Response Laboratory, Jacqui Wood Cancer Centre, Division of Cellular and Systems Medicine, School of Medicine, University of Dundee, Dundee, DD1 9SY, UK.
Julia StellzigStress Response Laboratory, Jacqui Wood Cancer Centre, Division of Cellular and Systems Medicine, School of Medicine, University of Dundee, Dundee, DD1 9SY, UK.
Motoharu OnoStress Response Laboratory, Jacqui Wood Cancer Centre, Division of Cellular and Systems Medicine, School of Medicine, University of Dundee, Dundee, DD1 9SY, UK.
Ludwig A KuebelsbeckDepartment of Surgery, School of Medicine, Klinikum Rechts der Isar, Technical University of Munich, Munich, Germany.ORCID http://orcid.org/0000-0002-2888-6558
Klaus-Peter JanssenDepartment of Surgery, School of Medicine, Klinikum Rechts der Isar, Technical University of Munich, Munich, Germany.ORCID http://orcid.org/0000-0002-4707-7887
Bernhard HolzmannDepartment of Surgery, School of Medicine, Klinikum Rechts der Isar, Technical University of Munich, Munich, Germany.
Jennifer P MortonInstitute of Cancer Sciences, Garscube Estate, Switchback Road, Glasgow, G61 1QH, UK.
Owen J SansomInstitute of Cancer Sciences, Garscube Estate, Switchback Road, Glasgow, G61 1QH, UK.ORCID http://orcid.org/0000-0001-9540-3010
Christopher J CauntDepartment of Biology and Biochemistry, University of Bath, Claverton Down, Bath, BA2 7AY, UK.
Stephen M KeyseStress Response Laboratory, Jacqui Wood Cancer Centre, Division of Cellular and Systems Medicine, School of Medicine, University of Dundee, Dundee, DD1 9SY, UK. s.m.keyse@dundee.ac.uk.ORCID http://orcid.org/0000-0002-5150-8221
University of Dundee · GBTUM Klinikum · DECancer Research UK · GBUniversity of Bath · GB

Funding

Cancer Research UK 12053Cancer Research UK 29996Cancer Research UK A12053Cancer Research UK A17196Cancer Research UK A21139Cancer Research UK A25142Cancer Research UK A25233Cancer Research UK A29996Medical Research Council MR/N020790/1
6 · The paper itself

Abstract

The cytoplasmic phosphatase DUSP6 and its nuclear counterpart DUSP5 are negative regulators of RAS/ERK signalling. Here we use deletion of either Dusp5 or Dusp6 to explore the roles of these phosphatases in a murine model of KRAS

Indexed as

Carcinoma, Pancreatic DuctalDual Specificity Phosphatase 6Dual-Specificity PhosphatasesPancreatic NeoplasmsAnimalsAtrophyCarcinogenesisHyperplasiaMicePancreasProto-Oncogene Proteins p21(ras)Weight LossDual Specificity Phosphatase 6Dual-Specificity PhosphatasesDusp5 protein, mouseDusp6 protein, mouseHras protein, mouseProto-Oncogene Proteins p21(ras)

Identifiers

PMID35418690
PMCPMC9106580
OpenAlexW4223911362

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.