Evidence map›Paper›PMID 23402742›Full record

ReviewSteroids2013

New insights on the role of hormonal therapy in ovarian cancer.

Fiona Simpkins, Arlene Garcia-Soto, Joyce Slingerland

Abstract readReview
In one paragraph

Review in Steroids, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
10.7field-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

36 citing papers in PubMed, 62 citations in OpenAlex.

  1. Article
  2. The Role of Estrogen across Multiple Disease Mechanisms.Current issues in molecular biology · 2024
    Review
  3. Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Estrogens, Estrogen Receptors and Tumor Microenvironment in Ovarian Cancer.International journal of molecular sciences · 2023
    Review
  9. Article
  10. Article
  11. Review
  12. Review
  13. Review
  14. Article
  15. Review
  16. Article
  17. Article
  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

3 authors at 1 institution in 1 country.

Fiona SimpkinsDivision of Gynecology Oncology, University of Miami, Miller School of Medicine, Miami, FL, United States. fsimpkins@med.miami.edu
Arlene Garcia-Soto
Joyce Slingerland
University of Miami · US

Funding

Targeting SRC Signaling Pathways to Promote Cell Cycle Arrest in Ovarian CancerK08CA151892 · NCI · UNIVERSITY OF PENNSYLVANIA · PI SIMPKINS, FIONA · 2011 to 2016
$807k
NCI NIH HHS K08 CA151892NCI NIH HHS L30 CA162168
6 · The paper itself

Abstract

Ovarian cancer (OVCA) is the most lethal gynecological malignancy. It is often diagnosed in advanced stages and despite therapy, 70% relapse within 2years with incurable disease. Regimens with clinical benefit and minimal toxicity are urgently needed. More effective hormonal therapies would be appealing in this setting. Estrogens (E2) are implicated in the etiology of OVCA. Estrogens drive proliferation and anti-estrogens inhibit ovarian cancer growth in vitro and in vivo. Despite estrogen receptor (ER) expression in 67% of OVCAs, small anti-estrogen therapy trials have been disappointing and the benefit of hormonal therapy has not been systematically studied in large well-designed trials. OVCAs often manifest de novo anti-estrogen resistance and those that initially respond invariably develop resistance. Estrogens stimulate ovarian cancer progression by transcriptional activation and cross talk between liganded ER and mitogenic pathways, both of which drive cell cycle progression. Estrogen deprivation and estrogen receptor (ER) blockade cause cell cycle arrest in susceptible OVCAs by increasing the cell cycle inhibitor, p27. This review summarizes and discusses scientific and epidemiological evidence supporting estrogen's role in ovarian carcinogenesis, provides an overview of clinical trials of ER blockade and aromatase inhibitors in OVCA and reviews potential causes of antiestrogen resistance. Anti-estrogen resistance was recently shown to be reversed by dual ER and Src signaling blockade. Blocking cross-talk between ER and constitutively activated kinase pathways may improve anti-estrogen therapeutic efficacy in OVCA, as has been demonstrated in other cancers. Novel strategies to improve benefit from anti-estrogens by combining them with targeted therapies are reviewed.

Indexed as

Antineoplastic Agents, HormonalCell CycleFemaleHumansOvarian NeoplasmsReceptors, EstrogenAntineoplastic Agents, HormonalReceptors, Estrogen

Identifiers

PMID23402742
PMCPMC4551472
OpenAlexW2076238082

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.