Evidence map›Paper›PMID 25410484›Full record

ArticleBreast cancer research : BCR2014

Shift in GATA3 functions, and GATA3 mutations, control progression and clinical presentation in breast cancer.

Helit Cohen, Rotem Ben-Hamo, Moriah Gidoni, Ilana Yitzhaki, Renana Kozol, Alona Zilberberg, Sol Efroni

Open access · goldAbstract read
In one paragraph

Article in Breast cancer research : BCR, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

32 citing papers in PubMed, 61 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

7 authors at 1 institution in 1 country.

Helit CohenThe Mina and Everard Goodman Faculty of Life Science, Bar Ilan University, Ramat Gan, 52900, Israel. helit.c@gmail.com.
Rotem Ben-HamoThe Mina and Everard Goodman Faculty of Life Science, Bar Ilan University, Ramat Gan, 52900, Israel. rotem@systemsbiomed.org.
Moriah GidoniThe Mina and Everard Goodman Faculty of Life Science, Bar Ilan University, Ramat Gan, 52900, Israel. moriahcohen@gmail.com.
Ilana YitzhakiThe Mina and Everard Goodman Faculty of Life Science, Bar Ilan University, Ramat Gan, 52900, Israel. ilana.brt@gmail.com.
Renana KozolThe Mina and Everard Goodman Faculty of Life Science, Bar Ilan University, Ramat Gan, 52900, Israel. renko1989@gmail.com.
Alona ZilberbergThe Mina and Everard Goodman Faculty of Life Science, Bar Ilan University, Ramat Gan, 52900, Israel. alona.zilberberg@gmail.com.
Sol EfroniThe Mina and Everard Goodman Faculty of Life Science, Bar Ilan University, Ramat Gan, 52900, Israel. sol.efroni@biu.ac.il.
Bar-Ilan University · IL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionGATA binding protein 3 (GATA3) is a regulator of mammary luminal cell differentiation, and an estrogen receptor (ER) associated marker in breast cancer. Tumor suppressor functions of GATA3 have been demonstrated primarily in basal-like breast cancers. Here, we focused on its function in luminal breast cancer, where GATA3 is frequently mutated, and its levels are significantly elevated.

methodsGATA3 target genes were identified in normal- and luminal cancer- mammary cells by ChIP-seq, followed by examination of the effects of GATA3 expressions and mutations on tumorigenesis-associated genes and processes. Additionally, mutations and expression data of luminal breast cancer patients from The Cancer Genome Atlas were analyzed to characterize genetic signatures associated with GATA3 mutations.

resultsWe show that some GATA3 effects shift from tumor suppressing to tumor promoting during tumorigenesis, with deregulation of three genes, BCL2, DACH1, THSD4, representing major GATA3-controlled processes in cancer progression. In addition, we identify an altered activity of mutant GATA3, and distinct associated genetic signatures. These signatures depend on the functional domain mutated; and, for a specific subgroup, are shared with basal-like breast cancer patients, who are a clinical group with regard to considerations of mode of treatment.

conclusionsThe GATA3 dependent mechanisms may call for special considerations for proper prognosis and treatment of patients.

Indexed as

Gene Expression Regulation, NeoplasticADAM ProteinsBreast NeoplasmsCell LineCell Transformation, NeoplasticEye ProteinsFemaleGATA3 Transcription FactorHumansMammary Glands, HumanMutationProto-Oncogene Proteins c-bcl-2ThrombospondinsTranscription FactorsADAM ProteinsBCL2 protein, humanDACH1 protein, humanEye ProteinsGATA3 protein, humanGATA3 Transcription FactorProto-Oncogene Proteins c-bcl-2ThrombospondinsTHSD4 protein, humanTranscription Factors

Identifiers

PMID25410484
PMCPMC4303202
OpenAlexW2148240072

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.