Evidence map›Paper›PMID 30510993›Full record

ArticleCellular and molecular gastroenterology and hepatology2019

The Loss of ATRX Increases Susceptibility to Pancreatic Injury and Oncogenic KRAS in Female But Not Male Mice.

Claire C Young, Ryan M Baker, Christopher J Howlett, Todd Hryciw, Joshua E Herman, Douglas Higgs, Richard Gibbons, Howard Crawford, Arthur Brown, Christopher L Pin

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

Article in Cellular and molecular gastroenterology and hepatology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
2.2field-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

13 citing papers in PubMed, 31 citations in OpenAlex.

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  13. ATRX Links Chromatin Remodeling to Inflammation and Tumorigenesis in the Pancreas.Cellular and molecular gastroenterology and hepatology · 2019
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 4 institutions in 3 countries.

Claire C YoungDepartment of Paediatrics, University of Western Ontario, London, Ontario, Canada; Department of Physiology and Pharmacology, University of Western Ontario, London, Ontario, Canada; Department of Oncology, University of Western Ontario, London, Ontario, Canada; Children's Health Research Institute, London, Ontario, Canada.
Ryan M BakerDepartment of Paediatrics, University of Western Ontario, London, Ontario, Canada; Children's Health Research Institute, London, Ontario, Canada.
Christopher J HowlettDepartment of Pathology and Laboratory Medicine, University of Western Ontario, London, Ontario, Canada.
Todd HryciwDepartment of Anatomy and Cell Biology, Schulich School of Medicine & Dentistry, University of Western Ontario, London, Ontario, Canada; Robarts Research Institute, London, Ontario, Canada.
Joshua E HermanRobarts Research Institute, London, Ontario, Canada.
Douglas HiggsMRC Molecular Haematology Unit, Institute of Molecular Medicine, John Radcliffe Hospital, Oxford, United Kingdom.
Richard GibbonsMRC Molecular Haematology Unit, Institute of Molecular Medicine, John Radcliffe Hospital, Oxford, United Kingdom.
Howard CrawfordMolecular & Integrative Physiology and Internal Medicine, University of Michigan, Ann Arbor, Michigan.
Arthur BrownDepartment of Anatomy and Cell Biology, Schulich School of Medicine & Dentistry, University of Western Ontario, London, Ontario, Canada; Robarts Research Institute, London, Ontario, Canada; Children's Health Research Institute, London, Ontario, Canada.
Christopher L PinDepartment of Paediatrics, University of Western Ontario, London, Ontario, Canada; Department of Physiology and Pharmacology, University of Western Ontario, London, Ontario, Canada; Department of Oncology, University of Western Ontario, London, Ontario, Canada; Children's Health Research Institute, London, Ontario, Canada. Electronic address: cpin@uwo.ca.
Western University · CAJohn Radcliffe Hospital · GBRobarts Clinical Trials · CAUniversity of Michigan · US

Funding

Medical Research Council MC_U137961147Medical Research Council MC_UU_00016/3
6 · The paper itself

Abstract

Background: Pancreatic ductal adenocarcinoma (PDAC) is the third leading cause of cancer death in North America, accounting for >30,000 deaths annually. Although somatic activating mutations in Methods: Mice allowing conditional loss of Results: Mice lacking Conclusions: Our results indicate the absence of ATRX increases sensitivity to injury and oncogenic KRAS only in female mice. This is an instance of a sex-specific mutation that enhances oncogenic KRAS's ability to promote pancreatic intraepithelial lesion formation.

Indexed as

OncogenesAcinar CellsAnimalsApoptosisBasic Helix-Loop-Helix ProteinsDNA Mutational AnalysisFemaleGene DeletionMaleMicePancreasPancreatic NeoplasmsPrecancerous ConditionsProto-Oncogene Proteins p21(ras)X-linked Nuclear ProteinAtrx protein, mouseBasic Helix-Loop-Helix ProteinsBhlha15 protein, mouseHras protein, mouseProto-Oncogene Proteins p21(ras)X-linked Nuclear ProteinADM, acinar-to-duct cell metaplasiaANOVA, analysis of varianceATRX, ɑ-thalassemia, mental-retardation, X-linkedCIP, cerulein induced pancreatitisCPA, carboxypeptidaseDAXX, death associated protein 6ds, double strandedEpigeneticsEZH2, Enhancer of Zeste Homologue 2, MKA, Mist1creERT/+KrasLSL-G12D/+AtrxflΔ18MIST1Pancreatic Ductal AdenocarcinomaPanIN, pancreatic intraepithelial lesionPDAC, pancreatic ductal adenocarcinomaSOX9WT, wild-type

Identifiers

PMID30510993
PMCPMC6260375
OpenAlexW2889678507

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.