Evidence map›Paper›PMID 10819502›Full record

ReviewJournal of mammary gland biology and neoplasia1998

Estrogen responsiveness and control of normal human breast proliferation.

E Anderson, R B Clarke, A Howell

Abstract readReview
PubMed Publisher
In one paragraph

Review in Journal of mammary gland biology and neoplasia, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed
3.7field-weighted citation impact, top 7% 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

59 citing papers in PubMed, 184 citations in OpenAlex.

  1. Review
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  6. Review
  7. Article
  8. Mechanisms for estrogen receptor expression in human cancer.Experimental hematology & oncology · 2018
    Review
  9. DNA methylation age is elevated in breast tissue of healthy women.Breast cancer research and treatment · 2017
    Article
  10. Review
  11. Article
  12. Review
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  16. Review
  17. Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

E AndersonClinical Research Department, Christie Hospital NHS Trust, Manchester. eanderson@picr.man.ac.uk
R B Clarke
A Howell
The Christie Hospital · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Our understanding of the hormonal control of the proliferation of normal human breast epithelium is still surprisingly meager. However, the results of a number of recent studies have confirmed that estrogen is the major steroid mitogen for the luminal epithelial cell population (the usual targets for neoplastic transformation). Estrogen seemingly exerts its effects on cell division indirectly as there is complete dissociation between the population of luminal epithelial cells expressing the estrogen receptor (ER)4 and those that proliferate. We suggest that the ER-negative proliferating cells represent a precursor or stem cell population that differentiates to ER-containing, nonproliferative cells. In turn, these ER-positive cells act as 'estrogen sensors' and transmit positive or negative paracrine growth signals to the precursor cells depending on the prevailing hormonal environment. As yet there is no direct evidence supporting this hypothesis but we suggest ways in which it may be obtained. The implication of these studies is that inhibition of luminal epithelial proliferation with tamoxifen or pure antiestrogens or by preventing ovarian steroid secretion should be an effective strategy for the prevention of breast cancer. In addition, we may be able to predict the risk of breast cancer in an individual by measuring the intrinsic estrogen sensitivity of her breast epithelium. Finally, study of the paracrine mechanisms of growth control in the normal human breast may provide new, more specific, therapeutic targets for breast cancer prevention.

Indexed as

BreastCell DifferentiationCell DivisionEstrogensFemaleHumansReceptors, EstrogenEstrogensReceptors, Estrogen

Identifiers

PMID10819502
OpenAlexW1550578788

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.