Evidence map›Paper›PMID 26567630›Full record

ArticleScientific reports2015

Role of YAP and TAZ in pancreatic ductal adenocarcinoma and in stellate cells associated with cancer and chronic pancreatitis.

Susan Morvaridi, Deepti Dhall, Mark I Greene, Stephen J Pandol, Qiang Wang

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.

0numbers the graph read from it
0cells of the map it votes in
65citing papers in PubMed
4.4field-weighted citation impact, top 5% 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

65 citing papers in PubMed, 97 citations in OpenAlex.

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  20. TAZ promotes PDX1-mediated insulinogenesis.Cellular and molecular life sciences : CMLS · 2022
    Article

5 more citing papers are in PubMed but not listed here.

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

5 authors at 2 institutions in 1 country.

Susan MorvaridiDepartment of Medicine; Cedars-Sinai Medical Center, Los Angeles, CA 90048.
Deepti DhallDepartment of Pathology and Laboratory Medicine; Cedars-Sinai Medical Center, Los Angeles, CA 90048.
Mark I GreeneDepartment of Pathology and Laboratory Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104.
Stephen J PandolDepartment of Medicine; Cedars-Sinai Medical Center, Los Angeles, CA 90048.
Qiang WangDepartment of Medicine; Cedars-Sinai Medical Center, Los Angeles, CA 90048.
Cedars-Sinai Medical Center · USUniversity of Pennsylvania · 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
RECEPTOR MEDIATED BREAST CANCER THERAPYR01CA089481 · NCI · UNIVERSITY OF PENNSYLVANIA · PI GREENE, MARK I · 2001 to 2015
$3.3M
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 TR000124NCATS NIH HHS UL1TR000124NCI NIH HHS P01 CA163200NCI NIH HHS P01CA163200NCI NIH HHS R01 CA089481NCI NIH HHS R01CA089481NIAAA NIH HHS P50 AA011999NIAAA NIH HHS P50 AA11999NIDDK NIH HHS P01 DK098108NIDDK NIH HHS P01DK098108
6 · The paper itself

Abstract

Pancreatic ductal adenocarcinoma (PDAC) is characterized by a fibrotic and inflammatory microenvironment that is formed primarily by activated, myofibroblast-like, stellate cells. Although the stellate cells are thought to contribute to tumorigenesis, metastasis and drug resistance of PDAC, the signaling events involved in activation of the stellate cells are not well defined. Functioning as transcription co-factors, Yes-associated protein (YAP) and its homolog transcriptional co-activator with PDZ-binding motif (TAZ) modulate the expression of genes involved in various aspects of cellular functions, such as proliferation and mobility. Using human tissues we show that YAP and TAZ expression is restricted to the centroacinar and ductal cells of normal pancreas, but is elevated in cancer cells. In particular, YAP and TAZ are expressed at high levels in the activated stellate cells of both chronic pancreatitis and PDAC patients as well as in the islets of Langerhans in chronic pancreatitis tissues. Of note, YAP is up regulated in both acinar and ductal cells following induction of acute and chronic pancreatitis in mice. These findings indicate that YAP and TAZ may play a critical role in modulating pancreatic tissue regeneration, neoplastic transformation, and stellate cell functions in both PDAC and pancreatitis.

Indexed as

Acinar CellsAdaptor Proteins, Signal TransducingAnimalsCarcinoma, Pancreatic DuctalHumansImmunohistochemistryIntracellular Signaling Peptides and ProteinsIslets of LangerhansMiceMice, Inbred C57BLMice, TransgenicMicroscopy, FluorescencePancreatic NeoplasmsPancreatic Stellate CellsPancreatitis, ChronicPhosphoproteinsAdaptor Proteins, Signal TransducingIntracellular Signaling Peptides and ProteinsPhosphoproteinsTrans-ActivatorsTranscriptional Coactivator with PDZ-Binding Motif ProteinsTranscription FactorsWWTR1 protein, humanYAP1 protein, humanYAP-Signaling Proteins

Identifiers

PMID26567630
PMCPMC4645184
OpenAlexW2418179841

What OpenQuestion holds

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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.