Evidence map›Paper›PMID 17495520›Full record

ArticleCancer biology & therapy2007

Epidermal growth factor receptor plays a significant role in hepatocyte growth factor mediated biological responses in mammary epithelial cells.

Alyssa R Bonine-Summers, Mary E Aakre, Kimberly A Brown, Carlos L Arteaga, Jennifer A Pietenpol, Harold L Moses, Nikki Cheng

Open access · bronzeAbstract read
In one paragraph

Article in Cancer biology & therapy, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed, 1 pooled it
2.2field-weighted citation impact, top 14% 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

29 citing papers in PubMed, 1 synthesis or guideline pooled it, 52 citations in OpenAlex.

  1. Pooled it
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  16. Met interacts with EGFR and Ron in canine osteosarcoma.Veterinary and comparative oncology · 2013
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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

7 authors at 1 institution in 1 country.

Alyssa R Bonine-SummersDepartment of Cancer Biology, Vanderbilt-lngram Cancer Center, Vanderbilt University Medical Center, Nashville, Tennessee 37232-6838, USA.
Mary E Aakre
Kimberly A Brown
Carlos L Arteaga
Jennifer A Pietenpol
Harold L Moses
Nikki Cheng
Vanderbilt University · US

Funding

MULTIDISCIPLINARY BASIC RESEARCH TRAINING IN CANCERT32CA009592 · NCI · VANDERBILT UNIVERSITY · PI Justin M Balko, Julie A Rhoades (Sterling) · 1987 to 2026
$10.4M
TGF BETA SUPPRESSION AND PROMOTION OF MAMMARY CARCINOMASR01CA085492 · NCI · VANDERBILT UNIVERSITY · PI MOSES, HAROLD L, WEAVER, VALERIE MARIE · 2000 to 2015
$6.4M
TGF-beta in Mammary Development and TumorigenesisR01CA102162 · NCI · VANDERBILT UNIVERSITY · PI MOSES, HAROLD L · 2003 to 2013
$4.5M
NCI NIH HHS CA 085492NCI NIH HHS CA 102162NCI NIH HHS R01 CA085492NCI NIH HHS R01 CA102162NCI NIH HHS T32 CA009592
6 · The paper itself

Abstract

Breast cancers often have deregulated hepatocyte growth factor (HGF) and c-Met signaling that results in increased tumor growth and invasion. Elucidating the mechanism responsible for HGF/c-Met action in breast cancer progression has been difficult as c-Met communicates with a number of secondary receptors that can lead to various pathological outcomes. Understanding how these secondary receptors facilitate HGF/c-Met cellular responses will aid in the development of better therapeutic treatment options for breast cancer patients with elevated HGF signaling. In the present study it was shown that the epidermal growth factor receptor (EGFR) plays a significant role in HGF/c-Met mediated biological activities indicative of advanced tumor pathology, including enhanced proliferation and invasion. The clinically relevant EGFR inhibitor gefitinib was used to determine the role of EGFR in HGF-induced proliferation and motility in several mammary carcinoma cells including PyVmT, MDA-MB-231 and 4T1. Our analyses indicated that EGFR inhibition significantly blocked HGF activation of c-Met and EGFR and that inhibition of these pathways mitigated HGF induced proliferation and motility. The data indicate that this inhibition was not through a direct effect of gefitinib on c-Met, but that EGFR is necessary for c-Met activation in the assays performed. These results provide a novel mechanism of action for EGFR as a mediator of HGF signaling thereby linking EGFR to the oncogenic potential of c-Met in mammary carcinomas cells.

Indexed as

Drug Resistance, NeoplasmAntineoplastic AgentsBreast NeoplasmsCarcinomaCell Line, TumorCell MovementCell ProliferationEpithelial CellsErbB ReceptorsFemaleGefitinibHepatocyte Growth FactorHumansMammary Glands, HumanProtein Kinase InhibitorsQuinazolinesAntineoplastic AgentsErbB ReceptorsGefitinibHepatocyte Growth FactorProtein Kinase InhibitorsQuinazolinesReceptor Protein-Tyrosine KinasesRON protein

Identifiers

PMID17495520
PMCPMC3395216
OpenAlexW2018456517

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.