Evidence map›Paper›PMID 20833339›Full record

ReviewBest practice & research. Clinical endocrinology & metabolism2010

Clinical and molecular genetics of parathyroid neoplasms.

John M Sharretts, William F Simonds

Open access · greenAbstract readReview
In one paragraph

Review in Best practice & research. Clinical endocrinology & metabolism, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed, 1 pooled it
6.0field-weighted citation impact, top 3% 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

50 citing papers in PubMed, 1 synthesis or guideline pooled it, 146 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Review
  4. Article
  5. Article
  6. NovelCancers · 2023
    Article
  7. Article
  8. Review
  9. Parathyroid Carcinoma: a Review.Indian journal of surgical oncology · 2022
    Review
  10. Management of Primary Hyperparathyroidism.Indian journal of surgical oncology · 2022
    Review
  11. Article
  12. Article
  13. Review
  14. Genomic Analysis of Abnormal DNAM Methylation in Parathyroid Tumors.International journal of endocrinology · 2022
    Article
  15. Article
  16. Review
  17. Review
  18. Article
  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.

John M SharrettsMetabolic Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bldg. 10 Room 8C-101, 10 Center Dr. MSC 1752 Bethesda, MD 20892-1752, USA. sharrettsj@niddk.nih.gov
William F Simonds
National Institute of Diabetes and Digestive and Kidney Diseases · US

Funding

Clinical Investigation of FIHP, Parathyroid Cancer & the HPT-JT SyndromeZIADK043012 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI SIMONDS, WILLIAM F · 2009 to 2025
$4.3M
Mechanism of Action of the HRPT2 Tumor Suppressor Gene Product ParafibrominZIADK043320 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI SIMONDS, WILLIAM F · 2009 to 2017
$4.0M
Investigation of Familial Isolated Hyperparathyroidism aZ01DK043012 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI SIMONDS, WILLIAM F · 2002 to 2008
$534k
Intramural NIH HHS Z01 DK043012
6 · The paper itself

Abstract

Primary hyperparathyroidism (HPT) results from the excessive secretion of parathyroid hormone from parathyroid tumours. While most HPT is sporadic, it is associated with a familial syndrome in a minority of cases. The study of these syndromes has helped define the pathophysiology of both familial and sporadic parathyroid neoplasms. Investigation of kindred with multiple endocrine neoplasia type 1 (MEN1) and the hyperparathyroidism-jaw tumour syndrome (HPT-JT) led to the discovery of the tumour suppressor genes MEN1 and HRPT2. We now recognise that somatic mutations in MEN1 and HRPT2 tumour suppressor genes are frequent events in sporadic parathyroid adenomas and carcinomas, respectively. Parathyroid tumours in the MEN2A syndrome result from mutational activation of the RET oncogene. The CCND1/PRAD1 oncogene was discovered by analysis of sporadic parathyroid tumours. Studies of familial isolated HPT and analysis of chromosomal loss and gain in parathyroid tumours suggest that other genes relevant to parathyroid neoplasia await identification.

Indexed as

FemaleHumansHyperparathyroidism, PrimaryMaleMultiple Endocrine Neoplasia Type 1Parathyroid HormoneParathyroid NeoplasmsProto-Oncogene Proteins c-retTumor Suppressor ProteinsCDC73 protein, humanParathyroid HormoneProto-Oncogene Proteins c-retRET protein, humanTumor Suppressor Proteins

Identifiers

PMID20833339
PMCPMC2939004
OpenAlexW2087730167

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.