Evidence map›Paper›PMID 31557131›Full record

ArticleJCI insight2019

YAP1 oncogene is a context-specific driver for pancreatic ductal adenocarcinoma.

Bo Tu, Jun Yao, Sammy Ferri-Borgogno, Jun Zhao, Shujuan Chen, Qiuyun Wang, Liang Yan, Xin Zhou, Cihui Zhu, Seungmin Bang and 14 more

Open access · goldAbstract read
In one paragraph

Article in JCI insight, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
5.3field-weighted citation impact, top 4% 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

46 citing papers in PubMed, 75 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article
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

24 authors at 6 institutions in 4 countries.

Bo TuMolecular and Cellular Oncology Department.
Jun YaoMolecular and Cellular Oncology Department.
Sammy Ferri-BorgognoPathology Department, and.
Jun ZhaoPathology Department, and.
Shujuan ChenMolecular and Cellular Oncology Department.
Qiuyun WangMolecular and Cellular Oncology Department.
Liang YanMolecular and Cellular Oncology Department.
Xin ZhouMolecular and Cellular Oncology Department.
Cihui ZhuMolecular and Cellular Oncology Department.
Seungmin BangDepartment of Internal Medicine, Institute of Gastroenterology, Yonsei University College of Medicine, Seoul, South Korea.
Qing ChangInstitute for Applied Cancer Science and.
Christopher A BristowInstitute for Applied Cancer Science and.
Ya'an KangSurgical Oncology Department, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA.
Hongwu ZhengDepartment of Pathology and Laboratory Medicine, Weill Cornell Medical College, New York, New York, USA.
Huamin WangPathology Department, and.
Jason B FlemingSurgical Oncology Department, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA.
Michael KimSurgical Oncology Department, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA.
Timothy P HeffernanInstitute for Applied Cancer Science and.
Giulio F DraettaGenomic Medicine Department, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA.
Duojia PanDepartment of Physiology, Howard Hughes Medical Institute, University of Texas Southwestern Medical Center, Dallas, Texas, USA.
Anirban MaitraPathology Department, and.
Wantong YaoGenomic Medicine Department, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA.
Sonal GuptaPathology Department, and.
Haoqiang YingMolecular and Cellular Oncology Department.
Cellular Research (United States) · USThe University of Texas MD Anderson Cancer Center · USInstitute for Applied Science · GBCornell University · USHoward Hughes Medical Institute · USYonsei University · KR

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Scott Kopetz · 1985 to 2026
$290.8M
The RAS and P13K Pathways in Pancreatic AdenocarcinomaP01CA117969 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI DEPINHO, RONALD ANTHONY · 2006 to 2025
$41.7M
Elucidating and targeting subtype-specific driver in pancreatic cancerR01CA214793 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI YING, HAOQIANG · 2019 to 2023
$1.8M
Howard Hughes Medical InstituteNCI NIH HHS P01 CA117969NCI NIH HHS P30 CA016672NCI NIH HHS R01 CA214793
6 · The paper itself

Abstract

Transcriptomic profiling classifies pancreatic ductal adenocarcinoma (PDAC) into several molecular subtypes with distinctive histological and clinical characteristics. However, little is known about the molecular mechanisms that define each subtype and their correlation with clinical outcome. Mutant KRAS is the most prominent driver in PDAC, present in over 90% of tumors, but the dependence of tumors on oncogenic KRAS signaling varies between subtypes. In particular, the squamous subtype is relatively independent of oncogenic KRAS signaling and typically displays much more aggressive clinical behavior versus the progenitor subtype. Here, we identified that yes-associated protein 1 (YAP1) activation is enriched in the squamous subtype and associated with poor prognosis. Activation of YAP1 in progenitor subtype cancer cells profoundly enhanced malignant phenotypes and transformed progenitor subtype cells into squamous subtype. Conversely, depletion of YAP1 specifically suppressed tumorigenicity of squamous subtype PDAC cells. Mechanistically, we uncovered a significant positive correlation between WNT5A expression and YAP1 activity in human PDAC and demonstrated that WNT5A overexpression led to YAP1 activation and recapitulated a YAP1-dependent but Kras-independent phenotype of tumor progression and maintenance. Thus, our study identifies YAP1 oncogene as a major driver of squamous subtype PDAC and uncovers the role of WNT5A in driving PDAC malignancy through activation of the YAP pathway.

Indexed as

OncogenesAdaptor Proteins, Signal TransducingCarcinoma, Pancreatic DuctalHumansPancreatic NeoplasmsTranscription FactorsWnt-5a ProteinYAP-Signaling ProteinsAdaptor Proteins, Signal TransducingTranscription FactorsWnt-5a ProteinWNT5A protein, humanYAP1 protein, humanYAP-Signaling ProteinsCancerGeneticsMouse modelsOncogenesOncology

Identifiers

PMID31557131
PMCPMC6948828
OpenAlexW2974998460

What OpenQuestion holds

Textmetadata
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.