Evidence map›Paper›PMID 31672974›Full record

ArticleNature communications2019

Clinically relevant molecular subtypes and genomic alteration-independent differentiation in gynecologic carcinosarcoma.

Osamu Gotoh, Yuko Sugiyama, Yutaka Takazawa, Kazuyoshi Kato, Norio Tanaka, Kohei Omatsu, Nobuhiro Takeshima, Hidetaka Nomura, Kosei Hasegawa, Keiichi Fujiwara and 4 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
78citing papers in PubMed, 3 pooled it
12.8field-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

78 citing papers in PubMed, 3 syntheses or guidelines pooled it, 147 citations in OpenAlex.

  1. Pooled it
  2. Prognostic value of the TCGA molecular classification in uterine carcinosarcoma.International journal of gynaecology and obstetrics: the official organ of the International Federation of Gynaecology and Obstetrics · 2022
    Pooled it
  3. Pooled it
  4. Trial
  5. Article
  6. Article
  7. A Single-Cell Atlas of Uterine Carcinosarcoma from Diverse Ancestries.bioRxiv : the preprint server for biology · 2026
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Impact ofFujita medical journal · 2025
    Article
  14. Article
  15. Endometrial carcinosarcoma without myoinvasion.International journal of gynecological cancer : official journal of the International Gynecological Cancer Society · 2025
    Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. Review

18 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

14 authors at 3 institutions in 1 country.

Osamu GotohProject for Development of Innovative Research on Cancer Therapeutics, Cancer Precision Medicine Center, Japanese Foundation for Cancer Research, 3-8-31 Ariake, Koto-ku, Tokyo, Japan.ORCID http://orcid.org/0000-0002-9363-4584
Yuko SugiyamaDepartment of Gynecology, Cancer Institute Hospital, Japanese Foundation for Cancer Research, 3-8-31 Ariake, Koto-ku, Tokyo, Japan.
Yutaka TakazawaDepartment of Pathology, Cancer Institute Hospital, Japanese Foundation for Cancer Research, 3-8-31 Ariake, Koto-ku, Tokyo, Japan.
Kazuyoshi KatoDepartment of Gynecology, Cancer Institute Hospital, Japanese Foundation for Cancer Research, 3-8-31 Ariake, Koto-ku, Tokyo, Japan.
Norio TanakaProject for Development of Innovative Research on Cancer Therapeutics, Cancer Precision Medicine Center, Japanese Foundation for Cancer Research, 3-8-31 Ariake, Koto-ku, Tokyo, Japan.ORCID http://orcid.org/0000-0003-2724-8009
Kohei OmatsuDepartment of Gynecology, Cancer Institute Hospital, Japanese Foundation for Cancer Research, 3-8-31 Ariake, Koto-ku, Tokyo, Japan.
Nobuhiro TakeshimaDepartment of Gynecology, Cancer Institute Hospital, Japanese Foundation for Cancer Research, 3-8-31 Ariake, Koto-ku, Tokyo, Japan.
Hidetaka NomuraDepartment of Gynecology, Cancer Institute Hospital, Japanese Foundation for Cancer Research, 3-8-31 Ariake, Koto-ku, Tokyo, Japan.
Kosei HasegawaDepartment of Gynecologic Oncology, Saitama Medical University International Medical Center, 1397-1 Yamane, Hidaka-shi, Saitama, Japan.
Keiichi FujiwaraDepartment of Gynecologic Oncology, Saitama Medical University International Medical Center, 1397-1 Yamane, Hidaka-shi, Saitama, Japan.
Mana TakiDepartment of Gynecologic Oncology, Kyoto University Hospital, 54 Kawaharacho, Shogoin, Sakyo-ku, Kyoto, Japan.
Noriomi MatsumuraDepartment of Gynecologic Oncology, Kyoto University Hospital, 54 Kawaharacho, Shogoin, Sakyo-ku, Kyoto, Japan.
Tetsuo NodaProject for Development of Innovative Research on Cancer Therapeutics, Cancer Precision Medicine Center, Japanese Foundation for Cancer Research, 3-8-31 Ariake, Koto-ku, Tokyo, Japan.
Seiichi MoriProject for Development of Innovative Research on Cancer Therapeutics, Cancer Precision Medicine Center, Japanese Foundation for Cancer Research, 3-8-31 Ariake, Koto-ku, Tokyo, Japan. seiichi.mori@jfcr.or.jp.
Japanese Foundation For Cancer Research · JPKyoto University Hospital · JPSaitama Medical University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Carcinosarcoma (CS) of the uterus or ovary is a rare, aggressive and biphasic neoplasm composed of carcinoma and sarcoma elements. Previous genomic studies have identified the driver genes and genomic properties associated with CS. However, there is still no molecular subtyping scheme with clinical relevance for this disease. Here, we sequence 109 CS samples, focusing on 596 genes. We identify four molecular subtypes that resemble those observed in endometrial carcinoma: POLE-mutated, microsatellite instability, copy number high, and copy number low subtypes. These molecular subtypes are linked with DNA repair deficiencies, potential therapeutic strategies, and multiple clinicopathological features, including patient outcomes. Multi-regional comparative sequencing reveals genomic alteration-independent CS cell differentiation. Transcriptome and DNA methylome analyses confirm epithelial-mesenchymal transition as a mechanism of sarcoma differentiation. The current study thus provides therapeutic possibilities for CS as well as clues to understanding the molecular histogenic mechanism of its development.

Indexed as

AdultAgedAged, 80 and overCarcinoma, EndometrioidCarcinosarcomaCluster AnalysisDecision TreesDNA Copy Number VariationsDNA MethylationDNA Polymerase IIDNA Repair-Deficiency DisordersEpithelial-Mesenchymal TransitionFemaleGenital Neoplasms, FemaleHigh-Throughput Nucleotide SequencingHumansDNA Polymerase IIPOLE protein, humanPoly-ADP-Ribose Binding ProteinsRNA, Messenger

Identifiers

PMID31672974
PMCPMC6823358
OpenAlexW2982559021

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.