Evidence map›Paper›PMID 27588951›Full record

ArticlePLoS genetics2016

Gain- and Loss-of-Function Mutations in the Breast Cancer Gene GATA3 Result in Differential Drug Sensitivity.

Barbara Mair, Tomasz Konopka, Claudia Kerzendorfer, Katia Sleiman, Sejla Salic, Violeta Serra, Markus K Muellner, Vasiliki Theodorou, Sebastian M B Nijman

Open access · goldAbstract read
In one paragraph

Article in PLoS genetics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.8field-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

29 citing papers in PubMed, 58 citations in OpenAlex.

  1. The GATA3-RFPL3-ASK1 axis suppresses breast cancer growth and lung metastasis.Apoptosis : an international journal on programmed cell death · 2026
    Article
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  4. KLF transcription factors in bone diseases.Journal of cellular and molecular medicine · 2024
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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

9 authors at 4 institutions in 4 countries.

Barbara MairCeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences, Vienna, Austria.ORCID 0000-0001-6982-2529
Tomasz KonopkaLudwig Institute for Cancer Research, Nuffield Department of Clinical Medicine, University of Oxford, Oxford, United Kingdom.ORCID 0000-0003-3042-4712
Claudia KerzendorferCeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences, Vienna, Austria.
Katia SleimanCeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences, Vienna, Austria.ORCID 0000-0001-5808-1913
Sejla SalicLudwig Institute for Cancer Research, Nuffield Department of Clinical Medicine, University of Oxford, Oxford, United Kingdom.
Violeta SerraExperimental Therapeutics Group, Vall d'Hebron Institute of Oncology, Barcelona, Spain.
Markus K MuellnerCeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences, Vienna, Austria.
Vasiliki TheodorouInstitute of Molecular Biology and Biotechnology, Foundation for Research and Technology-Hellas, Heraklion, Crete, Greece.ORCID 0000-0003-1614-700X
Sebastian M B NijmanCeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences, Vienna, Austria.
Austrian Academy of Sciences · ATUniversity of Oxford · GBFoundation for Research and Technology Hellas · GRVall d'Hebron Institute of Oncology · ES

Funding

European Research Council 311166Medical Research Council G0900747 91070Wellcome TrustWellcome Trust 090532/Z/09/Z
6 · The paper itself

Abstract

Patterns of somatic mutations in cancer genes provide information about their functional role in tumourigenesis, and thus indicate their potential for therapeutic exploitation. Yet, the classical distinction between oncogene and tumour suppressor may not always apply. For instance, TP53 has been simultaneously associated with tumour suppressing and promoting activities. Here, we uncover a similar phenomenon for GATA3, a frequently mutated, yet poorly understood, breast cancer gene. We identify two functional classes of frameshift mutations that are associated with distinct expression profiles in tumours, differential disease-free patient survival and gain- and loss-of-function activities in a cell line model. Furthermore, we find an estrogen receptor-independent synthetic lethal interaction between a GATA3 frameshift mutant with an extended C-terminus and the histone methyltransferases G9A and GLP, indicating perturbed epigenetic regulation. Our findings reveal important insights into mutant GATA3 function and breast cancer, provide the first potential therapeutic strategy and suggest that dual tumour suppressive and oncogenic activities are more widespread than previously appreciated.

Indexed as

Epigenesis, GeneticBreast NeoplasmsDisease-Free SurvivalDrug Resistance, NeoplasmEstrogensFemaleFrameshift MutationGATA3 Transcription FactorGene Expression Regulation, NeoplasticHistocompatibility AntigensHistone-Lysine N-MethyltransferaseHumansMCF-7 CellsSmall Molecule LibrariesEHMT1 protein, humanEHMT2 protein, humanEstrogensGATA3 protein, humanGATA3 Transcription FactorHistocompatibility AntigensHistone-Lysine N-MethyltransferaseSmall Molecule Libraries

Identifiers

PMID27588951
PMCPMC5010247
OpenAlexW2514386502

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.