Evidence map›Paper›PMID 25458418›Full record

ReviewTrends in endocrinology and metabolism: TEM2014

Cholesterol and breast cancer pathophysiology.

Erik R Nelson, Ching-yi Chang, Donald P McDonnell

Open access · greenAbstract readReview
In one paragraph

Review in Trends in endocrinology and metabolism: TEM, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 105 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
105citing papers in PubMed, 1 pooled it
4.0field-weighted citation impact, top 6% 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

105 citing papers in PubMed, 1 synthesis or guideline pooled it, 192 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Review
  6. 27-Hydroxycholesterol in cancer development and drug resistance.Journal of enzyme inhibition and medicinal chemistry · 2025
    Review
  7. Article
  8. Observational
  9. Article
  10. Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. Article

45 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

3 authors at 2 institutions in 1 country.

Erik R NelsonDepartment of Molecular and Integrative Physiology, University of Illinois at Urbana-Champaign, IL 61801, USA.
Ching-yi ChangDepartment of Pharmacology and Cancer Biology, Duke University School of Medicine, Durham, NC 27710, USA.
Donald P McDonnellDepartment of Pharmacology and Cancer Biology, Duke University School of Medicine, Durham, NC 27710, USA. Electronic address: donald.mcdonnell@duke.edu.
Duke University · USUniversity of Illinois Urbana-Champaign · US

Funding

Mechanism of Action of Estrogens and AntiestrogensR37DK048807 · NIDDK · DUKE UNIVERSITY · PI MCDONNELL, DONALD P · 2005 to 2014
$5.0M
MECHANISM OF ESTROGENS AND ANTIESTROGENSR01DK048807 · NIDDK · DUKE UNIVERSITY · PI MCDONNELL, DONALD P · 1995 to 2019
$4.3M
27-hydroxycholesterol as a link between obesity and breast cancer pathogenesisR00CA172357 · NCI · UNIVERSITY OF ILLINOIS AT URBANA-CHAMPAIGN · PI NELSON, ERIK RUSSELL · 2014 to 2016
$727k
27-hydroxycholesterol as a link between obesity and breast cancer pathogenesisK99CA172357 · NCI · DUKE UNIVERSITY · PI NELSON, ERIK RUSSELL · 2013 to 2014
$190k
NCI NIH HHS K99 CA172357NCI NIH HHS K99CA172357NCI NIH HHS R00 CA172357NIDDK NIH HHS R01 DK048807NIDDK NIH HHS R37DK048807
6 · The paper itself

Abstract

Cholesterol is a risk factor for breast cancer although the mechanisms by which this occurs are not well understood. One hypothesis is that dyslipidemia results in increased cholesterol content in cell membranes, thus impacting upon membrane fluidity and subsequent signaling. In addition, studies demonstrate that the metabolite, 27-hydroxycholesterol (27HC), can function as an estrogen, increasing the proliferation of estrogen receptor (ER)-positive breast cancer cells. This was unexpected because 27HC and other oxysterols activate the liver X receptors (LXR), resulting in a reduction of intracellular cholesterol. Resolution of this paradox will require dissection of the molecular mechanisms by which ER and LXR converge in breast cancer cells. Regardless, the observation that 27HC influences breast cancer provides a rationale for strategies that target cholesterol metabolism.

Indexed as

Breast NeoplasmsCholesterolFemaleHumansHydroxycholesterolsLiver X ReceptorsOrphan Nuclear ReceptorsReceptors, Estrogen27-hydroxycholesterolCholesterolHydroxycholesterolsLiver X ReceptorsOrphan Nuclear ReceptorsReceptors, Estrogen

Identifiers

PMID25458418
PMCPMC4268141
OpenAlexW2012306194

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.