Evidence map›Paper›PMID 31310834›Full record

ArticleCellular and molecular gastroenterology and hepatology2019

Differential Cell Susceptibilities to Kras

Chanjuan Shi, Fong Cheng Pan, Jessica N Kim, M Kay Washington, Chandrasekhar Padmanabhan, Christian T Meyer, Janel L Kopp, Maike Sander, Maureen Gannon, R Daniel Beauchamp and 2 more

Open access · goldAbstract read
In one paragraph

Article in Cellular and molecular gastroenterology and hepatology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

15 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Review
  6. Review
  7. Review
  8. Review
  9. The pancreatic cancer genome revisited.Nature reviews. Gastroenterology & hepatology · 2021
    Review
  10. Article
  11. Review
  12. Kras mutation rate precisely orchestrates ductal derived pancreatic intraepithelial neoplasia and pancreatic cancer.Laboratory investigation; a journal of technical methods and pathology · 2021
    Article
  13. Article
  14. Review
  15. Putting the Cell of Origin for Pancreatic Cancer Into its Proper Context.Cellular and molecular gastroenterology and hepatology · 2019
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

12 authors at 3 institutions in 1 country.

Chanjuan ShiDepartment of Pathology, Microbiology, and Immunology, Vanderbilt University Medical Center, Nashville, Tennessee.
Fong Cheng PanDepartment of Cell and Developmental Biology, Vanderbilt University Medical Center, Nashville, Tennessee.
Jessica N KimSection of Surgical Sciences, Vanderbilt University Medical Center, Nashville, Tennessee.
M Kay WashingtonDepartment of Pathology, Microbiology, and Immunology, Vanderbilt University Medical Center, Nashville, Tennessee.
Chandrasekhar PadmanabhanSection of Surgical Sciences, Vanderbilt University Medical Center, Nashville, Tennessee.
Christian T MeyerDepartment of Biochemistry, Vanderbilt University Medical Center, Nashville, Tennessee.
Janel L KoppDepartments of Pediatrics and Cellular and Molecular Medicine, 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.
Maureen GannonDepartment of Cell and Developmental Biology, Vanderbilt University Medical Center, Nashville, Tennessee; Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee; Department of Veterans Affairs, Tennessee Valley Health System, Nashville, Tennessee.
R Daniel BeauchampDepartment of Cell and Developmental Biology, Vanderbilt University Medical Center, Nashville, Tennessee; Section of Surgical Sciences, Vanderbilt University Medical Center, Nashville, Tennessee.
Christopher V WrightDepartment of Cell and Developmental Biology, Vanderbilt University Medical Center, Nashville, Tennessee.
Anna L MeansDepartment of Cell and Developmental Biology, Vanderbilt University Medical Center, Nashville, Tennessee; Section of Surgical Sciences, Vanderbilt University Medical Center, Nashville, Tennessee. Electronic address: anna.means@vumc.org.
Vanderbilt University Medical Center · USUniversity of California San Diego · USValley Health System · US

Funding

Tumor Immunology and Microenvironment Research ProgramP30CA068485 · NCI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI STACIE B DUSETZINA · 1995 to 2026
$172.8M
Coordinating Center for Beta Cell Biology ConsortiumU01DK072473 · NIDDK · VANDERBILT UNIVERSITY · PI MAGNUSON, MARK A · 2005 to 2014
$61.0M
Understanding and Controlling p120 Dysfunction in CRCP50CA095103 · NCI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI COFFEY, ROBERT J. · 2002 to 2017
$33.6M
Translational Analysis CoreP30DK058404 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI RICHARD M. PEEK · 2002 to 2026
$29.9M
Novel insights into nutrient-dependent regulation of beta cell proliferationR01DK078803 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI SANDER, MAIKE · 2007 to 2022
$4.4M
Integrated Training in Engineering and DiabetesT32DK101003 · NIDDK · VANDERBILT UNIVERSITY · PI Jamey D. Young · 2014 to 2026
$3.9M
Formation and maturation of endocrine pancreas progenitorsR01DK105689 · NIDDK · UNIVERSITY OF PENNSYLVANIA · PI GANNON, MAUREEN A, STOFFERS, DORIS A · 2016 to 2019
$2.2M
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
The role of EGFR signaling in progression of Kras-induced pacreatic tumorsR21CA123061 · NCI · VANDERBILT UNIVERSITY · PI MEANS, ANNA L · 2006 to 2007
$308k
Origin of Pancreatic Ductal AdenocarcinomaF32CA136124 · NCI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI KOPP, JANEL LYNN · 2008 to 2010
$149k
BLRD VA I01 BX003744NCI NIH HHS F32 CA136124NCI NIH HHS P30 CA068485NCI NIH HHS P50 CA095103NCI NIH HHS R21 CA123061NCI NIH HHS R21 CA194839NIDDK NIH HHS P30 DK058404NIDDK NIH HHS R01 DK078803NIDDK NIH HHS R01 DK105689NIDDK NIH HHS U01 DK072473
6 · The paper itself

Abstract

BACKGROUND &

aimsActivating mutation of the KRAS gene is common in some cancers, such as pancreatic cancer, but rare in other cancers. Chronic pancreatitis is a predisposing condition for pancreatic ductal adenocarcinoma (PDAC), but how it synergizes with KRAS mutation is not known.

methodsWe used a mouse model to express an activating mutation of Kras in conjunction with obstruction of the main pancreatic duct to recapitulate a common etiology of human chronic pancreatitis. Because the cell of origin of PDAC is not clear, Kras mutation was introduced into either duct cells or acinar cells.

resultsAlthough Kras

conclusionsOne mechanism by which tissues may be susceptible or resistant to KRAS

Indexed as

Acinar CellsAnimalsCarcinogenesisCarcinoma, Pancreatic DuctalCell Transformation, NeoplasticDisease Models, AnimalGenes, rasMetaplasiaMiceMutationPancreatic NeoplasmsPancreatitis, ChronicPrecancerous ConditionsProto-Oncogene Proteins p21(ras)Signal TransductionHras protein, mouseProto-Oncogene Proteins p21(ras)Acinar-to-Ductal MetaplasiaCdkn1aCell of OriginPancreatic Duct Ligation

Identifiers

PMID31310834
PMCPMC6889613
OpenAlexW2958380790

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.