Evidence map›Paper›PMID 25815421›Full record

ArticleEndocrinology2015

The ovary is an alternative site of origin for high-grade serous ovarian cancer in mice.

Jaeyeon Kim, Donna M Coffey, Lang Ma, Martin M Matzuk

Abstract read
In one paragraph

Article in Endocrinology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed, 1 pooled it
11.8field-weighted citation impact, top 1% 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

60 citing papers in PubMed, 1 synthesis or guideline pooled it, 81 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Loss ofOncotarget · 2025
    Article
  6. Article
  7. Serum Lipidome Profiling Reveals a Distinct Signature of Ovarian Cancer in Korean Women.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2024
    Article
  8. Article
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  14. Review
  15. Expression and T cell regulatory action of the PD-1 immune checkpoint in the ovary and fallopian tube.American journal of reproductive immunology (New York, N.Y. : 1989) · 2023
    Article
  16. Article
  17. Article
  18. Article
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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

4 authors at 2 institutions in 1 country.

Jaeyeon KimDepartments of Pathology and Immunology (J.K., L.M., M.M.M.), Molecular and Cellular Biology (M.M.M.), Molecular and Human Genetics (M.M.M.), and Pharmacology (M.M.M.); Center for Drug Discovery (M.M.M.); Dan L. Duncan Cancer Center (J.K., M.M.M.), and Center for Reproductive Medicine (J.K., M.M.M.), Baylor College of Medicine; and Department of Pathology and Genomic Medicine (D.M.C.), Houston Methodist and Weill Medical College of Cornell University, Houston, Texas 77030.
Donna M Coffey
Lang Ma
Martin M Matzuk
Cornell University · USMethodist Hospital · US

Funding

Understanding the origin,initiation,and progression of high-grade serous ovarianK99CA179137 · NCI · BAYLOR COLLEGE OF MEDICINE · PI KIM, JAEYEON · 2013 to 2014
$193k
Understanding the origin and pathogenesis of epithelial ovarian cancerF32CA159523 · NCI · BAYLOR COLLEGE OF MEDICINE · PI KIM, JAEYEON · 2011 to 2013
$120k
NCI NIH HHS F32 CA159523NCI NIH HHS F32CA159523NCI NIH HHS K99 CA179137NCI NIH HHS K99CA179137
6 · The paper itself

Abstract

Although named "ovarian cancer," it has been unclear whether the cancer actually arises from the ovary, especially for high-grade serous carcinoma (HGSC), also known as high-grade serous ovarian cancer, the most common and deadliest ovarian cancer. In addition, the tumor suppressor p53 is the most frequently mutated gene in HGSC. However, whether mutated p53 can cause HGSC remains unknown. In this study, we bred a p53 mutation, p53(R172H), into conditional Dicer-Pten double-knockout (DKO) mice, a mouse model duplicating human HGSC, to generate triple-mutant (TKO) mice. Like DKO mice, these TKO mice develop metastatic HGSCs originating from the fallopian tube. Unlike DKO mice, however, even after fallopian tubes are removed in TKO mice, ovaries alone can develop metastatic HGSCs, indicating that a p53 mutation can drive HGSC arising from the ovary. To confirm this, we generated p53(R172H)-Pten double-mutant mice, one of the genetic control lines for TKO mice. As anticipated, these double-mutant mice also develop metastatic HGSCs from the ovary, verifying the HGSC-forming ability of ovaries with a p53 mutation. Our study therefore shows that ovaries harboring a p53 mutation, as well as fallopian tubes, can be a distinct tissue source of high-grade serous ovarian cancer in mice.

Indexed as

AnimalsCystadenocarcinoma, SerousDEAD-box RNA HelicasesDisease Models, AnimalFemaleImmunohistochemistryMiceMice, KnockoutOvarian NeoplasmsOvaryPTEN PhosphohydrolaseRibonuclease IIITumor Suppressor Protein p53DEAD-box RNA HelicasesDicer1 protein, mousePTEN PhosphohydrolaseRibonuclease IIITumor Suppressor Protein p53

Identifiers

PMID25815421
PMCPMC5393339
OpenAlexW2024022439

What OpenQuestion holds

Textmetadata
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.