Evidence map›Paper›PMID 26052034›Full record

ReviewMolecular and cellular endocrinology2015

The molecular, cellular and clinical consequences of targeting the estrogen receptor following estrogen deprivation therapy.

Ping Fan, Philipp Y Maximov, Ramona F Curpan, Balkees Abderrahman, V Craig Jordan

Open access · bronzeAbstract readReview
In one paragraph

Review in Molecular and cellular endocrinology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

18 citing papers in PubMed, 35 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Vaginal Aging-What We Know and What We Do Not Know.International journal of environmental research and public health · 2021
    Review
  6. Review
  7. Identifying novel sphingosine kinase 1 inhibitors as therapeutics against breast cancer.Journal of enzyme inhibition and medicinal chemistry · 2020
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Estrogen-regulated feedback loop limits the efficacy of estrogen receptor-targeted breast cancer therapy.Proceedings of the National Academy of Sciences of the United States of America · 2018
    Article
  13. Article
  14. Article
  15. Article
  16. Anticipatory UPR Activation: A Protective Pathway and Target in Cancer.Trends in endocrinology and metabolism: TEM · 2016
    Review
  17. Article
  18. 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

5 authors at 3 institutions in 3 countries.

Ping FanDepartment of Breast Medical Oncology, MD Anderson Cancer Center, Houston, TX, USA.
Philipp Y MaximovDepartment of Breast Medical Oncology, MD Anderson Cancer Center, Houston, TX, USA.
Ramona F CurpanInstitute of Chemistry, Romanian Academy, Timisoara, Romania.
Balkees AbderrahmanFaculty of Medicine, The University of Jordan, Amman, Jordan.
V Craig JordanDepartment of Breast Medical Oncology, MD Anderson Cancer Center, Houston, TX, USA. Electronic address: VCJordan@mdanderson.org.
The University of Texas MD Anderson Cancer Center · USRomanian Academy · ROUniversity of Jordan · JO

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Fabien Delerue · 1985 to 2026
$290.8M
NCI NIH HHS CA016672NCI NIH HHS P30 CA016672
6 · The paper itself

Abstract

During the past 20 years our understanding of the control of breast tumor development, growth and survival has changed dramatically. The once long forgotten application of high dose synthetic estrogen therapy as the first chemical therapy to treat any cancer has been resurrected, refined and reinvented as the new biology of estrogen-induced apoptosis. High dose estrogen therapy was cast aside once tamoxifen, from its origins as a failed "morning after pill", was reinvented as the first targeted therapy to treat any cancer. The current understanding of the mechanism of estrogen-induced apoptosis is described as a consequence of acquired resistance to long term antihormone therapy in estrogen receptor (ER) positive breast cancer. The ER signal transduction pathway remains a target for therapy in breast cancer despite "antiestrogen" resistance, but becomes a regulator of resistance. Multiple mechanisms of resistance come into play: Selective ER modulator (SERM) stimulated growth, growth factor/ER crosstalk, estrogen-induced apoptosis and mutations of ER. But it is with the science of estrogen-induced apoptosis that the next innovation in women's health will be developed. Recent evidence suggests that the glucocorticoid properties of medroxyprogesterone acetate blunt estrogen-induced apoptosis in estrogen deprived breast cancer cell populations. As a result breast cancer develops during long-term hormone replacement therapy (HRT). A new synthetic progestin with estrogen-like properties, such as the 19 nortestosterone derivatives used in oral contraceptives, will continue to protect the uterus from unopposed estrogen stimulation but at the same time, reinforce apoptosis in vulnerable populations of nascent breast cancer cells.

Indexed as

ApoptosisBreast NeoplasmsDrug Resistance, NeoplasmEstrogensFemaleHumansMedroxyprogesterone AcetateMutationNandroloneReceptors, EstrogenEstrogensMedroxyprogesterone AcetateNandroloneReceptors, EstrogenAntiestrogensBreast cancerEstrogen-induced apoptosisEstrogen receptorEstrogensResistance

Identifiers

PMID26052034
PMCPMC4760743
OpenAlexW614551470

What OpenQuestion holds

Textmetadata
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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.