Evidence map›Paper›PMID 27849608›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2016

Transposon mutagenesis identifies genes that cooperate with mutant Pten in breast cancer progression.

Roberto Rangel, Song-Choon Lee, Kenneth Hon-Kim Ban, Liliana Guzman-Rojas, Michael B Mann, Justin Y Newberg, Takahiro Kodama, Leslie A McNoe, Luxmanan Selvanesan, Jerrold M Ward and 5 more

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
3.1field-weighted citation impact, top 9% 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

35 citing papers in PubMed, 56 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

15 authors at 4 institutions in 4 countries.

Roberto RangelCancer Research Program, Houston Methodist Research Institute, Houston, TX 77030.
Song-Choon LeeDivision of Genomics and Genetics, Institute of Molecular and Cell Biology, Agency for Science, Technology and Research, Biopolis, Singapore 138673.
Kenneth Hon-Kim BanDivision of Genomics and Genetics, Institute of Molecular and Cell Biology, Agency for Science, Technology and Research, Biopolis, Singapore 138673.
Liliana Guzman-RojasCancer Research Program, Houston Methodist Research Institute, Houston, TX 77030.
Michael B MannCancer Research Program, Houston Methodist Research Institute, Houston, TX 77030.
Justin Y NewbergCancer Research Program, Houston Methodist Research Institute, Houston, TX 77030.
Takahiro KodamaCancer Research Program, Houston Methodist Research Institute, Houston, TX 77030.ORCID 0000-0002-6250-1324
Leslie A McNoeDepartment of Biochemistry, University of Otago, Dunedin 9016, New Zealand.
Luxmanan SelvanesanDepartment of Biochemistry, University of Otago, Dunedin 9016, New Zealand.
Jerrold M WardDivision of Genomics and Genetics, Institute of Molecular and Cell Biology, Agency for Science, Technology and Research, Biopolis, Singapore 138673.
Alistair G RustExperimental Cancer Genetics, Wellcome Trust Sanger Institute, Hinxton, Cambridge CB10 1HH, United Kingdom.
Kuan-Yew ChinDivision of Genomics and Genetics, Institute of Molecular and Cell Biology, Agency for Science, Technology and Research, Biopolis, Singapore 138673.
Michael A BlackDepartment of Biochemistry, University of Otago, Dunedin 9016, New Zealand.
Nancy A JenkinsCancer Research Program, Houston Methodist Research Institute, Houston, TX 77030.
Neal G CopelandCancer Research Program, Houston Methodist Research Institute, Houston, TX 77030; ncopeland@houstonmethodist.org.
Agency for Science, Technology and Research · SGHouston Methodist · USUniversity of Otago · NZWellcome Sanger Institute · GB

Funding

Cancer Research UKWellcome Trust
6 · The paper itself

Abstract

Triple-negative breast cancer (TNBC) has the worst prognosis of any breast cancer subtype. To better understand the genetic forces driving TNBC, we performed a transposon mutagenesis screen in a phosphatase and tensin homolog (Pten) mutant mice and identified 12 candidate trunk drivers and a much larger number of progression genes. Validation studies identified eight TNBC tumor suppressor genes, including the GATA-like transcriptional repressor TRPS1 Down-regulation of TRPS1 in TNBC cells promoted epithelial-to-mesenchymal transition (EMT) by deregulating multiple EMT pathway genes, in addition to increasing the expression of SERPINE1 and SERPINB2 and the subsequent migration, invasion, and metastasis of tumor cells. Transposon mutagenesis has thus provided a better understanding of the genetic forces driving TNBC and discovered genes with potential clinical importance in TNBC.

Indexed as

DNA Transposable ElementsAdenocarcinomaAnimalsCell Line, TumorDisease ProgressionDNA-Binding ProteinsFemaleFos-Related Antigen 1Gene ExpressionGene Expression Regulation, NeoplasticGenes, NeoplasmGenes, Tumor SuppressorHumansKaplan-Meier EstimateLung NeoplasmsMammary Neoplasms, ExperimentalDNA-Binding ProteinsDNA Transposable ElementsFos-Related Antigen 1Proto-Oncogene Proteins c-fosPTEN PhosphohydrolasePten protein, mouseRepressor ProteinsTranscription FactorsTRPS1 protein, humanbreast cancermetastasisSleeping BeautyTRPS1tumor suppressors

Identifiers

PMID27849608
PMCPMC5137755
OpenAlexW2554000031

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.