Evidence map›Paper›PMID 16049327›Full record

ArticleThe American journal of pathology2005

Proliferation of estrogen receptor-alpha-positive mammary epithelial cells is restrained by transforming growth factor-beta1 in adult mice.

Kenneth B R Ewan, Hellen A Oketch-Rabah, Shraddha A Ravani, G Shyamala, Harold L Moses, Mary Helen Barcellos-Hoff

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in The American journal of pathology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.

0numbers the graph read from it
0cells of the map it votes in
63citing papers in PubMed
4.7field-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

63 citing papers in PubMed, 111 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. miR-30a-3p Regulates Autophagy in the Involution of Mice Mammary Glands.International journal of molecular sciences · 2023
    Article
  6. Review
  7. Obesity reduces mammary epithelial cell TGFβ1 activity through macrophage-mediated extracellular matrix remodeling.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Mechanism of immune evasion in breast cancer.OncoTargets and therapy · 2017
    Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article

3 more citing papers are in PubMed but not listed here.

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

6 authors at 1 institution in 1 country.

Kenneth B R EwanLife Sciences Division, Bldg. 74-355, 1 Cyclotron Rd., Lawrence Berkeley National Laboratory, Berkeley CA 94720, USA.
Hellen A Oketch-Rabah
Shraddha A Ravani
G Shyamala
Harold L Moses
Mary Helen Barcellos-Hoff
Lawrence Berkeley National Laboratory · US

Funding

TGFb Regulation of ER Receptor Positive Mammary CellsR01AG022413 · NIA · UNIVERSITY OF CALIF-LAWRENC BERKELEY LAB · PI BARCELLOS-HOFF, MARY HELEN · 2003 to 2006
$1.3M
NIA NIH HHS R01 AG022413
6 · The paper itself

Abstract

Transforming growth factor (TGF)-beta1 is a potent inhibitor of mammary epithelial proliferation. In human breast, estrogen receptor (ER)-alpha cells rarely co-localize with markers of proliferation, but their increased frequency correlates with breast cancer risk. To determine whether TGF-beta1 is necessary for the quiescence of ER-alpha-positive populations, we examined mouse mammary epithelial glands at estrus. Approximately 35% of epithelial cells showed TGF-beta1 activation, which co-localized with nuclear receptor-phosphorylated Smad 2/3, indicating that TGF-beta signaling is autocrine. Nuclear Smad co-localized with nuclear ER-alpha. To test whether TGF-beta inhibits proliferation, we examined genetically engineered mice with different levels of TGF-beta1. ER-alpha co-localization with markers of proliferation (ie, Ki-67 or bromodeoxyuridine) at estrus was significantly increased in the mammary glands of Tgf beta1 C57/bl/129SV heterozygote mice. This relationship was maintained after pregnancy but was absent at puberty. Conversely, mammary epithelial expression of constitutively active TGF-beta1 via the MMTV promoter suppressed proliferation of ER-alpha-positive cells. Thus, TGF-beta1 activation functionally restrains ER-alpha-positive cells from proliferating in adult mammary gland. Accordingly, we propose that TGF-beta1 dysregulation may promote proliferation of ER-alpha-positive cells associated with breast cancer risk in humans.

Indexed as

Cell ProliferationAnimalsCrosses, GeneticDNA-Binding ProteinsEpithelial CellsEstrogen Receptor alphaEstrusFemaleHeterozygoteMammary Glands, AnimalMiceMice, Inbred BALB CMice, Inbred C57BLMice, KnockoutMice, TransgenicPhosphorylationDNA-Binding ProteinsEstrogen Receptor alphaSmad2 ProteinSmad2 protein, mouseTGFB1 protein, humanTgfb1 protein, mouseTrans-ActivatorsTransforming Growth Factor betaTransforming Growth Factor beta1Non-programmatic

Identifiers

PMID16049327
PMCPMC1603552
OpenAlexW2061176458

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.