Evidence map›Paper›PMID 30863319›Full record

ArticleFrontiers in physiology2019

MSP-RON Signaling Is Activated in the Transition From Pancreatic Intraepithelial Neoplasia (PanIN) to Pancreatic Ductal Adenocarcinoma (PDAC).

Ce Li, Susan Morvaridi, Gloria Lam, Chintan Chheda, Yoshiko Kamata, Makoto Katsumata, Mouad Edderkaoui, Xiaopu Yuan, Nicholas Nissen, Stephen J Pandol and 1 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in physiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed, 1 pooled it
2.7field-weighted citation impact, top 11% 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

14 citing papers in PubMed, 1 synthesis or guideline pooled it, 21 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Phenomics (Cham, Switzerland) · 2024
    Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Mucin Expression and Splicing Determine Novel Subtypes and Patient Mortality in Pancreatic Ductal Adenocarcinoma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2021
    Article
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  10. Review
  11. Article
  12. Article
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  14. Review
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

11 authors at 1 institution in 2 countries.

Ce LiDepartment of Medical Oncology, The First Affiliated Hospital of China Medical University, Shenyang, China.
Susan MorvaridiDepartment of Medicine, Cedars-Sinai Medical Center, Los Angeles, CA, United States.
Gloria LamDepartment of Medicine, Cedars-Sinai Medical Center, Los Angeles, CA, United States.
Chintan ChhedaDepartment of Medicine, Cedars-Sinai Medical Center, Los Angeles, CA, United States.
Yoshiko KamataDepartment of Biomedical Sciences, Cedars-Sinai Medical Center, Los Angeles, CA, United States.
Makoto KatsumataDepartment of Biomedical Sciences, Cedars-Sinai Medical Center, Los Angeles, CA, United States.
Mouad EdderkaouiDepartment of Medicine, Cedars-Sinai Medical Center, Los Angeles, CA, United States.
Xiaopu YuanDepartment of Pathology, Cedars-Sinai Medical Center, Los Angeles, CA, United States.
Nicholas NissenComprehensive Transplant Center, Cedars-Sinai Medical Center, Los Angeles, CA, United States.
Stephen J PandolDepartment of Medicine, Cedars-Sinai Medical Center, Los Angeles, CA, United States.
Qiang WangDepartment of Medicine, Cedars-Sinai Medical Center, Los Angeles, CA, United States.
Cedars-Sinai Medical Center · US

Funding

UCLA Clinical Translational Science InstituteUL1TR001881 · NCATS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI ARLEEN F. BROWN, ARASH NAEIM · 2016 to 2026
$118.1M
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
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 UL1 TR001881NCI NIH HHS P01 CA163200NIAAA NIH HHS P50 AA011999NIDDK NIH HHS P01 DK098108
6 · The paper itself

Abstract

Pancreatic ductal adenocarcinoma (PDAC) is among the deadliest epithelial malignancies and remains difficult to treat. Pancreatic intraepithelial neoplasias (PanINs) represent the majority of the pre-cancer lesions in the pancreas. The PDAC microenvironment consists of activated pancreatic stellate cells (PSCs) and immune cells, which are thought to contribute to neoplastic transformation. However, the signaling events involved in driving the transition from the neoplastic precursor to the more advanced and aggressive forms in the pancreas are not well understood. Recepteur d'Origine Nantais (RON) is a c-MET family receptor tyrosine kinase that is implicated in playing a role in cell proliferation, migration and other aspects of tumorigenesis. Macrophage stimulating protein (MSP) is the ligand for RON and becomes activated upon proteolytic cleavage by matriptase (also known as ST14), a type II transmembrane serine protease. In the current study, by immunohistochemistry (IHC) analysis of human pancreatic tissues, we found that the expression levels MSP and matriptase are drastically increased during the transition from the preneoplastic PanIN stages to the more advanced and aggressive PDAC. Moreover, RON is highly expressed in both PDAC and in cancer-associated stellate cells. In contrast, MSP, RON, and matriptase are expressed at low levels, if any, in normal pancreas. Our study underscores an emerging role of MSP-RON autocrine and paracrine signaling events in driving malignant progression in the pancreas.

Indexed as

matriptasemetastasisMSP/MST1pancreaspancreatic ductal adenocarcinomapancreatic intraepithelial neoplasiaRON/MST1Rstellate cell

Identifiers

PMID30863319
PMCPMC6399467
OpenAlexW2916630482

What OpenQuestion holds

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LicenceCC BY
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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.