Evidence map›Paper›PMID 28600574›Full record

ArticleScientific reports2017

Promoter hypermethylation inactivates CDKN2A, CDKN2B and RASSF1A genes in sporadic parathyroid adenomas.

Ashutosh Kumar Arya, Sanjay Kumar Bhadada, Priyanka Singh, Naresh Sachdeva, Uma Nahar Saikia, Divya Dahiya, Arunanshu Behera, Anil Bhansali, Sudhaker D Rao

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

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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

27 citing papers in PubMed, 44 citations in OpenAlex.

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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 2 institutions in 2 countries.

Ashutosh Kumar AryaDepartment of Endocrinology, Postgraduate Institute of Medical Education & Research (PGIMER), Chandigarh, India.
Sanjay Kumar BhadadaDepartment of Endocrinology, Postgraduate Institute of Medical Education & Research (PGIMER), Chandigarh, India. bhadadask@rediffmail.com.
Priyanka SinghDepartment of Endocrinology, Postgraduate Institute of Medical Education & Research (PGIMER), Chandigarh, India.
Naresh SachdevaDepartment of Endocrinology, Postgraduate Institute of Medical Education & Research (PGIMER), Chandigarh, India.
Uma Nahar SaikiaDepartment of Histopathology, Postgraduate Institute of Medical Education & Research (PGIMER), Chandigarh, India.
Divya DahiyaDepartment of General Surgery, Postgraduate Institute of Medical Education & Research (PGIMER), Chandigarh, India.
Arunanshu BeheraDepartment of General Surgery, Postgraduate Institute of Medical Education & Research (PGIMER), Chandigarh, India.
Anil BhansaliDepartment of Endocrinology, Postgraduate Institute of Medical Education & Research (PGIMER), Chandigarh, India.
Sudhaker D RaoBone & Mineral Research Laboratory, Henry Ford Hospital, Detroit, USA.
Post Graduate Institute of Medical Education and Research · INHenry Ford Hospital · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cyclin D1, a G1-S phase regulator, is upregulated in parathyroid adenomas. Since cyclin-dependent kinase (CDK) inhibitors, CDKN2A and CDKN2B, and RASSF1A (Ras-association domain family 1, isoform A) are involved in G1-S phase arrest and act as potential tumor suppressor genes, we aimed to study potential methylation-mediated inactivation of these genes in parathyroid adenomas. Gene expressions of cyclin D1 (CCND1) and regulatory molecules (CDKN2A, CDKN2B and RASSF1A) was analysed in parathyroid adenoma tissues (n = 30). DNA promoter methylation of cyclin D1 regulators were assessed and correlated with clinicopathological features of the patients. Gene expression analysis showed a relative fold reductions of 0.35 for CDKN2A (p = 0.01), 0.45 for CDKN2B (P = 0.02), and 0.39 for RASSF1A (p < 0.01) in adenomatous compared to normal parathyroid tissue. There was an inverse relationship between the expressions of CDKN2A and CDKN2B with CCND1. In addition, the promoter regions of CDKN2A, CDKN2B, and of RASSF1A were significantly hyper-methylated in 50% (n = 15), 47% (n = 14), and 90% (n = 27) of adenomas respectively. In contrast, no such aberrant methylation of these genes was observed in normal parathyroid tissue. So, promoter hypermethylation is associated with down-regulation of CCND1 regulatory genes in sporadic parathyroid adenomas. This dysregulated cell cycle mechanism may contribute to parathyroid tumorigenesis.

Indexed as

DNA MethylationDown-RegulationAdenomaAdolescentAdultCyclin D1Cyclin-Dependent Kinase Inhibitor p15Cyclin-Dependent Kinase Inhibitor p16Cyclin-Dependent Kinase Inhibitor p18Epigenesis, GeneticFemaleGene Expression ProfilingGene Expression Regulation, NeoplasticHumansMaleMiddle AgedCCND1 protein, humanCDKN2A protein, humanCDKN2B protein, humanCyclin D1Cyclin-Dependent Kinase Inhibitor p15Cyclin-Dependent Kinase Inhibitor p16Cyclin-Dependent Kinase Inhibitor p18RASSF1 protein, humanTumor Suppressor Proteins

Identifiers

PMID28600574
PMCPMC5466668
OpenAlexW2623356835

What OpenQuestion holds

Textmetadata
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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.