Evidence map›Paper›PMID 28650484›Full record

ArticleNature genetics2017

Insertional mutagenesis identifies drivers of a novel oncogenic pathway in invasive lobular breast carcinoma.

Sjors M Kas, Julian R de Ruiter, Koen Schipper, Stefano Annunziato, Eva Schut, Sjoerd Klarenbeek, Anne Paulien Drenth, Eline van der Burg, Christiaan Klijn, Jelle J Ten Hoeve and 6 more

Abstract read
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In one paragraph

Article in Nature genetics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed, 1 pooled it
4.5field-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

52 citing papers in PubMed, 1 synthesis or guideline pooled it, 73 citations in OpenAlex.

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  4. E-Cadherin-Mediated Cell-Cell Adhesion and Invasive Lobular Breast Cancer.Advances in experimental medicine and biology · 2025
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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

16 authors at 5 institutions in 2 countries.

Sjors M KasDivision of Molecular Pathology, The Netherlands Cancer Institute, Amsterdam, the Netherlands.
Julian R de RuiterDivision of Molecular Pathology, The Netherlands Cancer Institute, Amsterdam, the Netherlands.
Koen SchipperDivision of Molecular Pathology, The Netherlands Cancer Institute, Amsterdam, the Netherlands.
Stefano AnnunziatoDivision of Molecular Pathology, The Netherlands Cancer Institute, Amsterdam, the Netherlands.
Eva SchutDivision of Molecular Pathology, The Netherlands Cancer Institute, Amsterdam, the Netherlands.
Sjoerd KlarenbeekExperimental Animal Pathology, The Netherlands Cancer Institute, Amsterdam, the Netherlands.
Anne Paulien DrenthDivision of Molecular Pathology, The Netherlands Cancer Institute, Amsterdam, the Netherlands.
Eline van der BurgDivision of Molecular Pathology, The Netherlands Cancer Institute, Amsterdam, the Netherlands.
Christiaan KlijnDivision of Molecular Pathology, The Netherlands Cancer Institute, Amsterdam, the Netherlands.
Jelle J Ten HoeveDivision of Molecular Carcinogenesis, The Netherlands Cancer Institute, Amsterdam, the Netherlands.
David J AdamsExperimental Cancer Genetics, Wellcome Trust Sanger Institute, Hinxton, UK.
Marco J KoudijsDivision of Molecular Pathology, The Netherlands Cancer Institute, Amsterdam, the Netherlands.
Jelle WesselingDivision of Molecular Pathology, The Netherlands Cancer Institute, Amsterdam, the Netherlands.
Micha NetheDivision of Molecular Pathology, The Netherlands Cancer Institute, Amsterdam, the Netherlands.
Lodewyk F A WesselsDivision of Molecular Carcinogenesis, The Netherlands Cancer Institute, Amsterdam, the Netherlands.
Jos JonkersDivision of Molecular Pathology, The Netherlands Cancer Institute, Amsterdam, the Netherlands.
Oncode Institute · NLThe Netherlands Cancer Institute · NLCancer Genomics Centre · NLDelft University of Technology · NLWellcome Sanger Institute · GB

Funding

Cancer Research UK 13031
6 · The paper itself

Abstract

Invasive lobular carcinoma (ILC) is the second most common breast cancer subtype and accounts for 8-14% of all cases. Although the majority of human ILCs are characterized by the functional loss of E-cadherin (encoded by CDH1), inactivation of Cdh1 does not predispose mice to develop mammary tumors, implying that mutations in additional genes are required for ILC formation in mice. To identify these genes, we performed an insertional mutagenesis screen using the Sleeping Beauty transposon system in mice with mammary-specific inactivation of Cdh1. These mice developed multiple independent mammary tumors of which the majority resembled human ILC in terms of morphology and gene expression. Recurrent and mutually exclusive transposon insertions were identified in Myh9, Ppp1r12a, Ppp1r12b and Trp53bp2, whose products have been implicated in the regulation of the actin cytoskeleton. Notably, MYH9, PPP1R12B and TP53BP2 were also frequently aberrated in human ILC, highlighting these genes as drivers of a novel oncogenic pathway underlying ILC development.

Indexed as

Mutagenesis, InsertionalAnimalsBreast NeoplasmsCadherinsCarcinoma, LobularCell LineCell SurvivalCell Transformation, NeoplasticFemaleHaplotypesHumansMaleMiceMyosin Heavy ChainsMyosin-Light-Chain PhosphataseNonmuscle Myosin Type IIACadherinsCdh1 protein, mouseMyh9 protein, mouseMyosin Heavy ChainsMyosin-Light-Chain PhosphataseNonmuscle Myosin Type IIAPpp1r12a protein, mouseTransposasesTrp53bp2 protein, mouseTumor Suppressor Proteins

Identifiers

PMID28650484
OpenAlexW2675346956

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.