Evidence map›Paper›PMID 20388212›Full record

ArticleBMC cancer2010

p16INK4a hypermethylation and p53, p16 and MDM2 protein expression in esophageal squamous cell carcinoma.

Noushin Taghavi, Firouzeh Biramijamal, Masoud Sotoudeh, Hooman Khademi, Reza Malekzadeh, Omeed Moaven, Bahram Memar, Azadeh A'rabi, Mohammad Reza Abbaszadegan

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed, 1 pooled it
3.2field-weighted citation impact, top 8% 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

37 citing papers in PubMed, 1 synthesis or guideline pooled it, 80 citations in OpenAlex.

  1. Pooled it
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  5. Methylation as a critical epigenetic process during tumor progressions among Iranian population: an overview.Genes and environment : the official journal of the Japanese Environmental Mutagen Society · 2021
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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 3 institutions in 1 country.

Noushin TaghaviNational Institute of Genetic Engineering and Biotechnology, Tehran, Iran.
Firouzeh Biramijamal
Masoud Sotoudeh
Hooman Khademi
Reza Malekzadeh
Omeed Moaven
Bahram Memar
Azadeh A'rabi
Mohammad Reza Abbaszadegan
Mashhad University of Medical Sciences · IRTehran University of Medical Sciences · IRNational Institute of Genetic Engineering and Biotechnology · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundTumor suppressor genes p53 and p16INK4a and the proto-oncogene MDM2 are considered to be essential G1 cell cycle regulatory genes whose loss of function is associated with ESCC carcinogenesis. We assessed the aberrant methylation of the p16 gene and its impact on p16INK4a protein expression and correlations with p53 and MDM2 protein expressions in patients with ESCC in the Golestan province of northeastern Iran in which ESCC has the highest incidence of cancer, well above the world average.

methodsCancerous tissues and the adjacent normal tissue obtained from 50 ESCC patients were assessed with Methylation-Specific-PCR to examine the methylation status of p16. The expression of p16, p53 and MDM2 proteins was detected by immunohistochemical staining.

resultsAbnormal expression of p16 and p53, but not MDM2, was significantly higher in the tumoral tissue. p53 was concomitantly accumulated in ESCC tumor along with MDM2 overexpression and p16 negative expression. Aberrant methylation of the p16INK4a gene was detected in 31/50 (62%) of esophageal tumor samples, while two of the adjacent normal mucosa were methylated (P < 0.001). p16INK4a aberrant methylation was significantly associated with decreased p16 protein expression (P = 0.033), as well as the overexpression of p53 (P = 0.020).

conclusionsp16 hypermethylation is the principal mechanism of p16 protein underexpression and plays an important role in ESCC development. It is associated with p53 protein overexpression and may influence the accumulation of abnormally expressed proteins in p53-MDM2 and p16-Rb pathways, suggesting a possible cross-talk of the involved pathways in ESCC development.

Indexed as

Biomarkers, TumorDNA MethylationAdultAgedAged, 80 and overCarcinoma, Squamous CellChi-Square DistributionCpG IslandsCyclin-Dependent Kinase Inhibitor p16Esophageal NeoplasmsFemaleGene Expression Regulation, NeoplasticHumansImmunohistochemistryIranKaplan-Meier EstimateBiomarkers, TumorCyclin-Dependent Kinase Inhibitor p16MAS1 protein, humanMDM2 protein, humanProto-Oncogene MasProto-Oncogene Proteins c-mdm2TP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID20388212
PMCPMC2868052
OpenAlexW2001103234

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.