Evidence map›Paper›PMID 25577262›Full record

ReviewJournal of endocrinological investigation2015

MicroRNA deregulation in parathyroid tumours suggests an embryonic signature.

C Verdelli, I Forno, V Vaira, S Corbetta

Abstract readReview
PubMed Publisher
In one paragraph

Review 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 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
2.3field-weighted citation impact, top 13% 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

12 citing papers in PubMed, 27 citations in OpenAlex.

  1. Trial
  2. Review
  3. Review
  4. Review
  5. Review
  6. The Core Stem GenesBiomedicines · 2021
    Article
  7. Article
  8. Intratumor heterogeneity in human parathyroid tumors.Histology and histopathology · 2020
    Review
  9. Article
  10. Review
  11. Article
  12. Update on parathyroid carcinoma.Journal of endocrinological investigation · 2016
    Review
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

4 authors at 3 institutions in 1 country.

C VerdelliLaboratory of Molecular Biology, IRCCS Policlinico San Donato, San Donato Milanese, MI, Italy.
I FornoDivision of Pathology, Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico, Milan, Italy.
V VairaDivision of Pathology, Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico, Milan, Italy.
S CorbettaEndocrinology and Diabetology Unit, Department of Biomedical Sciences, University of Milan, IRCCS Policlinico San Donato, Via Morandi 30, 20097, San Donato Milanese, MI, Italy. sabrina.corbetta@unimi.it.
Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico · ITIRCCS Policlinico San Donato · ITUniversity of Milan · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Primary hyperparathyroidism is a common endocrine disorder caused by abnormal tumour parathyroid cell proliferation. Parathyroid tumours show a great variability both in clinical features, such as the severity of PTH secretion, the rate and the pattern of cell proliferation, and genetic background. Studies aiming to develop new diagnostic markers and therapeutic approaches need a deeper definition of this variability. Dysregulation of microRNAs (miRNAs) has been shown to play an essential role in the development and progression of cancer. MiRNAs are small noncoding RNAs that inhibit the translation and stability of messenger RNAs (mRNAs). Here, data about the miRNA expression pattern in parathyroid normal and tumour glands were reviewed. Though available data in parathyroid tumours are very limited, the expression pattern of a subset of specific miRNAs clearly discriminated parathyroid carcinomas from normal parathyroid glands and, more clinically relevant, from parathyroid adenomas. Investigation showed that parathyroid tumours were characterized by an embryonic expression pattern of miRNAs such as miR-296, or the miRNA clusters C19MC and miR-371-3, typically in stem cells committed to differentiation or during human embryonic development, respectively. Further, miRNA profiles were correlated with tumour aggressive behaviour. Moreover, the interaction with the oncosuppressor menin suggests that miRNAs might modulate the function of the known oncosuppressors or oncogenes involved in parathyroid tumourigenesis and thus overseeing the tumour phenotype. In conclusion, miRNAs might provide new diagnostic markers and new therapeutic approaches by developing molecular miRNA-targeted therapies for the cure of parathyroid tumours, whose unique option is surgery.

Indexed as

Gene Expression Regulation, DevelopmentalGene Expression Regulation, NeoplasticHumansHyperparathyroidismMicroRNAsParathyroid NeoplasmsMicroRNAsHyperparathyroidismMicroRNAsParathyroid tumours

Identifiers

PMID25577262
OpenAlexW2104723731

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.