Evidence map›Paper›PMID 21911935›Full record

ArticleThe Journal of clinical investigation2011

TRAF6 is an amplified oncogene bridging the RAS and NF-κB pathways in human lung cancer.

Daniel T Starczynowski, William W Lockwood, Sophie Deléhouzée, Raj Chari, Joanna Wegrzyn, Megan Fuller, Ming-Sound Tsao, Stephen Lam, Adi F Gazdar, Wan L Lam and 1 more

Abstract read
In one paragraph

Article in The Journal of clinical investigation, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 112 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
112citing papers in PubMed, 1 pooled it
5.5field-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

112 citing papers in PubMed, 1 synthesis or guideline pooled it, 172 citations in OpenAlex.

  1. Pooled it
  2. Mitochondrial double-stranded RNA fuels pancreatic cancer growth via RIG-I/TLR3 inflammation.Proceedings of the National Academy of Sciences of the United States of America · 2026
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52 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

11 authors at 3 institutions in 1 country.

Daniel T StarczynowskiBritish Columbia Cancer Agency, Vancouver, British Columbia, Canada.
William W Lockwood
Sophie Deléhouzée
Raj Chari
Joanna Wegrzyn
Megan Fuller
Ming-Sound Tsao
Stephen Lam
Adi F Gazdar
Wan L Lam
Aly Karsan
University of British Columbia · CABC Cancer Agency · CAUniversity of Toronto · CA

Funding

UNIVERSITY OF TEXAS--SPORE IN LUNG CANCERP50CA070907 · NCI · UT SOUTHWESTERN MEDICAL CENTER · PI HEYMACH, JOHN V., MINNA, JOHN D. · 1996 to 2024
$57.4M
Novel Reagents and New Biomarkers for Lung CancerU01CA084971 · NCI · UT SOUTHWESTERN MEDICAL CENTER · PI GAZDAR, ADI F. · 1999 to 2009
$4.5M
CIHR MOP 77903CIHR MOP 86731CIHR MOP 89976CIHR MOP 97744NCI NIH HHS 5U01 CA84971-10NCI NIH HHS P50 CA070907NCI NIH HHS U01 CA084971
6 · The paper itself

Abstract

Somatic mutations and copy number alterations (as a result of deletion or amplification of large portions of a chromosome) are major drivers of human lung cancers. Detailed analysis of lung cancer-associated chromosomal amplifications could identify novel oncogenes. By performing an integrative cytogenetic and gene expression analysis of non-small-cell lung cancer (NSCLC) and small-cell lung cancer (SCLC) cell lines and tumors, we report here the identification of a frequently recurring amplification at chromosome 11 band p13. Within this region, only TNF receptor-associated factor 6 (TRAF6) exhibited concomitant mRNA overexpression and gene amplification in lung cancers. Inhibition of TRAF6 in human lung cancer cell lines suppressed NF-κB activation, anchorage-independent growth, and tumor formation. In these lung cancer cell lines, RAS required TRAF6 for its oncogenic capabilities. Furthermore, TRAF6 overexpression in NIH3T3 cells resulted in NF-κB activation, anchorage-independent growth, and tumor formation. Our findings show that TRAF6 is an oncogene that is important for RAS-mediated oncogenesis and provide a mechanistic explanation for the previously apparent importance of constitutive NF-κB activation in RAS-driven lung cancers.

Indexed as

AnimalsCarcinoma, Non-Small-Cell LungCarcinoma, Small CellCell Line, TumorCell Transformation, NeoplasticChromosomes, Human, Pair 11Gene AmplificationHumansLung NeoplasmsMiceMice, Inbred NODMice, SCIDNF-kappa BNIH 3T3 CellsOncogenesras ProteinsNF-kappa Bras ProteinsTNF Receptor-Associated Factor 6

Identifiers

PMID21911935
PMCPMC3195480
OpenAlexW2007251599

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.