Evidence map›Paper›PMID 22193050›Full record

ReviewMolecular and cellular endocrinology2012

The biology of progesterone receptor in the normal mammary gland and in breast cancer.

Alison E Obr, Dean P Edwards

Abstract readReview
In one paragraph

Review in Molecular and cellular endocrinology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers.

0numbers the graph read from it
0cells of the map it votes in
79citing papers in PubMed
8.4field-weighted citation impact, top 2% 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

79 citing papers in PubMed, 187 citations in OpenAlex.

  1. Targeting Estrogen Receptor for Breast Cancer.Current issues in molecular biology · 2026
    Review
  2. Review
  3. Article
  4. Article
  5. Clinical implications of taurine in breast cancer.Biochemistry and biophysics reports · 2025
    Review
  6. Article
  7. Article
  8. Article
  9. Methods and Models in Mammary Gland Biology and Breast Cancer Research.Journal of mammary gland biology and neoplasia · 2025
    Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Review
  17. Article
  18. Review
  19. Article
  20. Review

19 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

2 authors at 1 institution in 1 country.

Alison E ObrDepartments of Molecular & Cellular Biology and Pathology & Immunology, Baylor College of Medicine, Houston, TX 77030, USA.
Dean P Edwards
Baylor College of Medicine · US

Funding

The functional role of microRNAs in the normal mammary glandP01HD038129 · NICHD · UNIVERSITY OF COLORADO DENVER · PI ANDERSON, STEVEN M · 2000 to 2015
$15.2M
REPRODUCTIVE BIOLOGY: REGULATORY MECHANISMST32HD007165 · NICHD · BAYLOR COLLEGE OF MEDICINE · PI O'MALLEY, BERT W · 1985 to 2015
$5.6M
STEROID ANTAGONISTS AND RESISTANCE IN BREAST CANCERR01DK049030 · NIDDK · UNIVERSITY OF COLORADO DENVER · PI EDWARDS, DEAN P · 1994 to 2012
$3.1M
NICHD NIH HHS HD038129NICHD NIH HHS P01 HD038129NICHD NIH HHS T32 HD007165NIDDK NIH HHS DK049030NIDDK NIH HHS R01 DK049030
6 · The paper itself

Abstract

This paper reviews work on progesterone and the progesterone receptor (PR) in the mouse mammary gland that has been used extensively as an experimental model. Studies have led to the concept that progesterone controls proliferation and morphogenesis of the luminal epithelium in a tightly orchestrated manner at distinct stages of development by paracrine signaling pathways, including receptor activator of nuclear factor κB ligand (RANKL) as a major paracrine factor. Progesterone also drives expansion of stem cells by paracrine signals to generate progenitors required for alveologenesis. During mid-to-late pregnancy, progesterone has another role to suppress secretory activation until parturition mediated in part by crosstalk between PR and prolactin/Stat5 signaling to inhibit induction of milk protein gene expression, and by inhibiting tight junction closure. In models of hormone-dependent mouse mammary tumors, the progesterone/PR signaling axis enhances pre-neoplastic progression by a switch from a paracrine to an autocrine mode of proliferation and dysregulation of the RANKL signaling pathway. Limited experiments with normal human breast show that progesterone/PR signaling also stimulates epithelial cell proliferation by a paracrine mechanism; however, the signaling pathways and whether RANKL is a major mediator remains unknown. Work with human breast cancer cell lines, patient tumor samples and clinical studies indicates that progesterone is a risk factor for breast cancer and that alteration in progesterone/PR signaling pathways contributes to early stage human breast cancer progression. However, loss of PR expression in primary tumors is associated with a less differentiated more invasive phenotype and worse prognosis, suggesting that PR may limit later stages of tumor progression.

Indexed as

AnimalsBreast NeoplasmsFemaleHumansMammary Glands, AnimalMammary Glands, HumanMicePregnancyProgesteroneProgestinsRANK LigandReceptors, ProgesteroneSignal TransductionProgesteroneProgestinsRANK LigandReceptors, Progesterone

Identifiers

PMID22193050
PMCPMC3318965
OpenAlexW2032416959

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.