Evidence map›Paper›PMID 26383165›Full record

ArticleCancer research2015

Src Inhibition Blocks c-Myc Translation and Glucose Metabolism to Prevent the Development of Breast Cancer.

Shalini Jain, Xiao Wang, Chia-Chi Chang, Catherine Ibarra-Drendall, Hai Wang, Qingling Zhang, Samuel W Brady, Ping Li, Hong Zhao, Jessica Dobbs and 9 more

Open access · bronzeAbstract read
In one paragraph

Article in Cancer research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
2.2field-weighted citation impact, top 11% 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

32 citing papers in PubMed, 60 citations in OpenAlex.

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  12. Target c-Myc to treat pancreatic cancer.Cancer biology & therapy · 2022
    Article
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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

19 authors at 4 institutions in 2 countries.

Shalini JainDepartment of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas.
Xiao WangDepartment of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas.
Chia-Chi ChangDepartment of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas. Cancer Biology Program, University of Texas Graduate School of Biomedical Sciences, Houston, Texas.
Catherine Ibarra-DrendallDepartment of Medicine, Duke University, Durham, North Carolina.
Hai WangDepartment of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas.
Qingling ZhangDepartment of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas.
Samuel W BradyDepartment of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas. Cancer Biology Program, University of Texas Graduate School of Biomedical Sciences, Houston, Texas.
Ping LiDepartment of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas.
Hong ZhaoDepartment of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas.
Jessica DobbsBioengineering Department, Rice University, Houston, Texas.
Matt KyrishBioengineering Department, Rice University, Houston, Texas.
Tomasz S TkaczykBioengineering Department, Rice University, Houston, Texas.
Adrian AmbroseDepartment of Medicine, Duke University, Durham, North Carolina.
Christopher SistrunkDepartment of Medicine, Duke University, Durham, North Carolina.
Banu K ArunDepartment of Breast Medical Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas.
Rebecca Richards-KortumBioengineering Department, Rice University, Houston, Texas.
Wei JiaCancer Epidemiology Program, University of Hawaii Cancer Center, University of Hawaii at Monoa, Honolulu. Hawaii.
Victoria L SeewaldtDepartment of Medicine, Duke University, Durham, North Carolina.
Dihua YuDepartment of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas. Department of Breast Medical Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas. Center for Molecular Medicine, China Medical University, Taichung, Taiwan. dyu@mdanderson.org.
The University of Texas MD Anderson Cancer Center · USDuke University · USRice University · USUniversity of Hawaiʻi at Mānoa · US

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Fabien Delerue · 1985 to 2026
$290.8M
University of Hawaii Cancer Center CCSGP30CA071789 · NCI · UNIVERSITY OF HAWAII AT MANOA · PI GERTRAUD MASKARINEC · 1996 to 2026
$56.2M
Tyrosine Kinase-Dependant and - Independent Pathways of EGFR in Breast Cancer ProP01CA099031 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI HUNG, MIEN-CHIE · 2003 to 2014
$11.6M
Stromal activation in the progression of high ErbB2/1433zeta DCIS to IBCR01CA112567 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI YU, DIHUA · 2005 to 2016
$3.0M
Target p70S6K for Chemodietary Prevention/Early Intervention of ER- Breast CancerR01CA184836 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI YU, DIHUA · 2015 to 2019
$1.8M
NCI NIH HHS P01 CA099031NCI NIH HHS P01-CA099031NCI NIH HHS P30 CA016672NCI NIH HHS P30 CA071789NCI NIH HHS R01 CA112567NCI NIH HHS R01-CA112567-06NCI NIH HHS R01 CA184836NCI NIH HHS R01-CA184836
6 · The paper itself

Abstract

Preventing breast cancer will require the development of targeted strategies that can effectively block disease progression. Tamoxifen and aromatase inhibitors are effective in addressing estrogen receptor-positive (ER(+)) breast cancer development, but estrogen receptor-negative (ER(-)) breast cancer remains an unmet challenge due to gaps in pathobiologic understanding. In this study, we used reverse-phase protein array to identify activation of Src kinase as an early signaling alteration in premalignant breast lesions of women who did not respond to tamoxifen, a widely used ER antagonist for hormonal therapy of breast cancer. Src kinase blockade with the small-molecule inhibitor saracatinib prevented the disorganized three-dimensional growth of ER(-) mammary epithelial cells in vitro and delayed the development of premalignant lesions and tumors in vivo in mouse models developing HER2(+) and ER(-) mammary tumors, extending tumor-free and overall survival. Mechanistic investigations revealed that Src blockade reduced glucose metabolism as a result of an inhibition in ERK1/2-MNK1-eIF4E-mediated cap-dependent translation of c-Myc and transcription of the glucose transporter GLUT1, thereby limiting energy available for cell growth. Taken together, our results provide a sound rationale to target Src pathways in premalignant breast lesions to limit the development of breast cancers.

Indexed as

AnimalsAntineoplastic AgentsBenzodioxolesBreast NeoplasmsDisease Models, AnimalFemaleGene Expression Regulation, NeoplasticGenes, mycGlucoseHumansMiceProtein BiosynthesisQuinazolinesReceptors, Estrogensrc-Family KinasesAntineoplastic AgentsBenzodioxolesGlucoseQuinazolinesReceptors, Estrogensaracatinibsrc-Family Kinases

Identifiers

PMID26383165
PMCPMC4651709
OpenAlexW2149106868

What OpenQuestion holds

Textmetadata
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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.