Evidence map›Paper›PMID 29273451›Full record

ArticleGastroenterology2018

Loss of Pten and Activation of Kras Synergistically Induce Formation of Intraductal Papillary Mucinous Neoplasia From Pancreatic Ductal Cells in Mice.

Janel L Kopp, Claire L Dubois, David F Schaeffer, Atefeh Samani, Farnaz Taghizadeh, Robert W Cowan, Andrew D Rhim, Bangyan L Stiles, Mark Valasek, Maike Sander

Abstract read
In one paragraph

Article in Gastroenterology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
3.5field-weighted citation impact, top 6% 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

49 citing papers in PubMed, 77 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Review
  6. Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Clinical and Molecular Attributes and Evaluation of Pancreatic Cystic Neoplasm.Biochimica et biophysica acta. Reviews on cancer · 2023
    Review
  12. Review
  13. Review
  14. Article
  15. Review
  16. Review
  17. Review
  18. Review
  19. Humoral Predictors of Malignancy in IPMN: A Review of the Literature.International journal of molecular sciences · 2021
    Review
  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

10 authors at 4 institutions in 2 countries.

Janel L KoppDepartments of Pediatrics and Cellular and Molecular Medicine, University of California-San Diego, La Jolla, California; Department of Cellular and Physiological Sciences, University of British Columbia, Vancouver, British Columbia, Canada.
Claire L DuboisDepartments of Pediatrics and Cellular and Molecular Medicine, University of California-San Diego, La Jolla, California.
David F SchaefferDepartment of Pathology and Laboratory and Medicine, University of British Columbia, Vancouver, British Columbia, Canada.
Atefeh SamaniDepartment of Cellular and Physiological Sciences, University of British Columbia, Vancouver, British Columbia, Canada.
Farnaz TaghizadehDepartment of Cellular and Physiological Sciences, University of British Columbia, Vancouver, British Columbia, Canada.
Robert W CowanAhmed Center for Pancreatic Cancer Research and Department of Gastroenterology, Hepatology and Nutrition, University of Texas M.D. Anderson Cancer Center, Houston, Texas.
Andrew D RhimAhmed Center for Pancreatic Cancer Research and Department of Gastroenterology, Hepatology and Nutrition, University of Texas M.D. Anderson Cancer Center, Houston, Texas.
Bangyan L StilesDepartment of Pharmaceutical Sciences, School of Pharmacy, Keck School of Medicine, University of Southern California, and the Norris Comprehensive Cancer Center, Los Angeles, California.
Mark ValasekDepartment of Pathology, University of California-San Diego, La Jolla, California.
Maike SanderDepartments of Pediatrics and Cellular and Molecular Medicine, University of California-San Diego, La Jolla, California. Electronic address: masander@ucsd.edu.
University of British Columbia · CAUniversity of California San Diego · USThe University of Texas MD Anderson Cancer Center · USUniversity of Southern California · US

Funding

Novel insights into nutrient-dependent regulation of beta cell proliferationR01DK078803 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI SANDER, MAIKE · 2007 to 2022
$4.4M
Mechanism of Pancreatic CarcinogenesisR01CA136526 · NCI · MAYO CLINIC ROCHESTER · PI FERNANDEZ-ZAPICO, MARTIN ERNESTO · 2009 to 2019
$3.0M
Role of Neurogenic Inflammation in Pancreatic CancerR01CA177857 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI DAVIS, BRIAN M · 2013 to 2017
$2.1M
The role of PTEN and AKT2 in the malignant transformation of liver progenitor celR01CA154986 · NCI · UNIVERSITY OF SOUTHERN CALIFORNIA · PI STILES, BANGYAN · 2013 to 2017
$1.7M
A novel mouse model to identify biomarkers of IPMN formation and progressionR21CA194839 · NCI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI SANDER, MAIKE · 2015 to 2016
$371k
Origin of Pancreatic Ductal AdenocarcinomaF32CA136124 · NCI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI KOPP, JANEL LYNN · 2008 to 2010
$149k
NCI NIH HHS F32 CA136124NCI NIH HHS R01 CA136526NCI NIH HHS R01 CA154986NCI NIH HHS R01 CA177857NCI NIH HHS R21 CA194839NIDDK NIH HHS R01 DK078803
6 · The paper itself

Abstract

BACKGROUND &

aimsIntraductal papillary mucinous neoplasias (IPMNs) are precancerous cystic lesions that can develop into pancreatic ductal adenocarcinomas (PDACs). These large macroscopic lesions are frequently detected during medical imaging, but it is unclear how they form or progress to PDAC. We aimed to identify cells that form IPMNs and mutations that promote IPMN development and progression.

methodsWe generated mice with disruption of Pten specifically in ductal cells (Sox9CreER

resultsMice with ductal cell-specific disruption of Pten but not control mice developed sporadic, macroscopic, intraductal papillary lesions with histologic and molecular features of human IPMNs. Pten

conclusionsIn analyses of mice with ductal cell-specific disruption of Pten, with or without activated Kras, we found evidence for a ductal cell origin of IPMNs. We also showed that PTEN loss and activated Kras have synergistic effects in promoting development of IPMN and progression to PDAC.

Indexed as

AnimalsCarcinoma, Pancreatic DuctalCell LineageCell MovementCell ProliferationCell Transformation, NeoplasticDisease ProgressionGene Expression Regulation, EnzymologicGene Expression Regulation, NeoplasticGenetic Predisposition to DiseaseHumansMice, Inbred C57BLMice, KnockoutMutationNeoplasm InvasivenessNeoplasms, Cystic, Mucinous, and SerousHras protein, mouseKRAS protein, humanProto-Oncogene Proteins p21(ras)PTEN PhosphohydrolasePTEN protein, humanPten protein, mouseGastricOncocyticPancreatic CancerPanIN

Identifiers

PMID29273451
PMCPMC5880733
OpenAlexW2779623685

What OpenQuestion holds

Textmetadata
LicenceTDM
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.