Evidence map›Paper›PMID 29055020›Full record

ArticleCancer research2017

Subtype-Specific Tumor-Associated Fibroblasts Contribute to the Pathogenesis of Uterine Leiomyoma.

Xin Wu, Vanida A Serna, Justin Thomas, Wenan Qiang, Michael L Blumenfeld, Takeshi Kurita

Abstract read
In one paragraph

Article in Cancer research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed, 1 pooled it
3.4field-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

29 citing papers in PubMed, 1 synthesis or guideline pooled it, 50 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. UTERINE FIBROIDS.Physiological reviews · 2025
    Review
  6. Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Review
  19. Uterine Fibroids: Hiding in Plain Sight.Physiology (Bethesda, Md.) · 2022
    Review
  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

6 authors at 3 institutions in 1 country.

Xin WuDepartment of Cancer Biology and Genetics, The Comprehensive Cancer Center, Ohio State University, Columbus, Ohio.
Vanida A SernaDepartment of Cancer Biology and Genetics, The Comprehensive Cancer Center, Ohio State University, Columbus, Ohio.
Justin ThomasDepartment of Cancer Biology and Genetics, The Comprehensive Cancer Center, Ohio State University, Columbus, Ohio.
Wenan QiangCenter for Developmental Therapeutics, Chemistry of Life Processes Institute, Northwestern University, Evanston, Illinois.
Michael L BlumenfeldDepartment of Obstetrics and Gynecology, Ohio State University, Columbus, Ohio.
Takeshi KuritaDepartment of Cancer Biology and Genetics, The Comprehensive Cancer Center, Ohio State University, Columbus, Ohio. takeshi.kurita@osumc.edu.
The Ohio State University Comprehensive Cancer Center – Arthur G. James Cancer Hospital and Richard J. Solove Research Institute · USNorthwestern University · USThe Ohio State University · US

Funding

Translational Therapeutics Research Program (TT)P30CA016058 · NCI · OHIO STATE UNIVERSITY · PI Tasleem J Padamsee · 1985 to 2026
$132.3M
Xenograft Study on Growth-Control of Human Uterine LeiomyomataR01HD064402 · NICHD · OHIO STATE UNIVERSITY · PI KURITA, TAKESHI · 2010 to 2014
$1.6M
Molecular Etiology of Cervicovaginal Adenosis by in Utero Hormone ExposureR01CA154358 · NCI · OHIO STATE UNIVERSITY · PI KURITA, TAKESHI · 2010 to 2014
$1.5M
NCI NIH HHS P30 CA016058NCI NIH HHS R01 CA154358NICHD NIH HHS R01 HD064402
6 · The paper itself

Abstract

Recent genomic studies have identified subtypes of uterine leiomyoma (LM) with distinctive genetic alterations. Here, we report the elucidation of the biological characteristics of the two most prevalent uterine leiomyoma subtypes, MED12-mutant (MED12-LM) and HMGA2-overexpressing (HMGA2-LM) uterine leiomyomas. Because each tumor carries only one genetic alteration, both subtypes are considered to be monoclonal. Approximately 90% of cells in HMGA2-uterine leiomyoma were smooth muscle cells (SMC) with HMGA2 overexpression. In contrast, MED12-LM consisted of similar numbers of SMC and non-SMC, which were mostly tumor-associated fibroblasts (TAF). Paradoxically, TAF carried no mutations in MED12, suggesting an interaction between SMC and TAF to coordinate their growth. The higher amount of extracellular matrix in MED12-LM than HMGA2-LM was partially due to the high concentration of collagen-producing TAF. SMC growth in a xenograft assay was driven by progesterone in both uterine leiomyoma subtypes. In contrast, TAF in MED12-LM proliferated in response to estradiol, whereas progesterone had no effect. The high concentration of estrogen-responsive TAF in MED12-LM explains the inconsistent discoveries between

Indexed as

AdultAnimalsCancer-Associated FibroblastsFemaleGene Expression Regulation, NeoplasticHMGA2 ProteinHumansLeiomyomaMiceMice, Inbred NODMice, TransgenicMiddle AgedPhenotypeUterine NeoplasmsHMGA2 Protein

Identifiers

PMID29055020
PMCPMC6015476
OpenAlexW2767062467

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.