Evidence map›Paper›PMID 30250993›Full record

ArticleMolecular biology reports2018

Expression profiles of histone modification genes in gastric cancer progression.

Seda Orenay-Boyacioglu, Elmas Kasap, Emre Gerceker, Hakan Yuceyar, Ufuk Demirci, Fahri Bilgic, Mehmet Korkmaz

Abstract read
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In one paragraph

Article in Molecular biology reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.5field-weighted citation impact, top 17% 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

25 citing papers in PubMed, 39 citations in OpenAlex.

  1. Review
  2. Genomic analyses identify 15 risk loci and revealProceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  3. Article
  4. Review
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  8. Article
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  13. Article
  14. HighAnnals of translational medicine · 2022
    Article
  15. Differential molecular mechanistic behavior of HDACs in cancer progression.Medical oncology (Northwood, London, England) · 2022
    Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review
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

7 authors at 3 institutions in 1 country.

Seda Orenay-BoyaciogluDepartment of Medical Genetics, Faculty of Medicine, Adnan Menderes University, Aydin, Turkey. sorenay@adu.edu.tr.ORCID http://orcid.org/0000-0003-1651-1940
Elmas KasapDepartment of Gastroenterology, Faculty of Medicine, Celal Bayar University, Manisa, Turkey.ORCID http://orcid.org/0000-0002-4335-1156
Emre GercekerDepartment of Gastroenterology, Private Gazi Hospital, Izmir, Turkey.ORCID http://orcid.org/0000-0001-7494-2912
Hakan YuceyarDepartment of Gastroenterology, Faculty of Medicine, Celal Bayar University, Manisa, Turkey.ORCID http://orcid.org/0000-0003-1545-362X
Ufuk DemirciDepartment of Internal Medicine, Faculty of Medicine, Celal Bayar University, Manisa, Turkey.ORCID http://orcid.org/0000-0001-6923-1470
Fahri BilgicDepartment of Internal Medicine, Faculty of Medicine, Celal Bayar University, Manisa, Turkey.ORCID http://orcid.org/0000-0002-9302-4532
Mehmet KorkmazDepartment of Medical Biology, Faculty of Medicine, Celal Bayar University, Manisa, Turkey.ORCID http://orcid.org/0000-0003-2420-3681
Manisa Celal Bayar University · TRAdnan Menderes University · TRGaziantep Children's Hospital · TR

Funding

Celal Bayar University Scientific Research Projects Coordination Unit 2016-095
6 · The paper itself

Abstract

Gastric cancer (GC) development can be attributed to several risk factors including atrophic gastritis (AG), intestinal metaplasia (IM), and the presence of Helicobacter pylori (HP). Also, histone modification is an epigenetic mechanism that plays a pivotal role in GC carcinogenesis. In this preliminary study, we aimed to describe the expression profiles of histone modification in the AG, IM, and GC patient groups. A total of 80 patients with AG (n = 27), IM (n = 25), and GC (n = 28) with an additional 20 control subjects were included in the study. Expression profiles of three histone phosphorylation genes (PAK1, NEK6, and AURKA) and five histone deacetylation genes (HDACs 1, 2, 3, 5, and 7) were examined based on the results of Real Time qPCR method. It was observed that AURKA and HDAC2 genes were significantly overexpressed in all groups compared to the control (P < 0.05). In GC patients, overexpression of HDAC2 gene was detected in the absence of metastasis, and overexpression of AURKA, HDAC2, and NEK6 genes was detected in the presence of metastasis. When cancer involvements were compared, significant overexpression of the HDAC2 gene was noted in overall and corpus involvements (P < 0.05). In addition, overexpression of AURKA, NEK6, HDAC1, and HDAC2 genes and underexpression of HDAC5 gene were detected in the antrum involvement (P < 0.05). In conclusion, decreased expression of HDAC5 in GC is reported for the first time in this study, while supporting the existing literature in AURKA, NEK6, HDAC1, and HDAC2 up regulations during GC development.

Indexed as

AdultAgedAurora Kinase ADisease ProgressionFemaleGastric MucosaGastritis, AtrophicGenetic VariationHelicobacter InfectionsHelicobacter pyloriHistone CodeHistone DeacetylasesHistonesHumansIntestinesMaleAURKA protein, humanAurora Kinase AHDAC5 protein, humanHistone DeacetylasesHistonesNEK6 protein, humanNIMA-Related Kinasesp21-Activated KinasesPAK1 protein, humanAtrophic gastritisEpigeneticsGastric cancerHistone modificationIntestinal metaplasia

Identifiers

PMID30250993
OpenAlexW2893627914

What OpenQuestion holds

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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.