Evidence map›Paper›PMID 24913706›Full record

ArticleTumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine2014

Epigenetic alteration of p16 and retinoic acid receptor beta genes in the development of epithelial ovarian carcinoma.

Rahul Bhagat, Sandeep Sriram Kumar, Shilpa Vaderhobli, Chennagiri S Premalata, Venkateshaiah Reddihalli Pallavi, Gawari Ramesh, Lakshmi Krishnamoorthy

Abstract read
PubMed Publisher
In one paragraph

Article in Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed, 1 pooled it
1.4field-weighted citation impact, top 19% 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

15 citing papers in PubMed, 1 synthesis or guideline pooled it, 28 citations in OpenAlex.

  1. Pooled it
  2. DNA Methylation and Transcript Variant Analysis ofInternational journal of molecular sciences · 2025
    Article
  3. Review
  4. Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Quantitative assessment of aberrantCancer management and research · 2018
    Review
  12. Article
  13. Review
  14. p16 hypermethylation: a biomarker for increased esophageal cancer susceptibility in high incidence region of North East India.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015
    Article
  15. 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

7 authors at 1 institution in 1 country.

Rahul BhagatDepartment of Biochemistry, Kidwai Memorial Institute of Oncology, Dr. M.H. Marigowda Road, Bangalore, 560029, India, rahulbhagat1234@gmail.com.
Sandeep Sriram Kumar
Shilpa Vaderhobli
Chennagiri S Premalata
Venkateshaiah Reddihalli Pallavi
Gawari Ramesh
Lakshmi Krishnamoorthy
Kidwai Memorial Institute of Oncology · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Silencing of tumor suppressor and tumor-related genes by promoter hypermethylation is one of the major events in ovarian carcinogenesis. In this study, we analyzed aberrant promoter methylation of p16 and RAR-β genes in 134 epithelial ovarian carcinomas (EOCs), 23 low malignant potential (LMP) tumors, 26 benign cystadenomas, and 15 normal ovarian tissues. Methylation was investigated by methylation-specific PCR (MSP), and the results were confirmed by bisulfite DNA sequencing. Relative gene expression of p16 and RAR-β was done using quantitative reverse transcriptase PCR (qRT-PCR) on 51 EOC cases, 9 LMP tumors, and 7 benign cystadenomas with 5 normal ovarian tissues. Aberrant methylation for p16 and RAR-β was present in 43 % (58/134) and 31 % (41/134) in carcinoma cases, 22 % (05/23) and 52 % (12/23) in LMP tumors, and 42 % (11/26) and 69 % (18/26) in benign cystadenomas. No methylation was observed in any of the normal ovarian tissues. The mRNA expression level of p16 and RAR-β was significantly downregulated in EOC and LMP tumors than the corresponding normal tissues whereas the expression level was normal in benign cystadenomas for p16 and slightly reduced for RAR-β. A significant correlation of p16 promoter methylation was observed with reduced gene expression in EOC. For RAR-β, no significant correlation was observed between promoter methylation and gene expression. Our results suggest that epigenetic alterations of p16 and RAR-β have an important role in ovarian carcinogenesis and that mechanism along with methylation plays a significant role in downregulation of RAR-β gene in ovarian cancer.

Indexed as

Epigenesis, GeneticAdultAgedBase SequenceCyclin-Dependent Kinase Inhibitor p16DNA MethylationDown-RegulationFemaleGene Expression Regulation, NeoplasticHumansMiddle AgedMolecular Sequence DataNeoplasms, Glandular and EpithelialOvarian NeoplasmsPromoter Regions, GeneticProportional Hazards ModelsCyclin-Dependent Kinase Inhibitor p16Receptors, Retinoic Acidretinoic acid receptor beta

Identifiers

PMID24913706
OpenAlexW2064070540

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.