Evidence map›Paper›PMID 16434963›Full record

ArticleOncogene2006

Thyroid hormone receptors mutated in liver cancer function as distorted antimorphs.

I H Chan, M L Privalsky

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

Article in Oncogene, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

29 citing papers in PubMed, 61 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Thyroid hormone actions in liver cancer.Cellular and molecular life sciences : CMLS · 2013
    Review
  12. Article
  13. Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. A case-control study of levothyroxine and the risk of colorectal cancer.Journal of the National Cancer Institute · 2010
    Article
  20. Article
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

2 authors at 1 institution in 1 country.

I H ChanSection of Microbiology, University of California at Davis, 95616, USA.
M L Privalsky
University of California, Davis · US

Funding

MECHANISM OF ACTION OF THE VERB A ONCOGENE OF AEVR37CA053394 · NCI · UNIVERSITY OF CALIFORNIA DAVIS · PI PRIVALSKY, MARTIN L. · 1994 to 2012
$3.4M
NCI NIH HHS R37 CA053394NCI NIH HHS R37-CA53394
6 · The paper itself

Abstract

Aberrant thyroid hormone receptors (TRs) are found in over 70% of the human hepatocellular carcinomas (HCCs) analysed. To better understand the role(s) of these TR mutants in this neoplasia, we analysed a panel of HCC mutant receptors for their molecular properties. Virtually all HCC-associated TR mutants tested retained the ability to repress target genes in the absence of T3, yet were impaired in T3-driven gene activation and functioned as dominant-negative inhibitors of wild-type TR activity. Intriguingly, the HCC TRalpha1 mutants exerted dominant-negative interference at all T3 concentrations tested, whereas the HCC TRbeta1 mutants were dominant-negatives only at low and intermediate T3 concentrations, reverting to transcriptional activators at higher hormone levels. The relative affinity for the SMRT versus N-CoR corepressors was detectably altered for several of the HCC mutant TRs, suggesting changes in corepressor preference and recruitment compared to wild type. Several of the TRalpha HCC mutations also altered the DNA recognition properties of the encoded receptors, indicating that these HCC TR mutants may regulate a distinct set of target genes from those regulated by wild-type TRs. Finally, whereas wild-type TRs interfere with c-Jun/AP-1 function in a T3-dependent fashion and suppress anchorage-independent growth when ectopically expressed in HepG2 cells, at least certain of the HCC mutants did not exert these inhibitory properties. These alterations in transcriptional regulation and DNA recognition appear likely to contribute to oncogenesis by reprogramming the differentiation and proliferative properties of the hepatocytes in which the mutant TRs are expressed.

Indexed as

Carcinoma, HepatocellularCell Line, TumorCloning, MolecularDNA-Binding ProteinsElectrophoretic Mobility Shift AssayGene ExpressionGene Expression RegulationHumansLiver NeoplasmsMutationNuclear Receptor Co-Repressor 2Receptors, Thyroid HormoneRepressor ProteinsTranscriptional ActivationTransfectionTriiodothyronineDNA-Binding ProteinsNCOR2 protein, humanNuclear Receptor Co-Repressor 2Receptors, Thyroid HormoneRepressor ProteinsTriiodothyronine

Identifiers

PMID16434963
PMCPMC2701908
OpenAlexW2049253602

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.