Evidence map›Paper›PMID 24035866›Full record

ReviewMolecular and cellular endocrinology2014

Genetic and epigenetic changes in sporadic endocrine tumors: parathyroid tumors.

Jessica Costa-Guda, Andrew Arnold

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Molecular and cellular endocrinology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed, 1 pooled it
3.9field-weighted citation impact, top 6% 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

44 citing papers in PubMed, 1 synthesis or guideline pooled it, 90 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Histone Modification on Parathyroid Tumors: A Review of Epigenetics.International journal of molecular sciences · 2022
    Review
  11. Review
  12. Review
  13. Genomic Analysis of Abnormal DNAM Methylation in Parathyroid Tumors.International journal of endocrinology · 2022
    Article
  14. Article
  15. Article
  16. Article
  17. Role of LncRNA score and PVT1 in primary hyperparathyroidism-- a preliminary study.Journal of otolaryngology - head & neck surgery = Le Journal d'oto-rhino-laryngologie et de chirurgie cervico-faciale · 2021
    Article
  18. Familial Hyperparathyroidism.Frontiers in endocrinology · 2021
    Review
  19. Article
  20. 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

2 authors at 1 institution in 1 country.

Jessica Costa-GudaCenter for Molecular Medicine and Division of Endocrinology & Metabolism, University of Connecticut School of Medicine, Farmington, CT 06030-3101, USA.
Andrew ArnoldCenter for Molecular Medicine and Division of Endocrinology & Metabolism, University of Connecticut School of Medicine, Farmington, CT 06030-3101, USA. Electronic address: molecularmedicine@uchc.edu.
University of Connecticut · US

Funding

MOLECULAR PATHOGENESIS OF HYPERPARATHYROIDISMR01DK066411 · NIDDK · UNIVERSITY OF CONNECTICUT SCH OF MED/DNT · PI ARNOLD, ANDREW · 2008 to 2012
$1.7M
Modeling of Hyperparathyroidism-Jaw Tumor Syndrome by Targeted Deletion of Hrpt2F32DE021307 · NIDCR · UNIVERSITY OF CONNECTICUT SCH OF MED/DNT · PI COSTA, JESSICA · 2010 to 2012
$110k
NIDCR NIH HHS F32 DE021307NIDDK NIH HHS R01 DK066411
6 · The paper itself

Abstract

Parathyroid neoplasia is most commonly due to benign parathyroid adenoma but rarely can be caused by malignant parathyroid carcinoma. Evidence suggests that parathyroid carcinomas rarely, if ever, evolve through an identifiable benign intermediate, with the notable exception of carcinomas associated with the familial hyperparathyroidism-jaw tumor syndrome. Several genes have been directly implicated in the pathogenesis of typical sporadic parathyroid adenoma; somatic mutations in the MEN1 tumor suppressor gene are the most frequent finding, and alterations in the cyclin D1/PRAD1 oncogene are also firmly established molecular drivers of sporadic adenomas. In addition, good evidence supports mutation in the CDKN1B/p27 cyclin-dependent kinase inhibitor (CDKI) gene, and in other CDKI genes as contributing to disease pathogenesis in this context. Somatic defects in additional genes, including β-catenin, POT1 and EZH2 may contribute to parathyroid adenoma formation but, for most, their ability to drive parathyroid tumorigenesis remains to be demonstrated experimentally. Further, genetic predisposition to sporadic presentations of parathyroid adenoma appears be conferred by rare, and probably low-penetrance, germline variants in CDKI genes and, perhaps, in other genes such as CASR and AIP. The HRPT2 tumor suppressor gene is commonly mutated in parathyroid carcinoma.

Indexed as

Epigenesis, GeneticGenetic Predisposition to DiseaseHumansMutationNeoplasm ProteinsParathyroid NeoplasmsNeoplasm ProteinsHyperparathyroidismParathyroid adenomaParathyroid carcinoma

Identifiers

PMID24035866
PMCPMC3943641
OpenAlexW1999673670

What OpenQuestion holds

Textmetadata
LicenceTDM
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.