Evidence map›Paper›PMID 27855278›Full record

ArticleThe American journal of pathology2017

Cadherin-11 Is a Cell Surface Marker Up-Regulated in Activated Pancreatic Stellate Cells and Is Involved in Pancreatic Cancer Cell Migration.

Chiara Birtolo, Hung Pham, Susan Morvaridi, Chintan Chheda, Vay Liang W Go, Andrzej Ptasznik, Mouad Edderkaoui, Michael H Weisman, Erika Noss, Michael B Brenner and 4 more

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.8field-weighted citation impact, top 8% 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

23 citing papers in PubMed, 44 citations in OpenAlex.

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  14. Epigenetic Mechanisms of Pancreatobiliary Fibrosis.Current treatment options in gastroenterology · 2019
    Review
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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 4 institutions in 2 countries.

Chiara BirtoloDepartment of Medicine, Cedars-Sinai Medical Center, Los Angeles, California; Department of Internal Medicine, S. Orsola-Malpighi Hospital, University of Bologna, Bologna, Italy.
Hung PhamDepartment of Medicine, Cedars-Sinai Medical Center, Los Angeles, California.
Susan MorvaridiDepartment of Medicine, Cedars-Sinai Medical Center, Los Angeles, California.
Chintan ChhedaDepartment of Medicine, Cedars-Sinai Medical Center, Los Angeles, California.
Vay Liang W GoDepartment of Medicine, David Geffen School of Medicine at the University of California, Los Angeles, Los Angeles, California.
Andrzej PtasznikDepartment of Medicine, Cedars-Sinai Medical Center, Los Angeles, California.
Mouad EdderkaouiDepartment of Medicine, Cedars-Sinai Medical Center, Los Angeles, California.
Michael H WeismanDepartment of Medicine, Cedars-Sinai Medical Center, Los Angeles, California.
Erika NossDivision of Rheumatology, Immunology, and Allergy, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts.
Michael B BrennerDivision of Rheumatology, Immunology, and Allergy, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts.
Brent LarsonDepartment of Pathology and Laboratory Medicine, Cedars-Sinai Medical Center, Los Angeles, California.
Maha GuindiDepartment of Pathology and Laboratory Medicine, Cedars-Sinai Medical Center, Los Angeles, California.
Qiang WangDepartment of Medicine, Cedars-Sinai Medical Center, Los Angeles, California. Electronic address: qiang.wang@cshs.org.
Stephen J PandolDepartment of Medicine, Cedars-Sinai Medical Center, Los Angeles, California; Department of Medicine, David Geffen School of Medicine at the University of California, Los Angeles, Los Angeles, California; Department of Veterans Affairs, VA Greater Los Angeles Health Care System, Los Angeles, California. Electronic address: stephen.pandol@cshs.org.
Cedars-Sinai Medical Center · USBrigham and Women's Hospital · USUniversity of Bologna · ITUniversity of California, Los Angeles · US

Funding

UCLA Clinical and Translational Science InstituteUL1TR000124 · NCATS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI DUBINETT, STEVEN M. · 2012 to 2015
$57.0M
The Southernearch Center for ALPD and CirrhosisP50AA011999 · NIAAA · UNIVERSITY OF SOUTHERN CALIFORNIA · PI ANNA S. GUKOVSKAYA · 1999 to 2026
$45.8M
Vector and Human Acinar CoreP01DK098108 · NIDDK · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI PANDOL, STEPHEN J. · 2014 to 2018
$8.1M
Targeting diet-induced promotion of Kras-initiated pancreatic adenocarcinomaP01CA163200 · NCI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI PANDOL, STEPHEN J. · 2012 to 2016
$6.2M
Pathophysiology, Epidemiology, and Prevention of Pancreatogenic Diabetes - Administrative SupplementU01DK108314 · NIDDK · CEDARS-SINAI MEDICAL CENTER · PI Mark Goodarzi, Stephen J. Pandol · 2015 to 2026
$6.1M
Cadherin11 in cancer & rheumatoid arthritis: Common target, common therapies? (5)R01CA170653 · NCI · GEORGETOWN UNIVERSITY · PI BYERS, STEPHEN W · 2012 to 2015
$2.4M
Smoking, Alcohol Abuse and the PancreasI01BX001484 · VA · VA GREATER LOS ANGELES HEALTHCARE SYSTEM · PI PANDOL, STEPHEN J. · 2012 to 2015
–
BLRD VA I01 BX001484NCATS NIH HHS UL1 TR000124NCI NIH HHS P01 CA163200NCI NIH HHS R01 CA170653NIAAA NIH HHS P50 AA011999NIDDK NIH HHS P01 DK098108NIDDK NIH HHS U01 DK108314
6 · The paper itself

Abstract

Chronic pancreatitis is a prominent risk factor for the development of pancreatic ductal adenocarcinoma. In both conditions, the activation of myofibroblast-like pancreatic stellate cells (PSCs) plays a predominant role in the formation of desmoplastic reaction through the synthesis of connective tissue and extracellular matrix, inducing local pancreatic fibrosis and an inflammatory response. Yet the signaling events involved in chronic pancreatitis and pancreatic cancer progression and metastasis remain poorly defined. Cadherin-11 (Cad-11, also known as OB cadherin or CDH11) is a cell-to-cell adhesion molecule implicated in many biological functions, including tissue morphogenesis and architecture, extracellular matrix-mediated tissue remodeling, cytoskeletal organization, epithelial-to-mesenchymal transition, and cellular migration. In this study, we show that, in human chronic pancreatitis and pancreatic cancer tissues, Cad-11 expression was significantly increased in PSCs and pancreatic cancer cells. In particular, an increased expression of Cad-11 can be detected on the plasma membrane of activated PSCs isolated from chronic pancreatitis tissues and in pancreatic cancer cells metastasized to the liver. Moreover, knockdown of Cad-11 in cancer cells reduced pancreatic cancer cell migration. Taken together, our data underline the potential role of Cad-11 in PSC activation and pancreatic cancer metastasis.

Indexed as

Cell MovementUp-RegulationBiomarkers, TumorCadherinsCell Line, TumorCell MembraneCell ProliferationGene Expression Regulation, NeoplasticGene Knockdown TechniquesHumansPancreasPancreatic NeoplasmsPancreatic Stellate CellsBiomarkers, TumorCadherinsosteoblast cadherin

Identifiers

PMID27855278
PMCPMC5225304
OpenAlexW2553124867

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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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.