Evidence map›Paper›PMID 17667909›Full record

ArticleBritish journal of cancer2007

Downstream signalling and specific inhibition of c-MET/HGF pathway in small cell lung cancer: implications for tumour invasion.

P C Ma, M S Tretiakova, V Nallasura, R Jagadeeswaran, A N Husain, R Salgia

Open access · hybridAbstract read
In one paragraph

Article in British journal of cancer, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers.

0numbers the graph read from it
0cells of the map it votes in
80citing papers in PubMed
5.9field-weighted citation impact, top 4% 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

80 citing papers in PubMed, 173 citations in OpenAlex.

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  14. Effect of Sugars onPathogens (Basel, Switzerland) · 2020
    Article
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20 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

6 authors at 2 institutions in 1 country.

P C MaDivision of Hematology/Oncology, Department of Medicine, University Hospitals of Case Medical Center and Ireland Cancer Center, Case Western Reserve University, Case Comprehensive Cancer Center, Cleveland, OH 44106, USA.
M S Tretiakova
V Nallasura
R Jagadeeswaran
A N Husain
R Salgia
Cancer Research Center · USUniversity of Chicago · US

Funding

Role of c-Met in SCLC and Potential for Novel TherapyR01CA100750 · NCI · UNIVERSITY OF CHICAGO · PI SALGIA, RAVI · 2004 to 2012
$2.2M
Studies of Alternations of c-MET in SCLCK08CA102545 · NCI · CASE WESTERN RESERVE UNIVERSITY · PI MA, PATRICK C. · 2005 to 2009
$763k
NCI NIH HHS 1K08 CA102545NCI NIH HHS CA109640NCI NIH HHS K08 CA102545NCI NIH HHS R01 CA100750
6 · The paper itself

Abstract

The c-MET receptor can be overexpressed, amplified, or mutated in solid tumours including small cell lung cancer (SCLC). In c-MET-overexpressing SCLC cell line NCI-H69, hepatocyte growth factor (HGF) dramatically induced c-MET phosphorylation at phosphoepitopes pY1230/1234/1235 (catalytic tyrosine kinase), pY1003 (juxtamembrane), and also of paxillin at pY31 (CRKL-binding site). We utilised a global proteomics phosphoantibody array approach to identify further c-MET/HGF signal transduction intermediates in SCLC. Strong HGF induction of specific phosphorylation sites in phosphoproteins involved in c-MET/HGF signal transduction was detected, namely adducin-alpha [S724], adducin-gamma [S662], CREB [S133], ERK1 [T185/Y187], ERK1/2 [T202/Y204], ERK2 [T185/Y187], MAPKK (MEK) 1/2 [S221/S225], MAPKK (MEK) 3/6 [S189/S207], RB [S612], RB1 [S780], JNK [T183/Y185], STAT3 [S727], focal adhesion kinase (FAK) [Y576/S722/S910], p38alpha-MAPK [T180/Y182], and AKT1[S473] and [T308]. Conversely, inhibition of phosphorylation by HGF in protein kinase C (PKC), protein kinase R (PKR), and also CDK1 was identified. Phosphoantibody-based immunohistochemical analysis of SCLC tumour tissue and microarray established the role of c-MET in SCLC biology. This supports a role of c-MET activation in tumour invasive front in the tumour progression and invasion involving FAK and AKT downstream. The c-MET serves as an attractive therapeutic target in SCLC, as shown through small interfering RNA (siRNA) and selective prototype c-MET inhibitor SU11274, inhibiting the phosphorylation of c-MET itself and its downstream molecules such as AKT, S6 kinase, and ERK1/2. Investigation of mechanisms of invasion and, ultimately, metastasis in SCLC would be very useful with these signal transduction molecules.

Indexed as

Neoplasm InvasivenessSignal TransductionCarcinoma, Small CellCell Line, TumorHepatocyte Growth FactorHumansLung NeoplasmsProto-Oncogene Proteins c-metRNA, Small InterferingHepatocyte Growth FactorProto-Oncogene Proteins c-metRNA, Small Interfering

Identifiers

PMID17667909
PMCPMC2360323
OpenAlexW1971382968

What OpenQuestion holds

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LicenceCC BY
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.