Evidence map›Paper›PMID 26265122›Full record

ReviewJournal of mammary gland biology and neoplasia2015

Steroid hormones, steroid receptors, and breast cancer stem cells.

Jessica Finlay-Schultz, Carol A Sartorius

Abstract readReview
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 53 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed, 3 pooled it
2.2field-weighted citation impact, top 11% 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

53 citing papers in PubMed, 3 syntheses or guidelines pooled it, 101 citations in OpenAlex.

  1. Pooled it
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  4. Trial
  5. Article
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  10. Article
  11. MicroRNAs as Endocrine Modulators of Breast Cancer.International journal of molecular sciences · 2025
    Review
  12. Article
  13. Article
  14. Review
  15. Multifunctional Nanomaterials Mediate Cholesterol Depletion for Cancer Treatment.Angewandte Chemie (International ed. in English) · 2024
    Review
  16. Article
  17. Article
  18. Review
  19. Article
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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.

Jessica Finlay-SchultzDepartment of Pathology, University of Colorado Anschutz Medical Campus, 12801 East 17th Avenue; MS 8104, Aurora, CO, 80045, USA. jessica.finlay-schultz@ucdenver.edu.
Carol A SartoriusDepartment of Pathology, University of Colorado Anschutz Medical Campus, 12801 East 17th Avenue; MS 8104, Aurora, CO, 80045, USA.
University of Colorado Anschutz Medical Campus · US

Funding

Hormones and Tumor Initiating Cells in Human Breast CancersR01CA140985 · NCI · UNIVERSITY OF COLORADO DENVER · PI SARTORIUS, CAROL ANN · 2011 to 2020
$3.0M
Tumor-specific actions of progestins in patient-derived breast cancer modelsF32CA177081 · NCI · UNIVERSITY OF COLORADO DENVER · PI FINLAY-SCHULTZ, JESSICA · 2014 to 2016
$173k
NCI NIH HHS 1F32CA177081NCI NIH HHS F32 CA177081NCI NIH HHS R01 CA140985
6 · The paper itself

Abstract

The ovarian hormones progesterone and estrogen play important roles in breast cancer etiology, proliferation, and treatment. Androgens may also contribute to breast cancer risk and progression. In recent years, significant advances have been made in defining the roles of these steroid hormones in stem cell homeostasis in the breast. Stem cells are potential origins of breast cancer and may dictate tumor phenotype. At least a portion of breast cancers are proposed to be driven by cancer stem cells (CSCs), cells that mimic the self-renewing and repopulating properties of normal stem cells, and can confer drug resistance. Progesterone has been identified as the critical hormone regulating normal murine mammary stem cell (MaSC) populations and normal human breast stem cells. Synthetic progestins increase human breast cancer risk; one theory speculates that this occurs through increased stem cells. Progesterone treatment also increases breast CSCs in established breast cancer cell lines. This is mediated in part through progesterone regulation of transcription factors, signal transduction pathways, and microRNAs. There is also emerging evidence that estrogens and androgens can regulate breast CSC numbers. The evolving concept that a breast CSC phenotype is dynamic and can be influenced by cell signaling and external cues emphasizes that steroid hormones could be crucial players in controlling CSC number and function. Here we review recent studies on steroid hormone regulation of breast CSCs, and discuss mechanisms by which this occurs.

Indexed as

Signal TransductionAndrogensBreast NeoplasmsEstrogensFemaleHumansMicroRNAsNeoplastic Stem CellsProgesteroneProgestinsReceptors, AndrogenReceptors, EstrogenReceptors, ProgesteroneAndrogensEstrogensMicroRNAsProgesteroneProgestinsReceptors, AndrogenReceptors, EstrogenReceptors, ProgesteroneBreast cancerCancer stem cellsHormone replacement therapyProgesteroneProgesterone receptorSteroid hormone

Identifiers

PMID26265122
PMCPMC4666507
OpenAlexW1418273540

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.