Evidence map›Paper›PMID 28400509›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2017

Oncogene KRAS activates fatty acid synthase, resulting in specific ERK and lipid signatures associated with lung adenocarcinoma.

Arvin M Gouw, Livia S Eberlin, Katherine Margulis, Delaney K Sullivan, Georgia G Toal, Ling Tong, Richard N Zare, Dean W Felsher

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 94 papers.

0numbers the graph read from it
0cells of the map it votes in
94citing papers in PubMed
4.1field-weighted citation impact, top 5% 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

94 citing papers in PubMed, 148 citations in OpenAlex.

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34 more citing papers are in PubMed but not listed here.

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

8 authors at 2 institutions in 1 country.

Arvin M GouwDivision of Oncology, Department of Medicine, Stanford University School of Medicine, Stanford, CA 94305.
Livia S EberlinDepartment of Chemistry, Stanford University, Stanford, CA 94305.
Katherine MargulisDepartment of Chemistry, Stanford University, Stanford, CA 94305.
Delaney K SullivanDivision of Oncology, Department of Medicine, Stanford University School of Medicine, Stanford, CA 94305.
Georgia G ToalDivision of Oncology, Department of Medicine, Stanford University School of Medicine, Stanford, CA 94305.
Ling TongDivision of Oncology, Department of Medicine, Stanford University School of Medicine, Stanford, CA 94305.
Richard N ZareDepartment of Chemistry, Stanford University, Stanford, CA 94305; zare@stanford.edu dfelsher@stanford.edu.
Dean W FelsherDivision of Oncology, Department of Medicine, Stanford University School of Medicine, Stanford, CA 94305; zare@stanford.edu dfelsher@stanford.edu.
Stanford University · USThe University of Texas at Austin · US

Funding

Translational Oncology Research Program (Project-005)P30CA124435 · NCI · STANFORD UNIVERSITY · PI Vittorio Sebastiano · 2007 to 2026
$71.4M
Modeling and Predicting Therapeutic Resistance of CancerU01CA188383 · NCI · STANFORD UNIVERSITY · PI FELSHER, DEAN W, GAMBHIR, SANJIV S · 2014 to 2018
$3.2M
Prognostic Metabolic Signatures of Cancers Through Mass Spectrometry ImagingR01CA184384 · NCI · STANFORD UNIVERSITY · PI FELSHER, DEAN W, ZARE, RICHARD N · 2014 to 2018
$2.7M
Mechanisms by which Oncogene Inactivation Elicits Tumor Cell DeathR01CA170378 · NCI · STANFORD UNIVERSITY · PI FELSHER, DEAN W · 2012 to 2015
$2.1M
Cancer-Translational Nanotechnology Training Program (Cancer-TNT)T32CA196585 · NCI · STANFORD UNIVERSITY · PI FELSHER, DEAN W, RAO, JIANGHONG · 2015 to 2019
$1.8M
NCI NIH HHS P30 CA124435NCI NIH HHS R01 CA170378NCI NIH HHS R01 CA184384NCI NIH HHS T32 CA196585NCI NIH HHS U01 CA188383
6 · The paper itself

Abstract

KRAS gene mutation causes lung adenocarcinoma. KRAS activation has been associated with altered glucose and glutamine metabolism. Here, we show that KRAS activates lipogenesis, and this activation results in distinct proteomic and lipid signatures. By gene expression analysis, KRAS is shown to be associated with a lipogenesis gene signature and specific induction of fatty acid synthase (FASN). Through desorption electrospray ionization MS imaging (DESI-MSI), specific changes in lipogenesis and specific lipids are identified. By the nanoimmunoassay (NIA), KRAS is found to activate the protein ERK2, whereas ERK1 activation is found in non-KRAS-associated human lung tumors. The inhibition of FASN by cerulenin, a small molecule antibiotic, blocked cellular proliferation of KRAS-associated lung cancer cells. Hence, KRAS is associated with activation of ERK2, induction of FASN, and promotion of lipogenesis. FASN may be a unique target for KRAS-associated lung adenocarcinoma remediation.

Indexed as

LipogenesisAdenocarcinomaAdenocarcinoma of LungFatty Acid SynthasesHumansLipid MetabolismLung NeoplasmsMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Proto-Oncogene Proteins p21(ras)Signal TransductionFatty Acid SynthasesKRAS protein, humanMAPK1 protein, humanMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Proto-Oncogene Proteins p21(ras)fatty acid synthaseKRASlipogenesislungMS

Identifiers

PMID28400509
PMCPMC5410819
OpenAlexW2605487687

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.