Evidence map›Paper›PMID 31352001›Full record

ArticleGastroenterology2019

Oncogenic KRAS Reduces Expression of FGF21 in Acinar Cells to Promote Pancreatic Tumorigenesis in Mice on a High-Fat Diet.

Yongde Luo, Yaying Yang, Muyun Liu, Dan Wang, Feng Wang, Yawei Bi, Juntao Ji, Suyun Li, Yan Liu, Rong Chen and 24 more

Open access · greenAbstract read
In one paragraph

Article in Gastroenterology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed, 1 pooled it
3.3field-weighted citation impact, top 7% 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

53 citing papers in PubMed, 1 synthesis or guideline pooled it, 85 citations in OpenAlex.

  1. Pooled it
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  8. Treating metabolic dysfunction-associated steatohepatitis: The fat-trimming FGF21 approach.Obesity reviews : an official journal of the International Association for the Study of Obesity · 2025
    Review
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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

34 authors at 9 institutions in 3 countries.

Yongde LuoSchool of Pharmaceutical Science, Wenzhou Medical University, Wenzhou, Zhejiang, China; Department of Medicine, Stony Brook University, Stony Brook, New York. Electronic address: yongdeluo08@gmail.com.
Yaying YangDepartment of Gastrointestinal Medical Oncology, University of Texas, MD Anderson Cancer Center, Houston, Texas.
Muyun LiuDepartment of Gastrointestinal Medical Oncology, University of Texas, MD Anderson Cancer Center, Houston, Texas.
Dan WangDepartment of Medicine, Stony Brook University, Stony Brook, New York.
Feng WangSun Yat-Sen University Cancer Center, State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Guangzhou, China.
Yawei BiDepartment of Medicine, Stony Brook University, Stony Brook, New York.
Juntao JiDepartment of Medicine, Stony Brook University, Stony Brook, New York.
Suyun LiDepartment of Medicine, Stony Brook University, Stony Brook, New York.
Yan LiuDepartment of Cancer Biology, University of Texas, MD Anderson Cancer Center, Houston, Texas.
Rong ChenDepartment of Experimental Therapeutics, University of Texas, MD Anderson Cancer Center, Houston, Texas.
Haojie HuangDepartment of Cancer Biology, University of Texas, MD Anderson Cancer Center, Houston, Texas.
Xiaojie WangSchool of Pharmaceutical Science, Wenzhou Medical University, Wenzhou, Zhejiang, China.
Agnieszka K Swidnicka-SiergiejkoDepartment of Cancer Biology, University of Texas, MD Anderson Cancer Center, Houston, Texas.
Tobias JanowitzCold Spring Harbor Laboratory, Cold Spring Harbor, New York.
Semir BeyazCold Spring Harbor Laboratory, Cold Spring Harbor, New York.
Guoqiang WangDepartment of Medicine, Stony Brook University, Stony Brook, New York.
Sulan XuDepartment of Medicine, Stony Brook University, Stony Brook, New York.
Agnieszka B BialkowskaDepartment of Medicine, Stony Brook University, Stony Brook, New York.
Catherine K LuoDepartment of Medicine, Stony Brook University, Stony Brook, New York.
Christoph L PinDepartments of Pediatrics, Oncology, and Physiology and Pharmacology, Schulich School of Medicine, University of Western Ontario Children's Health Research Institute, London, Ontario, Canada.
Guang LiangSchool of Pharmaceutical Science, Wenzhou Medical University, Wenzhou, Zhejiang, China.
Xiongbin LuDepartment of Medical and Molecular Genetics, Indiana University School of Medicine, Indianapolis, Indiana.
Maoxin WuDepartment of Pathology, Stony Brook University, Stony Brook, New York.
Kenneth R ShroyerDepartment of Pathology, Stony Brook University, Stony Brook, New York.
Robert A WolffDepartment of Gastrointestinal Medical Oncology, University of Texas, MD Anderson Cancer Center, Houston, Texas.
William PlunkettDepartment of Experimental Therapeutics, University of Texas, MD Anderson Cancer Center, Houston, Texas.
Baoan JiDepartment of Biochemistry and Molecular Biology, Mayo Clinic, Jacksonville, Florida.
Zhaoshen LiDepartment of Gastroenterology, Changhai Hospital, Shanghai, China.
Ellen LiDepartment of Medicine, Stony Brook University, Stony Brook, New York.
Xiaokun LiSchool of Pharmaceutical Science, Wenzhou Medical University, Wenzhou, Zhejiang, China.
Vincent W YangDepartment of Medicine, Stony Brook University, Stony Brook, New York.
Craig D LogsdonDepartment of Gastrointestinal Medical Oncology, University of Texas, MD Anderson Cancer Center, Houston, Texas; Department of Cancer Biology, University of Texas, MD Anderson Cancer Center, Houston, Texas.
James L AbbruzzeseDepartment of Gastrointestinal Medical Oncology, University of Texas, MD Anderson Cancer Center, Houston, Texas; Division of Medical Oncology, Department of Medicine, Duke Cancer Institute, Duke University, Durham, North Carolina.
Weiqin LuDepartment of Medicine, Stony Brook University, Stony Brook, New York; Department of Gastrointestinal Medical Oncology, University of Texas, MD Anderson Cancer Center, Houston, Texas. Electronic address: weiqin.lu@stonybrookmedicine.edu.
Stony Brook University · USThe University of Texas MD Anderson Cancer Center · USWenzhou Medical University · CNCold Spring Harbor Laboratory · USIndiana University School of MedicineJacksonville College · USSecond Military Medical University · CNSun Yat-sen University · CNWestern University · CA

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Scott Kopetz · 1985 to 2026
$290.8M
Women's Cancer Research ProgramP30CA014236 · NCI · DUKE UNIVERSITY · PI DONNA NIEDZWIECKI · 1985 to 2026
$174.8M
Single-Cell Biology Shared ResourceP30CA045508 · NCI · COLD SPRING HARBOR LABORATORY · PI John Edward Moses · 1987 to 2026
$118.9M
MOLECULAR MECHANISMS OF PANCREATITISR01DK052067 · NIDDK · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI LOGSDON, CRAIG D · 1998 to 2015
$4.4M
Training and Education ProgramP20CA192994 · NCI · STATE UNIVERSITY NEW YORK STONY BROOK · PI LI, ELLEN · 2015 to 2018
$1.6M
Training and Education ProgramP20CA192996 · NCI · COLD SPRING HARBOR LABORATORY · PI MCCOMBIE, WILLIAM RICHARD · 2015 to 2018
$620k
NCI NIH HHS P20 CA192994NCI NIH HHS P20 CA192996NCI NIH HHS P30 CA014236NCI NIH HHS P30 CA016672NCI NIH HHS P30 CA045508NIDDK NIH HHS R01 DK052067
6 · The paper itself

Abstract

BACKGROUND &

aimsObesity is a risk factor for pancreatic cancer. In mice, a high-fat diet (HFD) and expression of oncogenic KRAS lead to development of invasive pancreatic ductal adenocarcinoma (PDAC) by unknown mechanisms. We investigated how oncogenic KRAS regulates the expression of fibroblast growth factor 21, FGF21, a metabolic regulator that prevents obesity, and the effects of recombinant human FGF21 (rhFGF21) on pancreatic tumorigenesis.

methodsWe performed immunohistochemical analyses of FGF21 levels in human pancreatic tissue arrays, comprising 59 PDAC specimens and 45 nontumor tissues. We also studied mice with tamoxifen-inducible expression of oncogenic KRAS in acinar cells (Kras

resultsPancreatic tissues of mice expressed high levels of FGF21 compared with liver tissues. FGF21 and its receptor proteins were expressed by acinar cells. Acinar cells that expressed Kras

conclusionsNormal acinar cells from mice and humans express high levels of FGF21. In mice, acinar expression of oncogenic KRAS significantly reduces FGF21 expression. When these mice are placed on an HFD, they develop extensive inflammation, pancreatic cysts, PanINs, and PDACs, which are reduced by injection of FGF21. FGF21 also reduces the guanosine triphosphate binding capacity of RAS. FGF21 might be used in the prevention or treatment of pancreatic cancer.

Indexed as

Diet, High-FatAcinar CellsAnimalsCarcinoma, Pancreatic DuctalCell Transformation, NeoplasticDown-RegulationFibroblast Growth FactorsGene Expression Regulation, NeoplasticHumansKlotho ProteinsMembrane ProteinsMice, TransgenicMutationPancreatic CystPancreatic Intraductal NeoplasmsPancreatic NeoplasmsFgfr1 protein, mousefibroblast growth factor 21Fibroblast Growth FactorsHras protein, mouseKlb protein, mouseKlotho ProteinsKRAS protein, humanMembrane ProteinsPPAR gammaPparg protein, mouseProto-Oncogene Proteins p21(ras)Receptor, Fibroblast Growth Factor, Type 1transcription factor PTF1Transcription FactorsTrp53 protein, mouseTumor Suppressor Protein p53FGFR1Gene RegulationKLBSignaling

Identifiers

PMID31352001
PMCPMC6815712
OpenAlexW2964320731

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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.