Evidence map›Paper›PMID 23438512›Full record

ArticleJournal of proteome research2013

Phosphotyrosine profiling of NSCLC cells in response to EGF and HGF reveals network specific mediators of invasion.

Hannah Johnson, Rebecca S Lescarbeau, Jesus A Gutierrez, Forest M White

Abstract read
In one paragraph

Article in Journal of proteome research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.1field-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

17 citing papers in PubMed, 29 citations in OpenAlex.

  1. Tyrosine phosphoproteome profiling identifies cell-intrinsic signals limiting the efficacy of tyrosine kinase inhibitor therapies.Proceedings of the National Academy of Sciences of the United States of America · 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

4 authors at 2 institutions in 1 country.

Hannah JohnsonDepartment of Biological Engineering, Massachusetts Institute of Technology , Cambridge, Massachusetts, United States.
Rebecca S Lescarbeau
Jesus A Gutierrez
Forest M White
Massachusetts Institute of Technology · USEli Lilly (United States) · US

Funding

VIRUS PRODUCTION COREP30CA014051 · NCI · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI MATTHEW G. VANDER HEIDEN · 1985 to 2026
$93.9M
Tumor Cell Networks CenterU54CA112967 · NCI · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI LAUFFENBURGER, DOUGLAS A · 2004 to 2015
$26.2M
TOXICOLOGY CORE UNITP30ES002109 · NIEHS · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI LEVINE, STUART S · 1985 to 2020
$25.6M
Vanderbilt Proteome Characterization CenterU24CA159988 · NCI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI LIEBLER, DANIEL C · 2011 to 2016
$13.9M
Engineered Antibody EGFR Antagonist Cancer TherapeuticsR01CA096504 · NCI · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI WITTRUP, KARL DANE · 2002 to 2017
$9.7M
Understanding and Eliminating Oncogenic EGFR Signaling in Malignant GliomaU01CA141556 · NCI · TUFTS MEDICAL CENTER · PI CHAREST, ALAIN · 2009 to 2013
$3.3M
Quantitative Analysis of Epidermal Growth Factor Receptor Signaling NetworksR01CA118705 · NCI · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI WHITE, FOREST M · 2008 to 2012
$1.8M
NCI NIH HHS 5U01CA141556-03NCI NIH HHS P30 CA014051NCI NIH HHS R01 CA096504NCI NIH HHS R01 CA118705NCI NIH HHS R01CA118705NCI NIH HHS U01 CA141556NCI NIH HHS U24 CA159988NCI NIH HHS U24CA159988NCI NIH HHS U54 CA112967NCI NIH HHS U54CA112967NIEHS NIH HHS P30 ES002109
6 · The paper itself

Abstract

Growth factor signaling is deregulated in cancer and often leads to invasion, yet receptor tyrosine kinase signaling pathways driving invasion under different growth factor conditions are not well understood. To identify specific signaling molecules regulating invasion of A549 non-small cell lung carcinoma (NSCLC) cells downstream of the epidermal growth factor receptor (EGFR) and Met, quantitative site-specific mass spectrometric analysis of tyrosine phosphorylation was performed following epidermal growth factor (EGF) or hepatocyte growth factor (HGF) stimulation, at three different growth factor concentrations and at two time points. Through this analysis, the temporal and concentration dependent phosphorylation profiles were obtained for 131 and 139 sites downstream of EGF and HGF stimulation, respectively. To characterize the effect of these signaling network alterations, we quantified 3D cell migration/invasion through Matrigel. Partial least-squares regression (PLSR) analysis was performed to identify the tyrosine phosphorylation sites most strongly correlated with EGF and/or HGF mediated invasion. Potential common and specific signaling events required for driving invasion downstream of EGFR and Met were identified using either a combined or two independent PLSR models, based on the quantitative EGF or HGF data. Our data highlight the integration and compartmentalization of signaling required for invasion in cancer.

Indexed as

Carcinoma, Non-Small-Cell LungCell Line, TumorCell MovementEpidermal Growth FactorErbB ReceptorsHepatocyte Growth FactorHumansLung NeoplasmsPhosphorylationPhosphotyrosineProto-Oncogene Proteins c-metSignal TransductionEpidermal Growth FactorErbB ReceptorsHepatocyte Growth FactorMET protein, humanPhosphotyrosineProto-Oncogene Proteins c-met

Identifiers

PMID23438512
PMCPMC3950895
OpenAlexW2259144504

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.