Evidence map›Paper›PMID 25935255›Full record

ArticleJournal of endocrinological investigation2015

TP53 polymorphism may contribute to genetic susceptibility to develop Hashimoto's thyroiditis.

R M Ruggeri, T M Vicchio, S Giovinazzo, R Certo, A Alibrandi, F Trimarchi, S Benvenga, M Trovato

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In one paragraph

Article in Journal of endocrinological investigation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
–field-weighted citation impact
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

6 citing papers in PubMed.

  1. Review
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  3. Association ofBiomedicines · 2023
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4 · The record

Corrections and comments

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5 · Who and what money

Authors and funding

8 authors.

R M RuggeriDepartment of Clinical and Experimental Medicine, Endocrine Unit, University of Messina, Padiglione H, 4 Piano, AOU Policlinico Universitario "G. Martino", via Consolare Valeria, 1, 98125, Messina, Italy. rmruggeri@unime.it.
T M VicchioDepartment of Clinical and Experimental Medicine, Endocrine Unit, University of Messina, Padiglione H, 4 Piano, AOU Policlinico Universitario "G. Martino", via Consolare Valeria, 1, 98125, Messina, Italy.
S GiovinazzoDepartment of Clinical and Experimental Medicine, Endocrine Unit, University of Messina, Padiglione H, 4 Piano, AOU Policlinico Universitario "G. Martino", via Consolare Valeria, 1, 98125, Messina, Italy.
R CertoDepartment of Clinical and Experimental Medicine, Endocrine Unit, University of Messina, Padiglione H, 4 Piano, AOU Policlinico Universitario "G. Martino", via Consolare Valeria, 1, 98125, Messina, Italy.
A AlibrandiDepartment of Statistical Sciences (SEFISAST), University of Messina, Messina, Italy.
F TrimarchiDepartment of Clinical and Experimental Medicine, Endocrine Unit, University of Messina, Padiglione H, 4 Piano, AOU Policlinico Universitario "G. Martino", via Consolare Valeria, 1, 98125, Messina, Italy.
S BenvengaDepartment of Clinical and Experimental Medicine, Endocrine Unit, University of Messina, Padiglione H, 4 Piano, AOU Policlinico Universitario "G. Martino", via Consolare Valeria, 1, 98125, Messina, Italy.
M TrovatoDepartment of Clinical and Experimental Medicine, Endocrine Unit, University of Messina, Padiglione H, 4 Piano, AOU Policlinico Universitario "G. Martino", via Consolare Valeria, 1, 98125, Messina, Italy.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposep53, which is encoded by the tumor suppressor gene TP53, plays a crucial role in the regulation of mechanisms of cell cycle arrest and apoptosis. Some SNPs of TP53, involving a different apoptotic ability of p53, have been associated with increased susceptibility to develop autoimmune diseases as well as cancer. We investigated the genotypic distribution of TP53 exon 4 SNPs in a cohort of Caucasian patients affected by Hashimoto's thyroiditis (HT).

methodsPeripheral blood for DNA extraction was collected from 109 Caucasian unrelated subjects, 79 HT patients and 30 healthy controls. SNPs analysis was carried out by amplification and sequencing of exon 4 TP53.

resultsFor the Pro72Arg (rs 1042522) SNP we found these rates in HT patients: 11.4% wild-type C/C (Pro72Pro), 24.0% heterozygous G/C (Pro72Arg), 64.6% homozygous G/G (Arg72Arg). The corresponding rates in healthy controls were 10, 46.7 and 43.3%, respectively. Thus, significantly different were G/C heterozygosity (24.0 vs 46.7 %, p = 0.039) and G/G homozygosity (64.6 vs 43.3%, p = 0.042). These differences were also confirmed when comparing our study population to published Caucasian control groups. The other described SNPs (Pro34Pro rs 11575998, Pro36Pro rs1800370, Pro47Ser rs1800371, and Arg110Leu rs 11540654) were absent or very rare in our study population.

conclusionsOur preliminary data, the first on a Caucasian population, indicate an increased prevalence of the homozygous genotype Arg/Arg and a decreased prevalence of heterozygous genotype Arg/Pro of rs 1042522 in HT patients compared to controls, suggesting that such SNP may contribute to confer susceptibility to HT.

Indexed as

AdultExonsFemaleGenetic Predisposition to DiseaseHashimoto DiseaseHumansMaleMiddle AgedPolymorphism, Single NucleotideTumor Suppressor Protein p53White PeopleTP53 protein, humanTumor Suppressor Protein p53Hashimoto’s thyroiditisp53p53 mutationsSingle nucleotide polymorphism (SNP)

Identifiers

PMID25935255

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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.