Evidence map›Paper›PMID 22586128›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2012

The polymorphism rs944289 predisposes to papillary thyroid carcinoma through a large intergenic noncoding RNA gene of tumor suppressor type.

Jaroslaw Jendrzejewski, Huiling He, Hanna S Radomska, Wei Li, Jerneja Tomsic, Sandya Liyanarachchi, Ramana V Davuluri, Rebecca Nagy, Albert de la Chapelle

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 155 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
155citing papers in PubMed, 4 pooled it
8.5field-weighted citation impact, top 2% 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

155 citing papers in PubMed, 4 syntheses or guidelines pooled it, 251 citations in OpenAlex.

  1. Pooled it
  2. Perspectives of long non-coding RNAs in cancer.Molecular biology reports · 2017
    Pooled it
  3. Pooled it
  4. Pooled it
  5. Review
  6. Article
  7. Review
  8. Review
  9. Review
  10. Radiation-Related Thyroid Cancer.Endocrine reviews · 2024
    Review
  11. Review
  12. Review
  13. Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Genetic susceptibility to hereditary non-medullary thyroid cancer.Hereditary cancer in clinical practice · 2022
    Review
  20. Article

95 more citing papers are in PubMed but not listed here.

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

9 authors at 3 institutions in 1 country.

Jaroslaw JendrzejewskiHuman Cancer Genetics Program, Comprehensive Cancer Center, The Ohio State University, Columbus, OH 43210, USA.
Huiling He
Hanna S Radomska
Wei Li
Jerneja Tomsic
Sandya Liyanarachchi
Ramana V Davuluri
Rebecca Nagy
Albert de la Chapelle
The Ohio State University · USCancer Genetics (United States) · USThe Wistar Institute · US

Funding

Translational Therapeutics Research Program (TT)P30CA016058 · NCI · OHIO STATE UNIVERSITY · PI Tasleem J Padamsee · 1985 to 2026
$132.3M
Selective Modulation of Thyroidal RadioiodineP01CA124570 · NCI · OHIO STATE UNIVERSITY · PI RINGEL, MATTHEW D · 2008 to 2017
$23.4M
NCI NIH HHS P01 CA124570NCI NIH HHS P01CA124570NCI NIH HHS P30 CA016058NCI NIH HHS P30CA16058
6 · The paper itself

Abstract

A genome-wide association study of papillary thyroid carcinoma (PTC) pinpointed two independent SNPs (rs944289 and rs965513) located in regions containing no annotated genes (14q13.3 and 9q22.33, respectively). Here, we describe a unique, long, intergenic, noncoding RNA gene (lincRNA) named Papillary Thyroid Carcinoma Susceptibility Candidate 3 (PTCSC3) located 3.2 kb downstream of rs944289 at 14q.13.3 and the expression of which is strictly thyroid specific. By quantitative PCR, PTCSC3 expression was strongly down-regulated (P = 2.84 × 10(-14)) in thyroid tumor tissue of 46 PTC patients and the risk allele (T) was associated with the strongest suppression (genotype [TT] (n = 21) vs. [CT] (n = 19), P = 0.004). In adjacent unaffected thyroid tissue, the genotype [TT] was associated with up-regulation of PTCSC3 ([TT] (n = 21) vs. [CT] (n = 19), P = 0.034). The SNP rs944289 was located in a binding site for the CCAAT/enhancer binding proteins (C/EBP) α and β. The risk allele destroyed the binding site in silico. Both C/EBPα and C/EBPβ activated the PTCSC3 promoter in reporter assays (P = 0.0009 and P = 0.0014, respectively) and the risk allele reduced the activation compared with the nonrisk allele (C) (P = 0.026 and P = 0.048, respectively). Restoration of PTCSC3 expression in PTC cell line cells (TPC-1 and BCPAP) inhibited cell growth (P = 0.002 and P = 0.019, respectively) and affected the expression of genes involved in DNA replication, recombination and repair, cellular movement, tumor morphology, and cell death. Our data suggest that SNP rs944289 predisposes to PTC through a previously uncharacterized, long intergenic noncoding RNA gene (PTCSC3) that has the characteristics of a tumor suppressor.

Indexed as

Polymorphism, Single NucleotideAnimalsBinding SitesBlotting, NorthernCarcinoma, PapillaryCCAAT-Enhancer-Binding Protein-betaCell Line, TumorCell ProliferationChlorocebus aethiopsChromosomes, Human, Pair 14COS CellsGene Expression ProfilingGene Expression Regulation, NeoplasticGenes, Tumor SuppressorGenetic Predisposition to DiseaseGenotypeCCAAT-Enhancer-Binding Protein-betaRNA, Untranslated

Identifiers

PMID22586128
PMCPMC3365219
OpenAlexW2053255069

What OpenQuestion holds

Textmetadata
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.