Evidence map›Paper›PMID 30894372›Full record

ArticleCancer research2019

4E-BP1 Is a Tumor Suppressor Protein Reactivated by mTOR Inhibition in Head and Neck Cancer.

Zhiyong Wang, Xiaodong Feng, Alfredo A Molinolo, Daniel Martin, Lynn Vitale-Cross, Nijiro Nohata, Mizuo Ando, Amy Wahba, Panomwat Amornphimoltham, Xingyu Wu and 10 more

Open access · bronzeAbstract read
In one paragraph

Article in Cancer research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
3.9field-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

53 citing papers in PubMed, 81 citations in OpenAlex.

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  4. The 4E-BP1 deletion modestly mitigates mTORC1-deficient epidermal barrier defects.JID innovations : skin science from molecules to population health · 2026
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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

20 authors at 5 institutions in 4 countries.

Zhiyong WangMoores Cancer Center, University of California, San Diego, La Jolla, California.ORCID 0000-0002-3574-6078
Xiaodong FengMoores Cancer Center, University of California, San Diego, La Jolla, California.
Alfredo A MolinoloMoores Cancer Center, University of California, San Diego, La Jolla, California.ORCID 0000-0001-8412-2889
Daniel MartinNational Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, Maryland.ORCID 0000-0002-8880-9087
Lynn Vitale-CrossNational Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, Maryland.ORCID 0000-0001-7850-547X
Nijiro NohataMoores Cancer Center, University of California, San Diego, La Jolla, California.ORCID 0000-0002-6816-2984
Mizuo AndoMoores Cancer Center, University of California, San Diego, La Jolla, California.
Amy WahbaNational Cancer Institute, National Institutes of Health, Bethesda, Maryland.
Panomwat AmornphimolthamMoores Cancer Center, University of California, San Diego, La Jolla, California.
Xingyu WuMoores Cancer Center, University of California, San Diego, La Jolla, California.
Mara GilardiMoores Cancer Center, University of California, San Diego, La Jolla, California.
Michael AllevatoMoores Cancer Center, University of California, San Diego, La Jolla, California.
Victoria WuMoores Cancer Center, University of California, San Diego, La Jolla, California.
Dana J SteffenMoores Cancer Center, University of California, San Diego, La Jolla, California.
Philip TofilonNational Cancer Institute, National Institutes of Health, Bethesda, Maryland.
Nahum SonenbergDepartment of Biochemistry and Goodman Cancer Centre, McGill University, Montreal, Quebec, Canada.ORCID 0000-0002-4707-8759
Joseph CalifanoMoores Cancer Center, University of California, San Diego, La Jolla, California.
Qianming ChenState Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, China. sgutkind@ucsd.edu slippman@ucsd.edu qmchen@scu.edu.cn.
Scott M LippmanMoores Cancer Center, University of California, San Diego, La Jolla, California. sgutkind@ucsd.edu slippman@ucsd.edu qmchen@scu.edu.cn.
J Silvio GutkindMoores Cancer Center, University of California, San Diego, La Jolla, California. sgutkind@ucsd.edu slippman@ucsd.edu qmchen@scu.edu.cn.
University of California San Diego · USNational Institute of Dental and Craniofacial Research · USNational Institutes of Health · USSichuan University · CNMcGill University Health Centre · CA

Funding

VIRAL MALIGNANCYP30CA023100 · NCI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI Jesse Nodora · 1985 to 2026
$124.9M
GRADUATE TRAINING IN CELLULAR &MOLECULAR PHARMACOLOGYT32GM007752 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI BROWN, JOAN HELLER, HANDEL, TRACY M · 1985 to 2023
$13.5M
Radiation-induced translational control of gene expressionZIABC011373 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI TOFILON, PHILIP · 2011 to 2025
$11.7M
Targeting Signaling Vulnerabilities for Oral Cancer PreventionR01DE026644 · NIDCR · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI Jorge Silvio Gutkind, SCOTT M LIPPMAN · 2017 to 2026
$4.7M
Targeting the EGFR-PI3K/mTOR Signaling Circuitry: A Network-Based Approach for Oral Cancer Precision TherapyR01DE026870 · NIDCR · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI GUTKIND, JORGE SILVIO · 2018 to 2022
$2.3M
Area C: Genome-wide identification and targeting of resistance to cancer therapyR33CA225291 · NCI · UNIV OF MARYLAND, COLLEGE PARK · PI GUTKIND, JORGE SILVIO, RUPPIN, EYTAN · 2017 to 2017
$1.5M
NCI NIH HHS P30 CA023100NCI NIH HHS R33 CA225291NIDCR NIH HHS R01 DE026644NIDCR NIH HHS R01 DE026870NIGMS NIH HHS T32 GM007752
6 · The paper itself

Abstract

Aberrant activation of the PI3K-mTOR signaling pathway occurs in >80% of head and neck squamous cell carcinomas (HNSCC), and overreliance on this signaling circuit may in turn represent a cancer-specific vulnerability that can be exploited therapeutically. mTOR inhibitors (mTORi) promote tumor regression in genetically defined and chemically induced HNSCC animal models, and encouraging results have been recently reported. However, the mTOR-regulated targets contributing to the clinical response have not yet been identified. Here, we focused on

Indexed as

Adaptor Proteins, Signal TransducingAdenineAnimalsBenzoxazolesBiomarkers, TumorCell Cycle ProteinsCell Line, TumorCell ProliferationCRISPR-Cas SystemsHead and Neck NeoplasmsHumansMiceMice, KnockoutPhosphorylationPrognosisPyrimidinesAdaptor Proteins, Signal TransducingAdenineBenzoxazolesBiomarkers, TumorCell Cycle ProteinsEIF4EBP1 protein, humanMTOR protein, humanPyrimidinessapanisertibTOR Serine-Threonine KinasesTumor Suppressor Proteins

Identifiers

PMID30894372
PMCPMC6445709
OpenAlexW2923068106

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.