Evidence map›Paper›PMID 23435613›Full record

ArticleEndocrine2013

Allelic imbalance in sporadic parathyroid carcinoma and evidence for its de novo origins.

Jessica Costa-Guda, Yasuo Imanishi, Nallasivam Palanisamy, Norihiko Kawamata, H Phillip Koeffler, R S K Chaganti, Andrew Arnold

Abstract read
In one paragraph

Article in Endocrine, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

16 citing papers in PubMed, 36 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Clinical and Molecular Genetics of Primary Hyperparathyroidism.Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et metabolisme · 2020
    Review
  11. Journal of the Endocrine Society · 2020
    Article
  12. JBMR plus · 2020
    Article
  13. Article
  14. Article
  15. Update on parathyroid carcinoma.Journal of endocrinological investigation · 2016
    Review
  16. 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

7 authors at 4 institutions in 2 countries.

Jessica Costa-GudaUniversity of Connecticut Health Center, Farmington, CT, USA, costa@nso2.uchc.edu.
Yasuo Imanishi
Nallasivam Palanisamy
Norihiko Kawamata
H Phillip Koeffler
R S K Chaganti
Andrew Arnold
Cedars-Sinai Medical Center · USMemorial Sloan Kettering Cancer Center · USUConn Health · USUniversity of Connecticut · 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
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 5T32-DE07302NIDCR NIH HHS F32 DE021307NIDCR NIH HHS T32 DE007302NIDDK NIH HHS DK066411NIDDK NIH HHS R01 DK066411
6 · The paper itself

Abstract

Parathyroid cancer is a rare, clinically aggressive cause of primary hyperparathyroidism, and whether these malignancies generally evolve from pre-existing benign adenomas or arise de novo is unclear. Furthermore, while inactivation of the CDC73 (HRPT2) tumor suppressor gene, encoding parafibromin, is a major contributor, other genes essential to parathyroid carcinogenesis remain unknown. We sought to identify genomic regions potentially harboring such oncogenes or tumor suppressor genes, and to gain insight into the origins and molecular relationship of malignant versus benign parathyroid tumors. We performed genome-wide copy-number and loss of heterozygosity analysis using Affymetrix 50K SNP mapping arrays and/or comparative genomic hybridization on 16 primary parathyroid carcinomas, local recurrences or distant metastases, and matched normal controls, from 10 individuals. Recurrent regions of allelic loss were observed on chromosomes 1p, 3, and 13q suggesting that key parathyroid tumor suppressor genes are located in these chromosomal locations. Recurrent allelic gains were seen on chromosomes 1q and 16, suggesting the presence of parathyroid oncogenes on these chromosomes. Importantly, the most common alteration in benign parathyroid adenomas, loss of 11q, was not found as a recurrent change in the malignant parathyroid tissues. Molecular allelotyping using highly polymorphic microsatellite markers provided further confirmation that the prevalence of 11q loss is markedly and significantly lower in carcinomas as compared with adenomas. Our observations provide molecular support for the concept that sporadic parathyroid cancer usually arises de novo, rather than evolving from a pre-existing typical benign adenoma. Furthermore, these results help direct future investigation to ultimately determine which of the candidate genes in these chromosomal locations make significant contributions to the molecular pathogenesis of parathyroid cancer.

Indexed as

AdenomaAdultAgedAllelic ImbalanceCarcinomaCohort StudiesComparative Genomic HybridizationDNA Copy Number VariationsFemaleHumansHyperparathyroidism, PrimaryMaleMiddle AgedOligonucleotide Array Sequence AnalysisParathyroid NeoplasmsPolymorphism, Single Nucleotide

Identifiers

PMID23435613
PMCPMC3683451
OpenAlexW1992578997

What OpenQuestion holds

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Read underepoch 390

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.