Evidence map›Paper›PMID 26390871›Full record

ReviewJournal of mammary gland biology and neoplasia2015

Hormone-sensing mammary epithelial progenitors: emerging identity and hormonal regulation.

Gerard A Tarulli, Geraldine Laven-Law, Reshma Shakya, Wayne D Tilley, Theresa E Hickey

Abstract readReview
PubMed Publisher
In one paragraph

Review in Journal of mammary gland biology and neoplasia, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.7field-weighted citation impact, top 28% 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

9 citing papers in PubMed, 16 citations in OpenAlex.

  1. Article
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  7. 17Journal of the Endocrine Society · 2018
    Article
  8. Article
  9. Pathobiology of the 129:Stat1Breast cancer research : BCR · 2017
    Article
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

5 authors at 1 institution in 1 country.

Gerard A TarulliDame Roma Mitchell Cancer Research Laboratories (DRMCRL), School of Medicine, Faculty of Health Sciences, The University of Adelaide, Adelaide, SA, 5005, Australia. gerard.tarulli@adelaide.edu.au.
Geraldine Laven-LawDame Roma Mitchell Cancer Research Laboratories (DRMCRL), School of Medicine, Faculty of Health Sciences, The University of Adelaide, Adelaide, SA, 5005, Australia.
Reshma ShakyaBreast Cancer Genetics Laboratory, Centre for Personalised Cancer Medicine, School of Medicine, Faculty of Health Sciences, The University of Adelaide, Adelaide, SA, 5005, Australia.
Wayne D TilleyDame Roma Mitchell Cancer Research Laboratories (DRMCRL), School of Medicine, Faculty of Health Sciences, The University of Adelaide, Adelaide, SA, 5005, Australia.
Theresa E HickeyDame Roma Mitchell Cancer Research Laboratories (DRMCRL), School of Medicine, Faculty of Health Sciences, The University of Adelaide, Adelaide, SA, 5005, Australia.
University of Adelaide · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The hormone-sensing mammary epithelial cell (HS-MEC-expressing oestrogen receptor-alpha (ERα) and progesterone receptor (PGR)) is often represented as being terminally differentiated and lacking significant progenitor activity after puberty. Therefore while able to profoundly influence the proliferation and function of other MEC populations, HS-MECs are purported not to respond to sex hormone signals by engaging in significant cell proliferation during adulthood. This is a convenient and practical simplification that overshadows the sublime, and potentially critical, phenotypic plasticity found within the adult HS-MEC population. This concept is exemplified by the large proportion (~80 %) of human breast cancers expressing PGR and/or ERα, demonstrating that HS-MECs clearly proliferate in the context of breast cancer. Understanding how HS-MEC proliferation and differentiation is driven could be key to unraveling the mechanisms behind uncontrolled HS-MEC proliferation associated with ERα- and/or PGR-positive breast cancers. Herein we review evidence for the existence of a HS-MEC progenitor and the emerging plasticity of the HS-MEC population in general. This is followed by an analysis of hormones other than oestrogen and progesterone that are able to influence HS-MEC proliferation and differentiation: androgens, prolactin and transforming growth factor-beta1.

Indexed as

AndrogensAnimalsBreast NeoplasmsCCAAT-Enhancer-Binding Protein-betaCell DifferentiationCell PlasticityCell ProliferationCore Binding Factor alpha SubunitsDNA-Binding ProteinsEpithelial CellsEstrogen Receptor alphaFemaleGATA3 Transcription FactorHepatocyte Nuclear Factor 3-alphaHumansMammary Glands, AnimalAndrogensCCAAT-Enhancer-Binding Protein-betaCore Binding Factor alpha SubunitsDNA-Binding ProteinsELF5 protein, humanElf5 protein, mouseEstrogen Receptor alphaGATA3 Transcription FactorHepatocyte Nuclear Factor 3-alphaProlactinProto-Oncogene Proteins c-etsReceptors, ProgesteroneT-Box Domain ProteinsTBX3 protein, humanTbx3 protein, mouseTranscription FactorsTransforming Growth Factor beta1AndrogenEndocrine hormonesHormone-sensing cellsLuminal progenitorsProlactin

Identifiers

PMID26390871
OpenAlexW1704913944

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.