Evidence map›Paper›PMID 23112155›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2012

CDX2 is an amplified lineage-survival oncogene in colorectal cancer.

Keyan Salari, Mary E Spulak, Justin Cuff, Andrew D Forster, Craig P Giacomini, Stephanie Huang, Melissa E Ko, Albert Y Lin, Matt van de Rijn, Jonathan R Pollack

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed
3.7field-weighted citation impact, top 7% 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

52 citing papers in PubMed, 84 citations in OpenAlex.

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  11. Novel inheritedCold Spring Harbor molecular case studies · 2023
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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

10 authors at 2 institutions in 1 country.

Keyan SalariDepartment of Pathology, Stanford University School of Medicine, Stanford, CA 94305, USA.
Mary E Spulak
Justin Cuff
Andrew D Forster
Craig P Giacomini
Stephanie Huang
Melissa E Ko
Albert Y Lin
Matt van de Rijn
Jonathan R Pollack
Stanford University · USSanta Clara Valley Medical Center · US

Funding

Gene Amplification and Deletion in Pancreatic CancerR01CA112016 · NCI · STANFORD UNIVERSITY · PI POLLACK, JONATHAN R · 2006 to 2010
$1.4M
NCI NIH HHS CA112016NCI NIH HHS R01 CA112016
6 · The paper itself

Abstract

The mutational activation of oncogenes drives cancer development and progression. Classic oncogenes, such as MYC and RAS, are active across many different cancer types. In contrast, "lineage-survival" oncogenes represent a distinct and emerging class typically comprising transcriptional regulators of a specific cell lineage that, when deregulated, support the proliferation and survival of cancers derived from that lineage. Here, in a large collection of colorectal cancer cell lines and tumors, we identify recurrent amplification of chromosome 13, an alteration highly restricted to colorectal-derived cancers. A minimal region of amplification on 13q12.2 pinpoints caudal type homeobox transcription factor 2 (CDX2), a regulator of normal intestinal lineage development and differentiation, as a target of the amplification. In contrast to its described role as a colorectal tumor suppressor, CDX2 when amplified is required for the proliferation and survival of colorectal cancer cells. Further, transcriptional profiling, binding-site analysis, and functional studies link CDX2 to Wnt/β-catenin signaling, itself a key oncogenic pathway in colorectal cancer. These data characterize CDX2 as a lineage-survival oncogene deregulated in colorectal cancer. Our findings challenge a prevailing view that CDX2 is a tumor suppressor in colorectal cancer and uncover an additional piece in the multistep model of colorectal tumorigenesis.

Indexed as

Gene AmplificationAnimalsCDX2 Transcription FactorCell Line, TumorCell SurvivalCell Transformation, NeoplasticChromosomes, Human, Pair 13Colorectal NeoplasmsDisease Models, AnimalHomeodomain ProteinsHumansMiceNIH 3T3 CellsTranscription FactorsTumor Suppressor ProteinsWnt Signaling PathwayCDX2 protein, humanCdx2 protein, mouseCDX2 Transcription FactorHomeodomain ProteinsTranscription FactorsTumor Suppressor Proteins

Identifiers

PMID23112155
PMCPMC3503165
OpenAlexW2041434532

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.