ArticlePathology oncology research : POR1997
Clonality of the parathyroid nodules with uremic parathyroid hyperplasia.
Article in Pathology oncology research : POR, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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.
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
1 citing paper in PubMed, 8 citations in OpenAlex.
- Clonal emergence in uremic parathyroid hyperplasia is not related to MEN1 gene abnormality.Japanese journal of cancer research : Gann · 1999Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Clonal assessment suggests that most parathyroid adenomas and a subset of uremic parathyroid hyperplasia are monoclonal. A weakness that remains in the prior clonal studies is assessing the clonal status of the tissue fragments containing multiple nodules rather than a single nodule emerging in the uremic parathyroid hyperplasia. We applied the X chromosome-linked phosphoglycerate kinase (PGK) gene inactivation assay method for clonality to study individual nodules. Materials were obtained from 31 cases with parathyroid adenoma and 16 with uremic parathyroid hyperplasia. 17 cases were heterozygous in the PGK-1 locus. We were able to assess the clonality of 10 parathyroid adenomas and 7 hyperplastic glands. Monoclonality was demonstrable in 9 of the 10 parathyroid adenomas and in 4 of the 7 hyperplastic glands. Further analysis of 11 individual nodules microdissected from 3 monoclonal and 1 polyclonal hyperplastic glands revealed that 6 nodules were monoclonal and 5 were polyclonal. Nodules arising in a hyperplastic gland could be of monoclonal or polyclonal origin. Polyclonal and monoclonal nodules coexisted within single glands. Our findings indicate a progression from generalized hyperplasia to a monoclonal tumor in uremic parathyroid hyperplasia. Comparing clonality with the parathyroid hormone (PTH) immunoreactivity and histological features, we found that monoclonal nodules showed a homogeneous immunoreactivity against PTH antibody, whereas most of the polyclonal nodules showed a heterogeneous staining. Classic morphological criteria alone was inadequate to distinguish a monoclonal from a polyclonal nodule.
Identifiers
What OpenQuestion holds
Registered trials
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.