Evidence map›Paper›PMID 21654344›Full record

ArticleMelanoma research2011

Comprehensive analysis of receptor tyrosine kinase activation in human melanomas reveals autocrine signaling through IGF-1R.

Kerrington R Molhoek, Amber L Shada, Mark Smolkin, Sudhir Chowbina, Jason Papin, David L Brautigan, Craig L Slingluff

Abstract read
In one paragraph

Article in Melanoma research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.3field-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

25 citing papers in PubMed, 34 citations in OpenAlex.

  1. Clinical activity and safety of combination therapy with temsirolimus and bevacizumab for advanced melanoma: a phase II trial (CTEP 7190/Mel47).Clinical cancer research : an official journal of the American Association for Cancer Research · 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 2 institutions in 1 country.

Kerrington R MolhoekDepartment of Surgery, Division of Surgical Oncology, School of Medicine, University of Virginia Health System, Charlottesville, Virginia 22908, USA.
Amber L Shada
Mark Smolkin
Sudhir Chowbina
Jason Papin
David L Brautigan
Craig L Slingluff
University of Virginia · USUniversity of Virginia Health System · US

Funding

Women's Oncology Program - WONP30CA044579 · NCI · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI Thomas P. Loughran · 1987 to 2026
$72.1M
MELANOMA VACCINES USING MHC-ASSOCIATED PEPTIDESR01CA057653 · NCI · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI SLINGLUFF, CRAIG LEE · 1997 to 2012
$3.4M
RAPAMYCIN BLOCKADE OF PROTEIN PHOSPHATASE SIGNALINGR01CA077584 · NCI · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI BRAUTIGAN, DAVID L. · 1999 to 2007
$1.6M
NCI NIH HHS CA77584NCI NIH HHS P30 CA044579NCI NIH HHS P30 CA44579NCI NIH HHS P30CA44579NCI NIH HHS R01 CA057653NCI NIH HHS R01 CA077584NCI NIH HHS R01 CA57653
6 · The paper itself

Abstract

Melanomas depend on autocrine signals for proliferation and survival; however, no systematic screen of known receptor tyrosine kinases (RTKs) has been performed to identify which autocrine signaling pathways are activated in melanoma. Here, we performed a comprehensive analysis of 42 RTKs in six individual human melanoma tumor specimens as well as 17 melanoma cell lines, some of which were derived from the tumor specimens. We identified five RTKs that were active in almost every one of the melanoma tissue specimens and cell lines, including two previously unreported receptors, insulin-like growth factor receptor 1 (IGF-1R) and macrophage-stimulating protein receptor (MSPR), in addition to three receptors (vascular endothelial growth factor receptor, fibroblast growth factor receptor, and hepatocyte growth factor receptor) known to be autocrine activated in melanoma. We show, by quantitative real time PCR, that all melanoma cell lines expressed genes for the RTK ligands such as HGF, IGF-1, and MSP. Addition of antibodies to either IGF-1 or HGF, but not to MSP, to the culture medium blocked melanoma cell proliferation, and even caused net loss of melanoma cells. Antibody addition deactivated IGF-1R and hepatocyte growth factor receptors, as well as mitogen-activated protein kinase signaling. Thus, IGF-1 is a new growth factor for autocrine driven proliferation of human melanoma in vitro. Our results suggest that IGF-1-IGF-1R autocrine pathway in melanoma is a possible target for therapy in human melanomas.

Indexed as

Autocrine CommunicationSignal TransductionCell Line, TumorCell ProliferationGene Expression Regulation, NeoplasticHumansInsulin-Like Growth Factor ILigandsMelanomaMitogen-Activated Protein KinasesPhosphorylationReceptor, IGF Type 1Reverse Transcriptase Polymerase Chain ReactionTime FactorsInsulin-Like Growth Factor ILigandsMitogen-Activated Protein KinasesReceptor, IGF Type 1

Identifiers

PMID21654344
PMCPMC3131461
OpenAlexW2244368680

What OpenQuestion holds

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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.