Evidence map›Paper›PMID 29451304›Full record

ArticleInternational journal of cancer2018

Distinct methylation profile of mucinous ovarian carcinoma reveals susceptibility to proteasome inhibitors.

Phui-Ly Liew, Rui-Lan Huang, Yu-Chun Weng, Chia-Lang Fang, Tim Hui-Ming Huang, Hung-Cheng Lai

Open access · hybridAbstract readComparative Study
In one paragraph

Article in International journal of cancer, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

13 citing papers in PubMed, 22 citations in OpenAlex.

  1. Article
  2. Review
  3. Cellular origins of mucinous ovarian carcinoma.The Journal of pathology · 2025
    Review
  4. Article
  5. The Role ofInternational journal of women's health · 2025
    Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Bioinformatics analysis identifiesAnnals of translational medicine · 2022
    Article
  11. Review
  12. Article
  13. 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 4 institutions in 3 countries.

Phui-Ly LiewDepartment of Pathology, Shuang Ho Hospital, Taipei Medical University, New Taipei, Taiwan.ORCID 0000-0003-2156-5628
Rui-Lan HuangDepartment of Obstetrics and Gynecology, Shuang Ho Hospital, Taipei Medical University, New Taipei, Taiwan.ORCID 0000-0001-6458-4672
Yu-Chun WengTranslational epigenetic center, Shuang Ho Hospital, Taipei Medical University, New Taipei, Taiwan.
Chia-Lang FangDepartment of Pathology, School of Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan.
Tim Hui-Ming HuangDepartment of Molecular Medicine/Institute of Biotechnology, University of Texas Health Science Center at San Antonio, San Antonio, TX.
Hung-Cheng LaiDepartment of Obstetrics and Gynecology, Shuang Ho Hospital, Taipei Medical University, New Taipei, Taiwan.
Taipei Medical University-Shuang Ho Hospital · TWCentral South University · CNThe University of Texas Health Science Center at San Antonio · USWan Fang Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mucinous type of epithelial ovarian cancer (MuOC) is a unique subtype with a poor survival outcome in recurrent and advanced stages. The role of type-specific epigenomics and its clinical significance remains uncertain. We analyzed the methylomic profiles of 6 benign mucinous adenomas, 24 MuOCs, 103 serous type of epithelial ovarian cancers (SeOCs) and 337 nonepithelial ovarian cancers. MuOC and SeOC exhibited distinct DNA methylation profiles comprising 101 genes, 81 of which exhibited low methylation in MuOC and were associated with the response to glucocorticoid, ATP hydrolysis-coupled proton transport, proteolysis involved in the cellular protein catabolic process and ion transmembrane transport. Hierarchical clustering analysis showed that the profiles of MuOC were similar to colorectal adenocarcinoma and stomach adenocarcinoma. Genetic interaction network analysis of differentially methylated genes in MuOC showed a dominant network module is the proteasome subunit beta (PSMB) family. Combined functional module and methylation analysis identified PSMB8 as a candidate marker for MuOC. Immunohistochemical staining of PSMB8 used to validate in 94 samples of ovarian tumors (mucinous adenoma, MuOC or SeOC) and 62 samples of gastrointestinal cancer. PSMB8 was commonly expressed in MuOC and gastrointestinal cancer samples, predominantly as strong cytoplasmic and occasionally weak nuclei staining, but was not expressed in SeOC samples. Carfilzomib, a second-generation proteasome inhibitor, suppressed MuOC cell growth in vitro. This study unveiled a mucinous-type-specific methylation profile and suggests the potential use of a proteasome inhibitor to treat MuOC.

Indexed as

DNA MethylationAdenocarcinoma, MucinousCarcinoma, Ovarian EpithelialCell Line, TumorCell ProliferationCell SurvivalCluster AnalysisCystadenoma, MucinousEpigenomicsFemaleGastrointestinal NeoplasmsGene Expression Regulation, NeoplasticHumansOligopeptidesOvarian NeoplasmsProteasome Endopeptidase ComplexcarfilzomibLMP7 proteinOligopeptidesProteasome Endopeptidase ComplexProteasome Inhibitorsfunctional genetic interactionsmethylation profilesmucinous ovarian carcinomaproteasome inhibitorsPSMB8

Identifiers

PMID29451304
PMCPMC6001480
OpenAlexW2793819225

What OpenQuestion holds

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LicenceCC BY-NC
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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.