Evidence map›Paper›PMID 25625843›Full record

ArticleEpigenetics2014

Epigenetic analysis of sporadic and Lynch-associated ovarian cancers reveals histology-specific patterns of DNA methylation.

Anni Niskakoski, Sippy Kaur, Synnöve Staff, Laura Renkonen-Sinisalo, Heini Lassus, Heikki J Järvinen, Jukka-Pekka Mecklin, Ralf Bützow, Päivi Peltomäki

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In one paragraph

Article in Epigenetics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

19 citing papers in PubMed, 37 citations in OpenAlex.

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  9. Oncogenic and tumor suppressor function of MEIS and associated factors.Turkish journal of biology = Turk biyoloji dergisi · 2020
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  12. Molecular changes preceding endometrial and ovarian cancer: a study of consecutive endometrial specimens from Lynch syndrome surveillance.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2018
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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

9 authors at 4 institutions in 3 countries.

Anni Niskakoskia Department of Medical Genetics; Biomedicum Helsinki ; University of Helsinki ; Helsinki , Finland.
Sippy Kaur
Synnöve Staff
Laura Renkonen-Sinisalo
Heini Lassus
Heikki J Järvinen
Jukka-Pekka Mecklin
Ralf Bützow
Päivi Peltomäki
Helsinki University Hospital · FIUniversity of Helsinki · FICentral Finland Health Care District · FITampere University Hospital · FI

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Diagnosis and treatment of epithelial ovarian cancer is challenging due to the poor understanding of the pathogenesis of the disease. Our aim was to investigate epigenetic mechanisms in ovarian tumorigenesis and, especially, whether tumors with different histological subtypes or hereditary background (Lynch syndrome) exhibit differential susceptibility to epigenetic inactivation of growth regulatory genes. Gene candidates for epigenetic regulation were identified from the literature and by expression profiling of ovarian and endometrial cancer cell lines treated with demethylating agents. Thirteen genes were chosen for methylation-specific multiplex ligation-dependent probe amplification assays on 104 (85 sporadic and 19 Lynch syndrome-associated) ovarian carcinomas. Increased methylation (i.e., hypermethylation) of variable degree was characteristic of ovarian carcinomas relative to the corresponding normal tissues, and hypermethylation was consistently more prominent in non-serous than serous tumors for individual genes and gene sets investigated. Lynch syndrome-associated clear cell carcinomas showed the highest frequencies of hypermethylation. Among endometrioid ovarian carcinomas, lower levels of promoter methylation of RSK4, SPARC, and HOXA9 were significantly associated with higher tumor grade; thus, the methylation patterns showed a shift to the direction of high-grade serous tumors. In conclusion, we provide evidence of a frequent epigenetic inactivation of RSK4, SPARC, PROM1, HOXA10, HOXA9, WT1-AS, SFRP2, SFRP5, OPCML, and MIR34B in the development of non-serous ovarian carcinomas of Lynch and sporadic origin, as compared to serous tumors. Our findings shed light on the role of epigenetic mechanisms in ovarian tumorigenesis and identify potential targets for translational applications.

Indexed as

DNA MethylationEpigenesis, GeneticBiomarkers, TumorCarcinoma, EndometrioidCarcinoma, Ovarian EpithelialCell Line, TumorColorectal Neoplasms, Hereditary NonpolyposisCpG IslandsFemaleGene Expression Regulation, NeoplasticGenes, Tumor SuppressorHumansNeoplasms, Glandular and EpithelialOvarian NeoplasmsPromoter Regions, GeneticReference ValuesBiomarkers, TumorDm, methylation dosage ratioDNA methylationepigeneticsHOXA9LS, Lynch syndromeLynch syndromemiRNAs, microRNAsMS-MLPA, methylation-specific multiplex ligation-dependent probe amplificationMS-MLPA ovarian cancerRSK4SPARCTSG, tumor suppressor geneWT1-AS, Wilms tumor suppressor 1 antisenseWT1, Wilms tumor suppressor 1 sense

Identifiers

PMID25625843
PMCPMC4622692
OpenAlexW2069437138

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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.