Evidence map›Paper›PMID 17916247›Full record

ArticleBMC endocrine disorders2007

Mitochondrial DNA mutations in oxyphilic and chief cell parathyroid adenomas.

Jessica Costa-Guda, Takehiko Tokura, Sanford I Roth, Andrew Arnold

Open access · goldAbstract read
In one paragraph

Article in BMC endocrine disorders, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

20 citing papers in PubMed, 53 citations in OpenAlex.

  1. Article
  2. Observational
  3. Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Mitochondrial DNA somatic mutation in cancer.Toxicological research · 2014
    Article
  12. Review
  13. Review
  14. Relevance of mitochondrial genetics and metabolism in cancer development.Cold Spring Harbor perspectives in biology · 2013
    Review
  15. Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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 2 institutions in 1 country.

Jessica Costa-GudaCenter for Molecular Medicine, University of Connecticut School of Medicine, 263 Farmington Ave, Farmington, Connecticut 06030-3101, USA. costa@nso2.uchc.edu
Takehiko Tokura
Sanford I Roth
Andrew Arnold
University of Connecticut · USMassachusetts General Hospital · US

Funding

SKELETAL, CRANOFACIAL AND ORAL BIOLOGY TRAIINING GRANTT32DE007302 · NIDCR · UNIVERSITY OF CONNECTICUT SCH OF MED/DNT · PI LURIE, ALAN GORDON · 1996 to 2010
$6.1M
NIDCR NIH HHS T32 DE007302
6 · The paper itself

Abstract

backgroundThe potential pathogenetic significance of mitochondrial DNA (mtDNA) mutations in tumorigenesis is controversial. We hypothesized that benign tumorigenesis of a slowly replicating tissue like the human parathyroid might constitute an especially fertile ground on which a selective advantage conferred by mtDNA mutation could be manifested and might contribute to the oxyphilic phenotype observed in a subset of parathyroid tumors.

methodsWe sought acquired mitochondrial DNA mutations by sequencing the entire 16.6 kb mitochondrial genome of each of thirty sporadic parathyroid adenomas (18 chief cell and 12 oxyphil cell), eight independent, polyclonal, parathyroid primary chief cell hyperplasias plus corresponding normal control samples, five normal parathyroid glands, and one normal thyroid gland.

resultsTwenty-seven somatic mutations were identified in 15 of 30 (9 of 12 oxyphil adenomas, 6 of 18 chief cell) parathyroid adenomas studied. No somatic mutations were observed in the hyperplastic parathyroid glands.

conclusionFeatures of the somatic mutations suggest that they may confer a selective advantage and contribute to the molecular pathogenesis of parathyroid adenomas. Importantly, the statistically significant differences in mutation prevalence in oxyphil vs. chief cell adenomas also suggest that mtDNA mutations may contribute to the oxyphil phenotype.

Identifiers

PMID17916247
PMCPMC2099428
OpenAlexW2014256505

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Registered trials

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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.