Evidence map›Paper›PMID 19484750›Full record

ArticleMolecular reproduction and development2009

Profile of estrogen-responsive genes in an estrogen-specific mammary gland outgrowth model.

Bonnie J Deroo, Sylvia C Hewitt, Jennifer B Collins, Sherry F Grissom, Katherine J Hamilton, Kenneth S Korach

Abstract read
In one paragraph

Article in Molecular reproduction and development, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

20 citing papers in PubMed, 33 citations in OpenAlex.

  1. Molecular Regulatory Mechanisms of Mammary Gland Development: A Review.Animals : an open access journal from MDPI · 2025
    Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Estrogens regulate life and death in mitochondria.Journal of bioenergetics and biomembranes · 2017
    Review
  11. Transcriptional regulation of the sodium-coupled neutral amino acid transporter (SNAT2) by 17β-estradiol.Proceedings of the National Academy of Sciences of the United States of America · 2014
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. 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

6 authors at 3 institutions in 2 countries.

Bonnie J DerooReceptor Biology Section, NIEHS, NIH, Research Triangle Park, North Carolina 27709, USA.
Sylvia C Hewitt
Jennifer B Collins
Sherry F Grissom
Katherine J Hamilton
Kenneth S Korach
National Institute of Environmental Health Sciences · USTriangle · USLawson Health Research Institute · CA

Funding

Gene Expression and MicroarraysZICES102445 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI GERRISH, KEVIN · 2009 to 2025
$31.6M
Chemical Receptor Interactions In Reproduction And Hormonal ToxicityZIAES070065 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI KORACH, KENNETH S · 2009 to 2019
$29.6M
Chemical Receptor Interactions Reproduction/HormonalZ01ES070065 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI KORACH, KENNETH S · 1985 to 2008
$5.0M
Intramural NIH HHS Z01 ES070065
6 · The paper itself

Abstract

Both ovarian and pituitary hormones are required for the pubertal development of the mouse mammary gland. Estradiol directs ductal elongation and branching, while progesterone leads to tertiary branching and alveolar development. The purpose of this investigation was to identify estrogen-responsive genes associated with pubertal ductal growth in the mouse mammary gland in the absence of other ovarian hormones and at different stages of development. We hypothesized that the estrogen-induced genes and their associated functions at early stages of ductal elongation would be distinct from those induced after significant ductal elongation had occurred. Therefore, ovariectomized prepubertal mice were exposed to 17beta-estradiol from two to 28 days, and mammary gland global gene expression analyzed by microarray analysis at various times during this period. We found that: (a) gene expression changes in our estrogen-only model mimic those changes that occur in normal pubertal development in intact mice, (b) both distinct and overlapping gene profiles were observed at varying extents of ductal elongation, and (c) cell proliferation, the immune response, and metabolism/catabolism were the most common functional categories associated with mammary ductal growth. Particularly striking was the novel observation that genes active during carbohydrate metabolism were rapidly and robustly decreased in response to estradiol. Lastly, we identified mammary estradiol-responsive genes that are also co-expressed with estrogen receptor alpha in human breast cancer. In conclusion, our genomic data support the physiological observation that estradiol is one of the primary hormonal signals driving ductal elongation during pubertal mammary development.

Indexed as

AnimalsBreast NeoplasmsCarbohydrate MetabolismCell Growth ProcessesCluster AnalysisEstradiolEstrogen Receptor alphaFemaleGene Expression ProfilingGene Expression Regulation, DevelopmentalMammary Glands, AnimalMiceMice, Inbred C57BLOvariectomySexual MaturationEstradiolEstrogen Receptor alpha

Identifiers

PMID19484750
PMCPMC2737274
OpenAlexW2039361904

What OpenQuestion holds

Textmetadata
LicenceTDM
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.