Evidence map›Paper›PMID 39138354›Full record

ArticleScientific reports2024

Integrated genomic/epigenomic analysis stratifies subtypes of clear cell ovarian carcinoma, highlighting their cellular origin.

Akira Nishijima, Katsutoshi Oda, Kosei Hasegawa, Takahiro Koso, Kayo Asada, Yuji Ikeda, Ayumi Taguchi, Daichi Maeda, Genta Nagae, Shingo Tsuji and 12 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
–field-weighted citation impact
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

9 citing papers in PubMed.

  1. Trial
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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

22 authors.

Akira NishijimaGenome Science Division, Research Center for Advanced Science and Technology, The University of Tokyo, Tokyo, Japan.
Katsutoshi OdaDivision of Integrative Genomics, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan. katsutoshi-tky@umin.ac.jp.
Kosei HasegawaDepartment of Gynecologic Oncology, Saitama Medical University International Medical Center, Saitama, Japan.
Takahiro KosoGenome Science Division, Research Center for Advanced Science and Technology, The University of Tokyo, Tokyo, Japan.
Kayo AsadaGenome Science Division, Research Center for Advanced Science and Technology, The University of Tokyo, Tokyo, Japan.
Yuji IkedaDepartment of Obstetrics and Gynecology, Nihon University, Tokyo, Japan.
Ayumi TaguchiDepartment of Obstetrics and Gynecology, The University of Tokyo, Tokyo, Japan.
Daichi MaedaDepartment of Molecular and Cellular Pathology, Kanazawa University, Ishikawa, Japan.
Genta NagaeGenome Science Division, Research Center for Advanced Science and Technology, The University of Tokyo, Tokyo, Japan.
Shingo TsujiGenome Science Division, Research Center for Advanced Science and Technology, The University of Tokyo, Tokyo, Japan.
Kenji TatsunoGenome Science Division, Research Center for Advanced Science and Technology, The University of Tokyo, Tokyo, Japan.
Yuriko UeharaGenome Science Division, Research Center for Advanced Science and Technology, The University of Tokyo, Tokyo, Japan.
Akira KurosakiDepartment of Gynecologic Oncology, Saitama Medical University International Medical Center, Saitama, Japan.
Sho SatoDepartment of Gynecologic Oncology, Saitama Medical University International Medical Center, Saitama, Japan.
Michihiro TanikawaDepartment of Obstetrics and Gynecology, The University of Tokyo, Tokyo, Japan.
Kenbun SoneDepartment of Obstetrics and Gynecology, The University of Tokyo, Tokyo, Japan.
Mayuyo MoriDepartment of Obstetrics and Gynecology, The University of Tokyo, Tokyo, Japan.
Masako IkemuraDepartment of Pathology, The University of Tokyo, Tokyo, Japan.
Keiichi FujiwaraDepartment of Gynecologic Oncology, Saitama Medical University International Medical Center, Saitama, Japan.
Tetsuo UshikuDepartment of Pathology, The University of Tokyo, Tokyo, Japan.
Yutaka OsugaDepartment of Obstetrics and Gynecology, The University of Tokyo, Tokyo, Japan.
Hiroyuki AburataniGenome Science Division, Research Center for Advanced Science and Technology, The University of Tokyo, Tokyo, Japan. haburata-tky@umin.ac.jp.

Funding

Japan Agency for Medical Research and Development JP19cm0106502Japan Society for the Promotion of Science 24K02584Japan Society for the Promotion of Science 24K02591
6 · The paper itself

Abstract

The cellular origin of clear cell ovarian carcinoma (CCOC), a major histological subtype of ovarian carcinoma remains elusive. Here, we explored the candidate cellular origin and identify molecular subtypes using integrated genomic/epigenomic analysis. We performed whole exome-sequencing, microarray, and DNA methylation array in 78 CCOC samples according to the original diagnosis. The findings revealed that ARID1A and/or PIK3CA mutations were mutually exclusive with DNA repair related genes, including TP53, BRCA1, and ATM. Clustering of CCOC and other ovarian carcinomas (n = 270) with normal tissues from the fallopian tube, ovarian surface epithelium, endometrial epithelium, and pelvic peritoneum mesothelium (PPM) in a methylation array showed that major CCOC subtypes (with ARID1A and/or PIK3CA mutations) were associated with the PPM-lile cluster (n = 64). This cluster was sub-divided into three clusters: (1) mismatch repair (MMR) deficient with tumor mutational burden-high (n = 2), (2) alteration of ARID1A (n = 51), and (3) ARID1A wild-type (n = 11). The remaining samples (n = 14) were subdivided into (4) ovarian surface epithelium-like (n = 11) and (5) fallopian tube-like (considered as high-grade serous histotype; n = 3). Among these, subtypes (1-3) and others (4 and 5) were found to be associated with immunoreactive signatures and epithelial-mesenchymal transition, respectively. These results contribute to the stratification of CCOC into biological subtypes.

Indexed as

Adenocarcinoma, Clear CellDNA-Binding ProteinsDNA MethylationMutationOvarian NeoplasmsTranscription FactorsClass I Phosphatidylinositol 3-KinasesEpigenomicsExome SequencingFemaleGenomicsHumansMiddle AgedARID1A protein, humanClass I Phosphatidylinositol 3-KinasesDNA-Binding ProteinsPIK3CA protein, humanTranscription FactorsCellular originClear cell ovarian carcinomaEpigenomicsGenomicsMolecular subtypes

Identifiers

PMID39138354
PMCPMC11322660

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.