Evidence map›Paper›PMID 23322301›Full record

ArticleGenes & development2013

Integrated cistromic and expression analysis of amplified NKX2-1 in lung adenocarcinoma identifies LMO3 as a functional transcriptional target.

Hideo Watanabe, Joshua M Francis, Michele S Woo, Banafsheh Etemad, Wenchu Lin, Daniel F Fries, Shouyong Peng, Eric L Snyder, Purushothama Rao Tata, Francesca Izzo and 8 more

Open access · diamondAbstract read
In one paragraph

Article in Genes & development, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
–field-weighted citation impact
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

47 citing papers in PubMed, 70 citations in OpenAlex.

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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

18 authors at 4 institutions in 1 country.

Hideo WatanabeDepartment of Medical Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts 02215, USA.
Joshua M Francis
Michele S Woo
Banafsheh Etemad
Wenchu Lin
Daniel F Fries
Shouyong Peng
Eric L Snyder
Purushothama Rao Tata
Francesca Izzo
Anna C Schinzel
Jeonghee Cho
Peter S Hammerman
Roel G Verhaak
William C Hahn
Jayaraj Rajagopal
Tyler Jacks
Matthew Meyerson
Dana-Farber Cancer Institute · USMassachusetts Institute of Technology · USBroad Institute · USMassachusetts General Hospital · US

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Scott Kopetz · 1985 to 2026
$290.8M
Tumor Cell Biology Training ProgramT32CA009361 · NCI · DANA-FARBER CANCER INSTITUTE · PI GRAY, NATHANAEL SCHIANDER · 1985 to 2015
$8.9M
SPORE in Lung CancerP20CA090578 · NCI · DANA-FARBER CANCER INSTITUTE · PI JOHNSON, BRUCE E. · 2003 to 2007
$5.1M
NKX2-1, A Candidate Lineage Survival Oncogene in Lung AdenocarcinomaR01CA109038 · NCI · DANA-FARBER CANCER INSTITUTE · PI MEYERSON, MATTHEW L. · 2005 to 2014
$3.8M
The role of Nkx2-1 in lung adenocarcinomaK08CA154784 · NCI · UNIVERSITY OF UTAH · PI SNYDER, ERIC LEE · 2011 to 2015
$880k
NCI NIH HHS 5P20CA90578NCI NIH HHS 5R01CA109038NCI NIH HHS 5T32CA009361-28NCI NIH HHS K08 CA154784NCI NIH HHS P20 CA090578NCI NIH HHS P30 CA016672NCI NIH HHS R01 CA109038NCI NIH HHS T32 CA009361
6 · The paper itself

Abstract

The NKX2-1 transcription factor, a regulator of normal lung development, is the most significantly amplified gene in human lung adenocarcinoma. To study the transcriptional impact of NKX2-1 amplification, we generated an expression signature associated with NKX2-1 amplification in human lung adenocarcinoma and analyzed DNA-binding sites of NKX2-1 by genome-wide chromatin immunoprecipitation. Integration of these expression and cistromic analyses identified LMO3, itself encoding a transcription regulator, as a candidate direct transcriptional target of NKX2-1. Further cistromic and overexpression analyses indicated that NKX2-1 can cooperate with the forkhead box transcription factor FOXA1 to regulate LMO3 gene expression. RNAi analysis of NKX2-1-amplified cells compared with nonamplified cells demonstrated that LMO3 mediates cell survival downstream from NKX2-1. Our findings provide new insight into the transcriptional regulatory network of NKX2-1 and suggest that LMO3 is a transcriptional signal transducer in NKX2-1-amplified lung adenocarcinomas.

Indexed as

Gene Expression Regulation, NeoplasticAdaptor Proteins, Signal TransducingAdenocarcinomaAdenocarcinoma of LungCell Line, TumorChromatinGene Expression ProfilingHepatocyte Nuclear Factor 3-alphaHumansLIM Domain ProteinsLung NeoplasmsNuclear ProteinsProtein BindingProtein Interaction Domains and MotifsThyroid Nuclear Factor 1Transcription FactorsAdaptor Proteins, Signal TransducingChromatinFOXA1 protein, humanHepatocyte Nuclear Factor 3-alphaLIM Domain ProteinsLMO3 protein, humanNuclear ProteinsThyroid Nuclear Factor 1Transcription Factors

Identifiers

PMID23322301
PMCPMC3566312
OpenAlexW2153646780

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.