Evidence map›Paper›PMID 26463434›Full record

ReviewJournal of gynecologic oncology2016

Therapeutic options for management of endometrial hyperplasia.

Vishal Chandra, Jong Joo Kim, Doris Mangiaracina Benbrook, Anila Dwivedi, Rajani Rai

Open access · diamondAbstract readReview
In one paragraph

Review in Journal of gynecologic oncology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
66citing papers in PubMed, 1 pooled it
6.9field-weighted citation impact, top 3% 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

66 citing papers in PubMed, 1 synthesis or guideline pooled it, 218 citations in OpenAlex.

  1. Pooled it
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  4. Polymorphism of theLife (Basel, Switzerland) · 2026
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6 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

5 authors at 3 institutions in 3 countries.

Vishal ChandraDepartment of Obstetrics and Gynecology, University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA.ORCID http://orcid.org/0000-0002-5206-2313
Jong Joo KimSchool of Biotechnology, Yeungnam University, Gyeongsan, Korea.ORCID http://orcid.org/0000-0001-9687-0075
Doris Mangiaracina BenbrookDepartment of Obstetrics and Gynecology, University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA.ORCID http://orcid.org/0000-0001-7606-8245
Anila DwivediDivision of Endocrinology, CSIR-Central Drug Research Institute, Lucknow, India.ORCID http://orcid.org/0000-0001-8515-5551
Rajani RaiSchool of Biotechnology, Yeungnam University, Gyeongsan, Korea. rajaniraiims@gmail.com.ORCID http://orcid.org/0000-0003-3503-5265
Central Drug Research Institute · INYeungnam University · KRUniversity of Oklahoma Health Sciences Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Endometrial hyperplasia (EH) comprises a spectrum of changes in the endometrium ranging from a slightly disordered pattern that exaggerates the alterations seen in the late proliferative phase of the menstrual cycle to irregular, hyperchromatic lesions that are similar to endometrioid adenocarcinoma. Generally, EH is caused by continuous exposure of estrogen unopposed by progesterone, polycystic ovary syndrome, tamoxifen, or hormone replacement therapy. Since it can progress, or often occur coincidentally with endometrial carcinoma, EH is of clinical importance, and the reversion of hyperplasia to normal endometrium represents the key conservative treatment for prevention of the development of adenocarcinoma. Presently, cyclic progestin or hysterectomy constitutes the major treatment option for EH without or with atypia, respectively. However, clinical trials of hormonal therapies and definitive standard treatments remain to be established for the management of EH. Moreover, therapeutic options for EH patients who wish to preserve fertility are challenging and require nonsurgical management. Therefore, future studies should focus on evaluation of new treatment strategies and novel compounds that could simultaneously target pathways involved in the pathogenesis of estradiol-induced EH. Novel therapeutic agents precisely targeting the inhibition of estrogen receptor, growth factor receptors, and signal transduction pathways are likely to constitute an optimal approach for treatment of EH.

Indexed as

Antineoplastic Agents, HormonalDisease ManagementDisease ProgressionEndometrial HyperplasiaFemaleGonadotropin-Releasing HormoneHumansHysterectomyMolecular Targeted TherapyProgesterone CongenersRisk FactorsTamoxifenAntineoplastic Agents, HormonalGonadotropin-Releasing HormoneProgesterone CongenersTamoxifenEndometrial HyperplasiaProgestinsReceptors, EstrogenTherapy

Identifiers

PMID26463434
PMCPMC4695458
OpenAlexW2185449028

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.