Evidence map›Paper›PMID 30819189›Full record

ArticleCell communication and signaling : CCS2019

Obesogenic high-fat diet heightens aerobic glycolysis through hyperactivation of oncogenic KRAS.

Dan Wang, Yawei Bi, Lianghao Hu, Yongde Luo, Juntao Ji, Albert Z Mao, Craig D Logsdon, Ellen Li, James L Abbruzzese, Zhaoshen Li and 2 more

Open access · goldAbstract read
In one paragraph

Article in Cell communication and signaling : CCS, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 2 pooled it
1.1field-weighted citation impact, top 28% 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

19 citing papers in PubMed, 2 syntheses or guidelines pooled it, 21 citations in OpenAlex.

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  8. Frontiers in cell and developmental biology · 2023
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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

12 authors at 6 institutions in 2 countries.

Dan WangDivision of Gastroenterology and Hepatology, Department of Medicine, Stony Brook of University School of Medicine, Stony Brook, New York, 11794, USA.
Yawei BiDivision of Gastroenterology and Hepatology, Department of Medicine, Stony Brook of University School of Medicine, Stony Brook, New York, 11794, USA.
Lianghao HuDepartment of Gastroenterology, Changhai Hospital, Shanghai, China.
Yongde LuoSchool of Pharmaceutical Science, Wenzhou Medical University, Wenzhou, Zhejiang, China.
Juntao JiDivision of Gastroenterology and Hepatology, Department of Medicine, Stony Brook of University School of Medicine, Stony Brook, New York, 11794, USA.
Albert Z MaoDivision of Gastroenterology and Hepatology, Department of Medicine, Stony Brook of University School of Medicine, Stony Brook, New York, 11794, USA.
Craig D LogsdonDepartment of Cancer Biology, University of Texas MD Anderson Cancer Center, Houston, TX, 77030, USA.
Ellen LiDivision of Gastroenterology and Hepatology, Department of Medicine, Stony Brook of University School of Medicine, Stony Brook, New York, 11794, USA.
James L AbbruzzeseDivision of Medical Oncology, Department of Medicine, Duke Cancer Institute, Duke University, Durham, North Carolina, USA.
Zhaoshen LiDepartment of Gastroenterology, Changhai Hospital, Shanghai, China.
Vincent W YangDivision of Gastroenterology and Hepatology, Department of Medicine, Stony Brook of University School of Medicine, Stony Brook, New York, 11794, USA.
Weiqin LuDivision of Gastroenterology and Hepatology, Department of Medicine, Stony Brook of University School of Medicine, Stony Brook, New York, 11794, USA. weiqin.lu@stonybrookmedicine.edu.
Stony Brook University · USChanghai Hospital · CNSecond Military Medical University · CNDuke Medical Center · USIntegrated BioTherapeutics (United States) · USThe University of Texas MD Anderson Cancer Center · US

Funding

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 CA192996
6 · The paper itself

Abstract

Oncogenic KRAS plays a vital role in controlling tumor metabolism by enhancing aerobic glycolysis. Obesity driven by chronic consumption of high-fat diet (HFD) is a major risk factor for oncogenic KRAS-mediated pancreatic ductal adenocarcinoma (PDAC). However, the role of HFD in KRAS-mediated metabolic reprogramming has been obscure. Here, by using genetically engineered mouse models expressing an endogenous level of KRAS

Indexed as

Diet, High-FatGlycolysisOncogenesAerobiosisAnimalsCyclooxygenase 2Dietary CarbohydratesMiceModels, BiologicalObesityPancreatic NeoplasmsProto-Oncogene Proteins p21(ras)Cyclooxygenase 2Dietary CarbohydratesHras protein, mouseProto-Oncogene Proteins p21(ras)COX-2GlycolysisHexokinase 2High-fat dietKRASLactate dehydrogenaseObesityPancreatic cancer

Identifiers

PMID30819189
PMCPMC6396546
OpenAlexW2939515657

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.