Trial reportClinical medicine & research2012
Evaluation of a mitochondrial DNA mutation in maternally inherited and sporadic cases of Dupuytren disease.
Trial report in Clinical medicine & research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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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.
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.
Who cites it
4 citing papers in PubMed, 10 citations in OpenAlex.
- The Effect of Shock Wave Therapy on Improving the Symptoms and Function of Patients with Dupuytren's Contracture.Advanced biomedical research · 2022Article
- The presence of highly disruptive 16S rRNA mutations in clinical samples indicates a wider role for mutations of the mitochondrial ribosome in human disease.Mitochondrion · 2015Article
- RNA sequencing reveals a depletion of collagen targeting microRNAs in Dupuytren's disease.BMC medical genomics · 2015Article
- Structure of the large ribosomal subunit from human mitochondria.Science (New York, N.Y.) · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
objectiveThe purpose was to test the hypothesis that Dupuytren disease (DD) is associated with a previously reported mutation in mitochondrial DNA at position 2839.
methodsTwo hundred sixty-nine cases of DD and an equal number of matched controls were identified in Marshfield Clinic's Personalized Medicine Research Project (PMRP). Clinical data used to describe the cohort were abstracted from the electronic medical records of the population. Genetic analysis of all the cases and controls was done using a custom synthesis TaqMan assay, while genetic analysis of sixteen of the above cases with a familial history of DD was performed by mitochondrial DNA sequencing at position C2839A.
resultsCases and controls were evenly distributed with 167 (62%) men and 102 (38%) women. The majority, 264 (98%) of the cases and controls were white non-Hispanic. Of the 269 cases, 16 were found to have a familial history of DD. Two cases had a maternal history, eight a paternal history, five an affected sibling, and one a paternal grandfather. All cases and controls were found to have only the C allele at the site of the reported mitochondrial C2839A polymorphism.
conclusionsThe previously reported mitochondrial mutation was not present in our small, maternally inherited cohort or in the total population of 538 cases and controls. This finding does not support the reported incidence of this polymorphism in 90% of the affected population with a maternal inheritance, and calls into question the role of the C2839A mitochondrial DNA polymorphism in familial or sporadic cases of DD.
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Registered trials
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