Evidence map›Paper›PMID 21487943›Full record

ReviewLangenbeck's archives of surgery2011

Molecular pathogenesis of nodular goiter.

Ralf Paschke

Registry-linked trialAbstract readReview
PubMed Publisher
In one paragraph

Review in Langenbeck's archives of surgery, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT06868459 (Pressure-enabled Retrograde Occlusive Therapy With Embolization for Control of Thyroid Disease), which is not on this map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.9field-weighted citation impact, top 9% 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.

NCT06868459 enrolling by invitationnot on this mapstarted 2025, after this paper: background citation

Pressure-enabled Retrograde Occlusive Therapy With Embolization for Control of Thyroid Disease (PROTECT Registry): A Multicenter Registry

Typeobservational_patient_registrySponsorSarasota Memorial Health Care SystemRan2025 to 2028Enrolled100ConditionsHyperthyroidism, Goiter, Multinodular Goiter, Thyroid NodulesArmsData Collection
3 · Its place in the literature

Who cites it

15 citing papers in PubMed, 71 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Is Melanoma Progression Affected by Thyroid Diseases?International journal of molecular sciences · 2022
    Review
  5. Article
  6. Thyroid diseases and skin autoimmunity.Reviews in endocrine & metabolic disorders · 2018
    Review
  7. Article
  8. Investigation of the role of 8-OHdG and oxidative stress in papillary thyroid carcinoma.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015
    Article
  9. Article
  10. Oxidative stress and the ageing endocrine system.Nature reviews. Endocrinology · 2013
    Review
  11. Review
  12. Article
  13. Article
  14. 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

1 author at 1 institution in 1 country.

Ralf PaschkeDepartment for Endocrinology and Nephrology, University of Leipzig, Liebigstrasse 20, D-04103, Leipzig, Germany. Ralf.Paschke@medizin.uni-leipzig.de
University Hospital Leipzig · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionFamilial clustering of goiters mostly with an autosomal dominant pattern of inheritance has repeatedly been reported. Moreover, other environmental and etiologic factors are likely to be involved in the development of euthyroid goiter. Therefore, a multifactorial etiology based on complex interactions of both genetic predisposition and the individuals' environment is likely.

methodsThe line of events from early thyroid hyperplasia to multinodular goiter argues for the predominant neoplastic (i.e., originating from a single mutated cell) character of nodular structures. Etiologically, relevant somatic mutations are known in two thirds of papillary and follicular thyroid carcinomas and hot thyroid nodules. In contrast, the somatic mutations relevant for benign cold or benign isocaptant thyroid nodules which constitute the majority of thyroid nodules are unknown.

resultsThe nodular process is triggered by the oxidative nature of thyroid hormone synthesis or additional oxidative stress caused by iodine deficiency or smoking. If the antioxidant defense is not effective, this oxidative stress will cause DNA damage followed by an increase of the spontaneous mutation rate which is a substrate for tumorogenesis.

conclusionsTherefore, the hallmark of thyroid physiology--H(2)O(2) production during hormone synthesis--is very likely the ultimate cause for the frequent mutagenesis in the thyroid gland. Because iodine deficiency increases the oxidative burden, DNA damage and mutagenesis could provide the basis for the frequent nodular transformation of endemic goiters.

Indexed as

MutagenesisCell Transformation, NeoplasticDNA DamageFemaleGene Expression RegulationGenetic Predisposition to DiseaseGoiter, NodularHumansIncidenceMaleOxidative StressPrognosisRisk FactorsThyroidectomyThyroid Neoplasms

Identifiers

PMID21487943
OpenAlexW2084566479

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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.