Evidence map›Paper›PMID 12151601›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2002

Identification of oncogenes collaborating with p27Kip1 loss by insertional mutagenesis and high-throughput insertion site analysis.

Harry C Hwang, Carla P Martins, Yvon Bronkhorst, Erin Randel, Anton Berns, Matthew Fero, Bruce E Clurman

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed
4.3field-weighted citation impact, top 5% 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

61 citing papers in PubMed, 106 citations in OpenAlex.

  1. Article
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  3. The miR-106a~363Oncotarget · 2017
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1 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

7 authors at 3 institutions in 2 countries.

Harry C HwangDivision of Clinical Research and Human Biology, Fred Hutchinson Cancer Research Center, 1100 Fairview Avenue North, Seattle, WA 98109, USA.
Carla P Martins
Yvon Bronkhorst
Erin Randel
Anton Berns
Matthew Fero
Bruce E Clurman
Fred Hutch Cancer Center · USCancer Research Center · USThe Netherlands Cancer Institute · NL

Funding

Interdisciplinary Tranining in Cancer ResearchT32CA080416 · NCI · UNIVERSITY OF WASHINGTON · PI STODDARD, BARRY L. · 1998 to 2023
$9.7M
Tumor Suppression by the Fbw7 Ubiquitin LigaseR01CA084069 · NCI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI CLURMAN, BRUCE E · 2000 to 2015
$5.1M
Mechanism of tumor suppression by p27K22CA087731 · NCI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI FERO, MATTHEW L · 2001 to 2003
$466k
NCI NIH HHS CA80416-05NCI NIH HHS K22 CA087731NCI NIH HHS R01 CA084069NCI NIH HHS R01 CA84069NCI NIH HHS T32 CA080416
6 · The paper itself

Abstract

The p27(Kip1) protein is a cyclin-dependent kinase inhibitor that blocks cell division in response to antimitogenic cues. p27 expression is reduced in many human cancers, and p27 functions as a tumor suppressor that exhibits haploinsufficiency in mice. Despite the well characterized role of p27 as a cyclin-dependent kinase inhibitor, its mechanism of tumor suppression is unknown. We used Moloney murine leukemia virus to induce lymphomas in p27+/+ and p27-/- mice and observed that lymphomagenesis was accelerated in the p27-/- animals. To identify candidate oncogenes that collaborate with p27 loss, we used a high-throughput strategy to sequence 277 viral insertion sites derived from two distinct sets of p27-/- lymphomas and determined their chromosomal location by comparison with the Celera and public (Ensembl) mouse genome databases. This analysis identified a remarkable number of putative protooncogenes in these lymphomas, which included loci that were novel as well as those that were overrepresented in p27-/- tumors. We found that Myc activations occurred more frequently in p27-/- lymphomas than in p27+/+ tumors. We also characterized insertions within two novel loci: (i) the Jun dimerization protein 2 gene (Jundp2), and (ii) an X-linked locus termed Xpcl1. Each of the loci that we found to be frequently involved in p27-/- lymphomas represents a candidate oncogene collaborating with p27 loss. This study illustrates the power of high-throughput insertion site analysis in cancer gene discovery.

Indexed as

Gene DeletionGenes, Tumor SuppressorMutagenesis, InsertionalOncogenesAnimalsBase SequenceCell Cycle ProteinsCloning, MolecularCyclin-Dependent Kinase Inhibitor p27Cyclin-Dependent KinasesDNA, NeoplasmDNA PrimersLymphomaMiceMice, KnockoutMolecular Sequence DataCdkn1b protein, mouseCell Cycle ProteinsCyclin-Dependent Kinase Inhibitor p27Cyclin-Dependent KinasesDNA, NeoplasmDNA PrimersTumor Suppressor Proteins

Identifiers

PMID12151601
PMCPMC123250
OpenAlexW2018616901

What OpenQuestion holds

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Read underepoch 390

Registered trials

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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.