Evidence map›Paper›PMID 31526907›Full record

ArticleCellular and molecular gastroenterology and hepatology2020

Loss of Pancreatic E-Cadherin Causes Pancreatitis-Like Changes and Contributes to Carcinogenesis.

Yoshihiro Kaneta, Takeshi Sato, Yohko Hikiba, Makoto Sugimori, Soichiro Sue, Hiroaki Kaneko, Kuniyasu Irie, Tomohiko Sasaki, Masaaki Kondo, Makoto Chuma and 2 more

Open access · goldAbstract read
In one paragraph

Article in Cellular and molecular gastroenterology and hepatology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.2field-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

18 citing papers in PubMed, 23 citations in OpenAlex.

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  16. E-Cadherin: An Enigma in Pancreatic Diseases.Cellular and molecular gastroenterology and hepatology · 2020
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

12 authors at 2 institutions in 1 country.

Yoshihiro KanetaDepartment of Gastroenterology, Graduate School of Medicine, Yokohama City University, Yokohama, Japan.
Takeshi SatoDepartment of Gastroenterology, Graduate School of Medicine, Yokohama City University, Yokohama, Japan.
Yohko HikibaDepartment of Gastroenterology, Graduate School of Medicine, Yokohama City University, Yokohama, Japan.
Makoto SugimoriDepartment of Gastroenterology, Graduate School of Medicine, Yokohama City University, Yokohama, Japan.
Soichiro SueDepartment of Gastroenterology, Graduate School of Medicine, Yokohama City University, Yokohama, Japan.
Hiroaki KanekoDepartment of Gastroenterology, Graduate School of Medicine, Yokohama City University, Yokohama, Japan.
Kuniyasu IrieDepartment of Gastroenterology, Graduate School of Medicine, Yokohama City University, Yokohama, Japan.
Tomohiko SasakiDepartment of Gastroenterology, Graduate School of Medicine, Yokohama City University, Yokohama, Japan.
Masaaki KondoDepartment of Gastroenterology, Graduate School of Medicine, Yokohama City University, Yokohama, Japan.
Makoto ChumaGastroenterological Centre, Yokohama City University Medical Centre, Yokohama, Japan.
Wataru ShibataDepartment of Gastroenterology, Graduate School of Medicine, Yokohama City University, Yokohama, Japan; Advanced Medical Research Center, Yokohama City University, Yokohama, Japan.
Shin MaedaDepartment of Gastroenterology, Graduate School of Medicine, Yokohama City University, Yokohama, Japan. Electronic address: smaeda@yokohama-cu.ac.jp.
Yokohama City University · JPYokohama City University Medical Center · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND &

aimsE-cadherin (Cdh1) is a key molecule for adherence required for maintenance of structural homeostasis. Loss of E-cadherin leads to poor prognosis and the development of resistance to chemotherapy in pancreatic cancer. Here, we evaluated the physiological and pathologic roles of E-cadherin in the pancreas.

methodsWe crossbred Ptf1a-Cre mice with Cdh1

resultsNone of the Ptf1a-Cre mice crossbred with Cdh1

conclusionsUnder physiological conditions, E-cadherin is important for maintaining the tissue homeostasis of the pancreas. Under pathologic conditions with mutational Kras activation, E-cadherin plays an important role in tumor formation via the acquisition of tumorigenic activity.

Indexed as

AnimalsCadherinsCarcinogenesisDisease Models, AnimalEpithelial-Mesenchymal TransitionGene Expression Regulation, NeoplasticHistone Deacetylase 1HumansMetaplasiaMiceMice, KnockoutOrganoidsPancreasPancreatic NeoplasmsPancreatitisPrimary Cell CultureCadherinsCdh1 protein, mouseHdac1 protein, mouseHistone Deacetylase 1Hras protein, mouseProto-Oncogene Proteins p21(ras)transcription factor PTF1Transcription FactorsE-CadherinGene RegulationOncogenePancreasPancreatic Cancer

Identifiers

PMID31526907
PMCPMC6889596
OpenAlexW2972542006

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.